Loading content

Dr Craig Beall

Senior Lecturer

+44 (0)1392 408209

RILD Building 4.06

University of Exeter Medical School, RILD Building, RD&E Hospital Wonford, Barrack Road, Exeter, EX2 5DW, UK

Office hours:

Undergraduate teaching virtual office hours: Fridays 9-11am.

Beallacott Retreat, January 2017

Beallacott Christmas quiz and Secret Santa 2017

Beallacott Retreat 2018

Overview

Follow on Twitter @Craig_Beall

Techniques
Glucose clamping
Electrophysiology
Western blotting
Fixed and live-cell imaging
Enzyme/kinase assays
Calcium imaging
Biosensing (Sarissa probes)

Upcoming Talks

Invited talks/seminars/media engagement
• 11th May 2021: Using Twitter to develop your scientific career
• 24th Sept 2020: European Foundation for the Study of Diabetes; Oral presentation
• 6th June 2019: Rigel Pharmaceuticals, Inc., South San Francisco; Invited seminar
• 24th May 2019: Diabetes UK Gifts in Wills Event - public talk
• 21st February 2019: University of Bath Pharmacology Society
• 12th March 2019: Brain Awareness Week - public talk
• Sept 2018: Vanderbilt University, Diabetes Research and Training Center
• Dec 2017: University of Aberdeen, Institute of Medical Sciences
• Oct 2017: Sidmouth Science Festival: "Why our brains love sugar; in health and disease"
• Sept 2017: Exeter Dementia Day, Rougemont Hotel, Exeter
• Oct 2016: Diabetes UK Exeter group
• Oct 2016: JDRF Discovery Day; Eden Project
• Sept 2016: Diabetes UK Torbay group
• May 2016: Diabetes UK Gifts in Wills; Royal Albert Memorial Museum
• Nov 2015: BBC Radio Devon; Hypoglycaemia awareness week radio interview
• July 2015: Diabetes UK Legacies: Plymouth Aquarium
• Mar 2015: Diabetes UK South West Volunteering conference
• May 2015: Pint of Science Exeter; Beautiful minds team leader and presenter
• Oct 2014: JDRF Patrons event; Armorers Hall, London

Honours and Awards

• 2019: University of Exeter Above and Beyond Award for Collaboration
• 2018: University of Exeter Above and Beyond Award for Challenge; Excellent student feedback in Problem-Based Learning activities
• 2017: University of Exeter Above and Beyond Award for Teaching; Problem-based learning facilitation
• 2016: University of Exeter Above and Beyond Award for Collaboration
• 2012: College of Medicine Staff Poster Prize (1st prize)
• 2011: College of Medicine Staff Poster Prize (1st prize)
• 2003: Awarded Carl Zeiss Prize for Best Laboratory-Based Honours Project and short-listed for the UK-wide Science, Engineering and Technology Student of the Year Award
• 2000: Awarded Schering Group award for Academic Excellence and Dedication to Course (Fife College)

Professional Memberships

• Physiological society (2003-)
• Diabetes UK (2011-)
• Society for Endocrinology (2011-)
• British Society for Neuroendocrinology (2011-)
• British Pharmacological Society (2014-2018)

Qualifications

PhD
BSc(Hons) First Class

Career

Dr Craig Beall completed his degree in Pharmacology (BSc Hons; University of Dundee) in 2003 before obtaining a Wellcome Trust Prize Studentship to undertake doctoral studies in the laboratory of Prof Mike Ashford, University of Dundee. Doctoral studies focused on mechanisms of glucose sensing in pancreatic beta cells and hypothalamic neurons, with a particular focus on AMP-activated protein kinase and ATP-sensitive K+ channels.

Following a year in at the University of Liverpool investigating the role of K+ channels in skeletal muscle insulin sensitivity, Dr Beall moved back to the University of Dundee to work with Professors Rory McCrimmon and Prof Ashford to focus on mechanisms of hypoglycaemia detection. Dr Beall was a recipient of a Juvenile Diabetes Research Foundation postdoctoral fellowship (2010-2013) to develop and establish an in vitro model for investigating the mechanisms of hypothalamic glucose sensing.

Links

ADA 2017, San Diego

Research

Research interests

The Beall laboratory is interested in the integrated physiology of glucose homeostasis and Type 1 and Type 2 Diabetes. This includes regulation of alpha cell function, brain-alpha cell communication, neural regulation of hepatic glucose output and skeletal muscle insulin sensitivity/glucose disposal.

Working with Dr Kate Ellacott, we are also interested in astrocyte-neuron communication during energy excess, such as a high fat diet and whether astrocytes play in a role in regulating feeding behaviour.

In collaboration with Rigel Pharmaceuticals, we are examining whether brain permeable AMPK activators can influence hypoglycaemia glucose counterregulation in diabetes.

In collaboration with Prof Matt Whiteman, we are investigating the anti-hypoglycaemic actions of novel hydrogen sulfide donors in diabetes.

Current Lab Members (as DoS/line manager):
Dr Paul Weightman Potter, Postdoctoral research associate (JDRF postdoctoral fellow)
Dr Ana Miguel Cruz, Postdoctoral research associate
Katie Partridge (Diabetes UK funded PhD student)
Dr Jiping Zhang (MRC funded PhD student)

Second/Co-supervisor:
Asmaa Al-Khalidi (PhD student)
Wyn Firth (PhD student)

Alumni:
Tom Worthington (Placement student, University of Exeter)
Valentina Abba (Placement student; University of Surrey)
Cristina Lumbreras (E3 funded PhD student)
Nicole Morrissey (PhD student, currently a postdoc in Oxford)
Benjamin Hall (PhD student)
Hannah Smithers (Postdoc, Associate lecturer, University of Exeter)
Aishwarya Vaidya (PhD student)
Josephine Robb (PhD student, currently a postdoc in Canada)
Alice Pink (Final Year Research Project student, 2019-20)
Daria Shevtsova (Final Year Research Project student, 2019-20)
Brittannie Willis (BSN funding summer student 2019)
Kealan Jones (U/G final year research project, 2018-19)
Alice Crocker (U/G final year research project, 2018-19)
Lisa Logie (PhD student; University of Dundee; 2015-2018)
Dr Lydia Hanna (postdoctoral researcher)
Julia Vlachaki-Walker, P/T MPhil student/research technician (Diabetes UK)
Chloe Tredgett, professional training year student (2017-18)
Ellie Davis, summer intern (2018)
Dr Yasaman Malekizadeh, postdoctoral research associate (2017-18)
Brad Hoskin, U/G final year research project student (2017-18)
Khalid Bukhashem, U/G final year research project student (2017-18)
William Casasola, U/G final year research project student (2017-18)
Brenda Vescance Caroprese; Physiological Society funded summer student (summer 2017)
Magdalena Kowalska; Alzheimer's Society funded summer studentAimes Somes (U/G laboratory-based project student; summer 2017)
Jade Shoulder, associate researcher
Dr Ashley Nicholls (research assistant. Currently a postdoc at the University of Cambridge)
Amrinder Malhi (British Society for Neuroendocrinology funded summer studentship; 2015; currently an intern at the International Diabetes Federation, London)
Dr Amy Cameron (visiting postdoctoral research fellow; Society for Endocrinology; 2015-16)
Jennie Gabriel (Society for Endocrinology funded summer student; 2014, currently studying for a PhD studying dementia at the University of Dundee).

Research projects

The role of astroglial mitochondrial dysfunction in neurotransmitter recycling during hypoglycaemia in diabetes (European Foundation for the Study of Diabetes/Novo Nordisk Programme 2018-2020)
Does an orally active brain permeable AMPK activator amplify the counterregulatory response to hypoglycaemia in a model of type 1 diabetes; JDRF Innovative Grant (2017-2018)
The role of astroytes in the homeostatic control of food intake; MRC project grant (2016-2019)
Does acute and recurrent insulin-induced hypoglycaemia alter DNA methylation in human neural cells? Novo Nordisk Research Foundation UK; (2016-2017)
Defining the role of hypothalamic astroglia in the regulation of the homeostatic control of food intake; GW4 MRC doctoral training partnership (2016-2019)
Targeting the hypothalamic purinergic system for the regulation of whole body energy homeostasis; Diabetes UK (2013-2018)
Impact of diabetes glucose variability on neural signalling in human brain cells - relationship to dementia risk; Mary Kinross Charitable Trust PhD studentship; collaboration with Prof A Randall, Exeter (2015-2018)
Mechanisms of muscle anabolic resistance in diabetes and ageing; UEMS PhD studentship; collaboration with Dr B Wall, Exeter (2016-2019)

Grants/Funding

JDRF Innovative Grant (2020-2021)
Novonordisk UK Research Foundation (2020-2021; PI: Weightman Potter)
Diabetes UK PhD Studentship (2019-2022)
Diabetes UK Early Career Small Grant (2019)
European Foundation for the Study of Diabetes (2018-2020)
British Society for Neuroendocrinology Research Visit Grant (2017-18)
Physiological Society summer vacation scholarship to Brenda Vescance Caroprese (2017)
Alzheimer's Society biomedical vacation scholarship to Magdalena Kowalska (2017)
University of Exeter Summer vacation scholarship to Brad Hoskin ((2017)
Mary Kinross Charitable Trust PhD Studentship (2015-2018)
British Society for Neuroendocrinology Summer Studentship (Amrinder Malhi; summer 2015)
Diabetes UK RD Lawrence Fellowship (2013-2018)
Society for Endocrinology Early Career Grant (2014-2015)
Society for Endocrinology Summer Studentship (Jennie Gabriel; summer 2014)
Anonymous Trust (PI; Co-I: Professors Ashford & McCrimmon, University of Dundee, 2014-2015)
British Society for Neuroendocrinology (PI; 2013-2014)
Tenovus Scotland (PI; Co-I: Professors Ashford & Mccrimmon, 013-2014)
Anonymous Trust (2012-2013)
Juvenile Diabetes Research Foundation Postdoctoral Fellowship (2010-2013)

Research networks

Collaborations:

Dr Kate Ellacott (University of Exeter; neural mechanisms of energy sensing)
Dr Simon Shaw (Rigel Pharmaceuticals, Inc, CA, USA).
Prof Matt Whiteman (University of Exeter)

Anyone interested in working in the Beall laboratory, either undergraduate, postgraduate or postdoctoral, please get in touch with Dr Beall.

Research grants

2017 Medical Research Council
Title: IMPC - Understanding the role of 18kDa Translocator protein (TSPO) in the regulation of energy homeostasis in mice
2016 Medical Research Council
Title: The role of hypothalamic astrocytes in the homeostatic regulation of feeding behaviour
2016 Medical Research Council
GW4 MRC Doctoral Training Partnership PhD Studentship Title: Defining the contribution of hypothalamic astroglia to the homeostatic regulation of food intake
2016 Juvenile Diabetes Research Foundation
Title: Does an orally active, brain permeable AMPK activator improve hypoglycemia counterregulation in type 1 diabetes?

Publications

Key publications | Publications by category | Publications by year

Key publications

Weightman Potter P, Vlachaki Walker J, Robb J, Chilton J, Williamson R, Randall A, Ellacott K, Beall C (In Press). Basal fatty acid oxidation increases after recurrent low glucose in human primary astrocytes. Diabetologia

Cruz AM, Partridge KM, Malekizadeh Y, Vlachaki Walker JM, Weightman Potter PG, Pye KR, Shaw SJ, Ellacott KLJ, Beall C (2021). Brain Permeable AMP-Activated Protein Kinase Activator R481 Raises Glycaemia by Autonomic Nervous System Activation and Amplifies the Counterregulatory Response to Hypoglycaemia in Rats. Frontiers in Endocrinology, 12

AimWe evaluated the efficacy of a novel brain permeable “metformin-like” AMP-activated protein kinase activator, R481, in regulating glucose homeostasis.Materials and MethodsWe used glucose sensing hypothalamic GT1-7 neuronal cells and pancreatic αTC1.9 α-cells to examine the effect of R481 on AMPK pathway activation and cellular metabolism. Glucose tolerance tests and hyperinsulinemic-euglycemic and hypoglycemic clamps were used in Sprague-Dawley rats to assess insulin sensitivity and hypoglycemia counterregulation, respectively.ResultsIn vitro, we demonstrate that R481 increased AMPK phosphorylation in GT1-7 and αTC1.9 cells. In Sprague-Dawley rats, R481 increased peak glucose levels during a glucose tolerance test, without altering insulin levels or glucose clearance. The effect of R481 to raise peak glucose levels was attenuated by allosteric brain permeable AMPK inhibitor SBI-0206965. This effect was also completely abolished by blockade of the autonomic nervous system using hexamethonium. During hypoglycemic clamp studies, R481 treated animals had a significantly lower glucose infusion rate compared to vehicle treated controls. Peak plasma glucagon levels were significantly higher in R481 treated rats with no change to plasma adrenaline levels. In vitro, R481 did not alter glucagon release from αTC1.9 cells, but increased glycolysis. Non brain permeable AMPK activator R419 enhanced AMPK activity in vitro in neuronal cells but did not alter glucose excursion in vivo.ConclusionsThese data demonstrate that peripheral administration of the brain permeable “metformin-like” AMPK activator R481 increases blood glucose by activation of the autonomic nervous system and amplifies the glucagon response to hypoglycemia in rats. Taken together, our data suggest that R481 amplifies the counterregulatory response to hypoglycemia by a central rather than a direct effect on the pancreatic α-cell. These data provide proof-of-concept that central AMPK could be a target for future drug development for prevention of hypoglycemia in diabetes.

Abstract.

MacDonald AJ, Yang YHC, Cruz AM, Beall C, Ellacott KLJ (2021). Brain-Body Control of Glucose Homeostasis—Insights from Model Organisms. Frontiers in Endocrinology, 12 Abstract.

Cruz AM, Beall C (2020). Extracellular ATP Increases Glucose Metabolism in Skeletal Muscle Cells in a P2 Receptor Dependent Manner but Does Not Contribute to Palmitate-Induced Insulin Resistance. Frontiers in Physiology, 11

Robb JL, Morrissey NA, Weightman Potter PG, Smithers HE, Beall C, Ellacott KLJ (2020). Immunometabolic Changes in Glia – a Potential Role in the Pathophysiology of Obesity and Diabetes. Neuroscience, 447, 167-181.

Robb JL, Hammad NA, Weightman Potter PG, Chilton JK, Beall C, Ellacott KLJ (2020). The metabolic response to inflammation in astrocytes is regulated by nuclear factor‐kappa B signaling. Glia, 68(11), 2246-2263.

Publications by category

Journal articles

Potter PGW, Washer S, Jeffries AR, Holley JE, Gutowski NJ, Dempster E, Beall C (In Press). Analysis of the transcriptome and DNA methylome in response to acute and recurrent low glucose in human primary astrocytes. Abstract.

Cruz AM, Malekizadeh Y, Vlachaki Walker JM, Weightman Potter PG, Pye K, Shaw SJ, Ellacott KLJ, Beall C (In Press). Brain permeable AMPK activator R481 raises glycemia by autonomic nervous system activation and amplifies the counterregulatory response to hypoglycemia in rats. Abstract.

Weightman Potter PG, Walker JMV, Robb JL, Chilton JK, Williamson R, Randall A, Ellacott KLJ, Beall C (In Press). Human primary astrocytes increase basal fatty acid oxidation following recurrent low glucose to maintain intracellular nucleotide levels. Abstract.

MacDonald AJ, Holmes FE, Beall C, Pickering AE, Ellacott KLJ (In Press). Regulation of food intake by astrocytes in the brainstem dorsal vagal complex. Abstract.

Weightman Potter PG, Ellacott KLJ, Randall AD, Beall C (2022). Glutamate Prevents Altered Mitochondrial Function Following Recurrent Low Glucose in Hypothalamic but Not Cortical Primary Rat Astrocytes. Cells, 11(21), 3422-3422. Abstract.

Morrissey NA, Beall C, Ellacott KLJ (2021). Absence of the mitochondrial translocator protein 18 kDa in mice does not affect body weight or food intake responses to altered energy availability. Journal of Neuroendocrinology, 33(9).

Weightman Potter PG, Washer SJ, Jeffries AR, Holley JE, Gutowski NJ, Dempster EL, Beall C (2021). Attenuated Induction of the Unfolded Protein Response in Adult Human Primary Astrocytes in Response to Recurrent Low Glucose. FRONTIERS IN ENDOCRINOLOGY, 12 Author URL.

Abstract.

MacDonald AJ, Yang YHC, Cruz AM, Beall C, Ellacott KLJ (2021). Brain-Body Control of Glucose Homeostasis—Insights from Model Organisms. Frontiers in Endocrinology, 12 Abstract.

Potter PW, Randall A, Ellacott K, Beall C (2021). Rat primary hypothalamic, but not cortical, astrocytes increase use of glutamate to fuel metabolism after recurrent low glucose. Endocrine Abstracts

Hanna L, Kawalek TJ, Beall C, Ellacott KLJ (2020). Changes in neuronal activity across the mouse ventromedial nucleus of the hypothalamus in response to low glucose: Evaluation using an extracellular multi‐electrode array approach. Journal of Neuroendocrinology, 32(3).

MacDonald AJ, Holmes FE, Beall C, Pickering AE, Ellacott KLJ (2020). Regulation of food intake by astrocytes in the brainstem dorsal vagal complex. Glia, 68(6), 1241-1254.

CRUZ AML, MALEKIZADEH Y, VLACHAKI WALKER JM, SHAW SJ, ELLACOTT KL, BEALL C (2019). 119-OR: Amplified Glucagon Response to Hypoglycemia following AMP-Activated Protein Kinase (AMPK) Activator R481 Treatment in Healthy Rats. Diabetes, 68(Supplement_1).

WEIGHTMAN POTTER PG, WASHER SJ, JEFFRIES A, DEMPSTER EL, BEALL C (2019). 401-P: Acute Low Glucose Alters Human Primary Astrocyte Expression of Endoplasmic Reticulum Stress and Mitochondrial Associated Genes, Which is Blunted after Recurrent Low Glucose. Diabetes, 68(Supplement_1).

MacDonald AJ, Robb JL, Morrissey NA, Beall C, Ellacott KLJ (2019). Astrocytes in neuroendocrine systems: an overview. J Neuroendocrinol, 31(5). Abstract. Author URL.

Logie L, Lees Z, Allwood JW, McDougal G, Beall C, Rena G (2018). Regulation of hepatic glucose production and AMPK by AICAR but not metformin depends on drug uptake through the equilibrative nucleoside transporter 1 (ENT1). Diabetes, Obesity and Metabolism, (In press)

Vlachaki Walker JM, Robb JL, Cruz AM, Malhi A, Weightman Potter PG, Ashford MLJ, McCrimmon RJ, Ellacott KLJ, Beall C (2017). AMP-activated protein kinase (AMPK) activator A-769662 increases intracellular calcium and ATP release from astrocytes in an AMPK-independent manner. Diabetes, Obesity and Metabolism, 19(7), 997-1005. Abstract.

Beall C, Hanna L, Ellacott KLJ (2017). CNS Targets of Adipokines. Compr Physiol, 7(4), 1359-1406. Abstract. Author URL.

Dadak S, Beall C, Vlachaki Walker JM, Soutar MPM, McCrimmon RJ, Ashford MLJ (2017). Oleate induces K ATP channel-dependent hyperpolarization in mouse hypothalamic glucose-excited neurons without altering cellular energy charge. Neuroscience, 346, 29-42.

Jeffery N, Richardson S, Beall C, Harries LW (2017). The species origin of the cellular microenvironment influences markers of beta cell fate and function in EndoC-βH1 cells. Experimental Cell Research, 361(2), 284-291.

Cameron AR, Morrison VL, Levin D, Mohan M, Forteath C, Beall C, McNeilly AD, Balfour DJK, Savinko T, Wong AKF, et al (2016). Anti-Inflammatory Effects of Metformin Irrespective of Diabetes Status. Circ Res, 119(5), 652-665.

RATIONALE: the diabetes mellitus drug metformin is under investigation in cardiovascular disease, but the molecular mechanisms underlying possible benefits are poorly understood. OBJECTIVE: Here, we have studied anti-inflammatory effects of the drug and their relationship to antihyperglycemic properties. METHODS AND RESULTS: in primary hepatocytes from healthy animals, metformin and the IKKβ (inhibitor of kappa B kinase) inhibitor BI605906 both inhibited tumor necrosis factor-α-dependent IκB degradation and expression of proinflammatory mediators interleukin-6, interleukin-1β, and CXCL1/2 (C-X-C motif ligand 1/2). Metformin suppressed IKKα/β activation, an effect that could be separated from some metabolic actions, in that BI605906 did not mimic effects of metformin on lipogenic gene expression, glucose production, and AMP-activated protein kinase activation. Equally AMP-activated protein kinase was not required either for mitochondrial suppression of IκB degradation. Consistent with discrete anti-inflammatory actions, in macrophages, metformin specifically blunted secretion of proinflammatory cytokines, without inhibiting M1/M2 differentiation or activation. In a large treatment naive diabetes mellitus population cohort, we observed differences in the systemic inflammation marker, neutrophil to lymphocyte ratio, after incident treatment with either metformin or sulfonylurea monotherapy. Compared with sulfonylurea exposure, metformin reduced the mean log-transformed neutrophil to lymphocyte ratio after 8 to 16 months by 0.09 U (95% confidence interval, 0.02-0.17; P=0.013) and increased the likelihood that neutrophil to lymphocyte ratio would be lower than baseline after 8 to 16 months (odds ratio, 1.83; 95% confidence interval, 1.22-2.75; P=0.00364). Following up these findings in a double-blind placebo controlled trial in nondiabetic heart failure (trial registration: NCT00473876), metformin suppressed plasma cytokines including the aging-associated cytokine CCL11 (C-C motif chemokine ligand 11). CONCLUSION: We conclude that anti-inflammatory properties of metformin are exerted irrespective of diabetes mellitus status. This may accelerate investigation of drug utility in nondiabetic cardiovascular disease groups. CLINICAL TRIAL REGISTRATION: Name of the trial registry: TAYSIDE trial (Metformin in Insulin Resistant Left Ventricular [LV] Dysfunction). URL: https://www.clinicaltrials.gov. Unique identifier: NCT00473876.

Abstract. Author URL.

Yavari A, Stocker CJ, Ghaffari S, Wargent ET, Steeples V, Czibik G, Pinter K, Bellahcene M, Woods A, Martínez de Morentin PB, et al (2016). Chronic Activation of γ2 AMPK Induces Obesity and Reduces β Cell Function. Cell Metab, 23(5), 821-836. Abstract. Author URL.

Haythorne E, Hamilton DL, Findlay JA, Beall C, McCrimmon RJ, Ashford MLJ (2016). Chronic exposure to KATP channel openers results in attenuated glucose sensing in hypothalamic GT1-7 neurons. Neuropharmacology, 111, 212-222.

Walker JV, Ashford MLJ, McCrimmon RJ, Beall C (2016). Exposure of astrocytes to recurrent low glucose delays AMPK phosphorylation and alters ATP and lactate release. DIABETIC MEDICINE, 33, 54-54. Author URL.

Beall C, Walker JMV, Ashford MLJ, McCrimmon RJ (2015). A critical role for AMP-activated protein kinase in regulation of gliotransmitter release from astrocytes. DIABETIC MEDICINE, 32, 62-62. Author URL.

Cameron AR, Morrison V, McNeilly AD, Forteath C, Beall C, Stewart CA, Balfour DJK, Sutherland CD, Sakamoto K, Fagerholm SC, et al (2015). Anti-inflammatory effects of metformin. DIABETIC MEDICINE, 32, 54-55. Author URL.

Cameron A, Forteath C, Beall C, Rena G (2015). Anti-inflammatory effects of metformin and their relationship to the therapeutic action of the drug. Endocrine Abstracts

Walker JV, Ashford M, McCrimmon R, Beall C (2015). Characterisation of the astrocytic response to acute and recurrent hypoglycaemia. Endocrine Abstracts

Walker JMV, Gabriel J, Ashford MLJ, McCrimmon RJ, Beall C (2015). Modulation of astrocytic lactate release during hypoglycaemia by AMP-activated protein kinase and noradrenaline. DIABETIC MEDICINE, 32, 62-63. Author URL.

Hamilton DL, Beall C, Jeromson S, Chevtzoff C, Cuthbertson DJ, Ashford MLJ (2014). Kv1.3 inhibitors have differential effects on glucose uptake and AMPK activity in skeletal muscle cell lines and mouse ex vivo skeletal muscle. J Physiol Sci, 64(1), 13-20. Abstract. Author URL.

Beall C, Watterson KR, McCrimmon RJ, Ashford MLJ (2013). AMPK modulates glucose-sensing in insulin-secreting cells by altered phosphotransfer to KATP channels. J Bioenerg Biomembr, 45(3), 229-241. Abstract. Author URL.

Beall C, Haythorne E, Fan X, Du Q, Jovanovic S, Sherwin RS, Ashford MLJ, McCrimmon RJ (2013). Continuous hypothalamic K(ATP) activation blunts glucose counter-regulation in vivo in rats and suppresses K(ATP) conductance in vitro. Diabetologia, 56(9), 2088-2092. Abstract. Author URL.

Ashford M, Beall C, McCrimmon R (2012). Hypoglycaemia: exercise for the brain?. J Neuroendocrinol, 24(10), 1365-1366. Abstract. Author URL.

Beall C, Hamilton DL, Gallagher J, Logie L, Wright K, Soutar MP, Dadak S, Ashford FB, Haythorne E, Du Q, et al (2012). Mouse hypothalamic GT1-7 cells demonstrate AMPK-dependent intrinsic glucose-sensing behaviour. Diabetologia, 55(9), 2432-2444.

AIMS/HYPOTHESIS: Hypothalamic glucose-excited (GE) neurons contribute to whole-body glucose homeostasis and participate in the detection of hypoglycaemia. This system appears defective in type 1 diabetes, in which hypoglycaemia commonly occurs. Unfortunately, it is at present unclear which molecular components required for glucose sensing are produced in individual neurons and how these are functionally linked. We used the GT1-7 mouse hypothalamic cell line to address these issues. METHODS: Electrophysiological recordings, coupled with measurements of gene expression and protein levels and activity, were made from unmodified GT1-7 cells and cells in which AMP-activated protein kinase (AMPK) catalytic subunit gene expression and activity were reduced. RESULTS: Hypothalamic GT1-7 neurons express the genes encoding glucokinase and ATP-sensitive K(+) channel (K(ATP)) subunits K ( ir ) 6.2 and Sur1 and exhibit GE-type glucose-sensing behaviour. Lowered extracellular glucose concentration hyperpolarised the cells in a concentration-dependent manner, an outcome that was reversed by tolbutamide. Inhibition of glucose uptake or metabolism hyperpolarised cells, showing that energy metabolism is required to maintain their resting membrane potential. Short hairpin (sh)RNA directed to Ampkα2 (also known as Prkaa2) reduced GT1-7 cell AMPKα2, but not AMPKα1, activity and lowered the threshold for hypoglycaemia-induced hyperpolarisation. shAmpkα1 (also known as Prkaa1) had no effect on glucose-sensing or AMPKα2 activity. Decreased uncoupling protein 2 (Ucp2) mRNA was detected in AMPKα2-reduced cells, suggesting that AMPKα2 regulates UCP2 levels. CONCLUSIONS/INTERPRETATION: We have demonstrated that GT1-7 cells closely mimic GE neuron glucose-sensing behaviour, and reducing AMPKα2 blunts their responsiveness to hypoglycaemic challenge, possibly by altering UCP2 activity. These results show that suppression of AMPKα2 activity inhibits normal glucose-sensing behaviour and may contribute to defective detection of hypoglycaemia.

Abstract. Author URL.

Beall C, Ashford ML, McCrimmon RJ (2012). The physiology and pathophysiology of the neural control of the counterregulatory response. Am J Physiol Regul Integr Comp Physiol, 302(2), R215-R223. Abstract. Author URL.

Beall C, Piipari K, Al-Qassab H, Smith MA, Parker N, Carling D, Viollet B, Withers DJ, Ashford MLJ (2010). Loss of AMP-activated protein kinase alpha2 subunit in mouse beta-cells impairs glucose-stimulated insulin secretion and inhibits their sensitivity to hypoglycaemia. Biochem J, 429(2), 323-333. Abstract. Author URL.

Conferences

Partridge KM, Morgan NG, Ellacott KLJ, Beall C (2022). Recurrent low glucose exposure (RLG) induces intrinsic metabolic adaptations in pancreatic alphaTC1.9 cells. Author URL.

Beall C, Cruz AM, Potter PGW, Walker JMV, Malekizadeh Y, Pye KR, Shaw SJ, Ellacott KLJ (2020). Amp-activated protein kinase (AMPK) activator R481 amplifies the glucagon response to hypoglycaemia without worsening hyperglycaemia in diabetic rats. Author URL.

Cruz A, Potter PW, Pye K, Shaw S, Ellacott K, Beall C (2020). Brain permeable AMPK activator R481 acutely raises blood glucose by activating the autonomic nervous system without altering insulin sensitivity. Author URL.

Potter PGW, Randall A, Beall C (2020). Cellular metabolism and Ca2+ signalling are modified differentially in rat hypothalamic and cortical primary astrocytes by acute and recurrent low glucose. Author URL.

Cruz AM, Beall C (2020). Exogenous ATP promotes glucose uptake and utilisation in skeletal muscle cells but does not alter glucose clearance in vivo. Author URL.

Robb JL, Hammad NA, Beall C, Ellacott KL (2019). A role for translocator protein 18kDa (TSPO) in immunometabolic regulation in astrocytes. Author URL.

Cruz AM, Malekizadeh Y, Walker JMV, Shaw S, Ellacott KLJ, Beall C (2019). AMP-activated protein kinase (AMPK) activator R481 improves the counterregulatory response to hypoglycaemia by amplifying glucagon release in healthy rats. Author URL.

Cruz AML, Malekizadeh Y, Vlachaki Walker J, Ellacott K, Shaw S, Beall C (2019). Amplified Glucagon Response to Hypoglycemia following AMP-Activated Protein Kinase (AMPK) Activator R481 Treatment in Healthy Rats. American Diabetes Association. 7th - 11th Jun 2019. Abstract.

Hall BC, Beall C, Randall AD (2018). Alzheimer's disease drug Memantine inhibits Adenosine triphosphate (ATP)-sensitive potassium (KATP) channel activation in hypothalamic GT1-7 cells. Author URL.

Logie L, Beall C, Rena G (2018). Effect of metformin but not AICAR on total adenosine triphosphate (ATP) levels in primary hepatocytes. Author URL.

Potter PGW, Walker JMV, Robb JL, Chilton J, Williamson R, Randall A, Ellacott KLJ, Beall C (2018). Recurrent hypoglycaemia increases human primary astrocyte oxygen consumption, fatty acid dependency and pentose phosphate pathway activity. Author URL.

Robb J, Hammad N, Beall C, Ellacott K (2018). The 18-kDa translocator protein (TSPO) regulates cellular metabolism in astrocytes. Author URL.

Walker JMV, Potter PGW, Somes A, Beall C (2017). Altered adenosine triphosphate (ATP)-induced calcium responses in glucosensing GT1-7 neurons during hypoglycaemia and in astrocytes following recurrent hypoglycaemia. Author URL.

Walker JMV, Potter PGW, Robb J, Ellacott KLJ, Beall C (2017). Exposure of Astrocytes to Recurrent Hypoglycemia in Vitro Alters Gliotransmission and Purinergic Signaling. Author URL.

Potter PGW, Cruz JMV, Cruz AM, Williamson R, Randall A, Beall C (2017). Human astrocytes are altered following chronic glucose variation: differential regulation of cytokine release and increased basal metabolism. Author URL.

Beall C, Dadak S, Walker JMV, Soutar MPM, McCrimmon RJ, Ashford MLJ (2017). Oleate induces ATP-sensitive channel (K-ATP)-dependent hyperpolarisation of mouse hypothalamic glucose-excited neurons without altering cellular energy charge. Author URL.

Logie L, Beall C, Rena G (2017). Repression of hepatic glucose production by 5-aminoimidazole-4-carboxamide ribonucleotide (AICAR) is inhibited by 8-CPT-cAMP mediated blockade of equilibrative nucleotide transporter 1 (ENT1). Author URL.

Walker JMV, Malhi A, Hardy H, Chilton J, Beall C (2016). A769662 regulates intracellular calcium and extracellular ATP independent of AMPK. Author URL.

Piipari K, Beall C, Al-Qassab H, Smith MA, Carling D, Viollet B, Ashford MLJ, Withers DJ (2010). Key Role of AMP-Activated Protein Kinase in Pancreatic Beta Cell Glucose-Sensing and Whole Body Glucose Homeostasis. Author URL.

Publications by year

In Press

MacDonald AJ, Holmes FE, Beall C, Pickering AE, Ellacott KLJ (In Press). Regulation of food intake by astrocytes in the brainstem dorsal vagal complex. Abstract.

2022

Weightman Potter PG, Ellacott KLJ, Randall A, Beall C (2022). Glutamate Rescues Altered Mitochondrial Function Following Recurrent Low Glucose in Hypothalamic But not Cortical Primary Rat Astrocytes.

Partridge KM, Morgan NG, Ellacott KLJ, Beall C (2022). Recurrent low glucose exposure (RLG) induces intrinsic metabolic adaptations in pancreatic alphaTC1.9 cells. Author URL.

2021

MacDonald AJ, Pye KR, Beall C, Ellacott KLJ (2021). Astrocytes in the dorsal vagal complex are not activated by systemic glucoprivation and their chemogenetic activation does not elicit homeostatic glucoregulatory responses in mice.

Abstract.

MacDonald AJ, Yang YHC, Cruz AM, Beall C, Ellacott KLJ (2021). Brain-Body Control of Glucose Homeostasis—Insights from Model Organisms. Frontiers in Endocrinology, 12 Abstract.

2020

Hall B (2020). An investigation into the effect of acute and chronic KATP channel modulation on membrane conductance and cellular metabolism.

The ATP-sensitive potassium (KATP) channel is a vital link between cellular metabolism and electrical excitability in a variety of cell types, including pancreatic beta cells and hypothalamic neurons where they are involved in the response to changing plasma glucose levels. Blockade of KATP channels using sulfonylureas is a common therapeutic target for Type 2 diabetes (T2D) treatment. However, long-term sulfonylurea therapy is associated with a 33% chance of failure, reducing overall drug efficacy and pancreatic beta cell function, reducing their lasting effectiveness. Furthermore, gain-of-function mutations in KATP channels, leading to NDM and DEND syndrome, can drastically alter basal cellular metabolism and mitochondrial function, indicating a potential role of KATP channel activity in the regulation of glucose metabolism. In addition, DEND mutations have been shown to cause a wide array of neurological conditions, currently untreatable with sulfonylurea therapy.
The aim of these studies was to answer three main questions; what is the impact of chronic blockade on membrane conductance and KATP channel activity after removal of the drug? does the alteration of KATP channel activity to regulate cellular glucose metabolism? and lastly, what concentration does memantine block native KATP channels at? Chapter 3 presents evidence that both gliclazide (5 μM) and tolbutamide (50 μM) caused a significant augmentation of KATP-mediated membrane conductance in GT1-7 cells after 48 hours of treatment of ~2x and 1.5x, respectively. Overall, these data provide an alternative explanation to the increased rate of drug failure after long term therapy with sulfonylureas. Chapter 4 shows that the acute modulation of KATP channel activity caused little to no significant alterations in either glycolysis or mitochondrial activity, as has been previously described. However, chronic KATP channel blockade with glibenclamide increased mitochondrial ATP production and decreased basal glycolysis, potentially as a response to increased cellular excitability. Chapter 5 shows that external exposure of GT1-7 cells to memantine (100 μM) caused significant reduction in KATP-dependent whole-cell membrane conductance (~80% maximal). However, no significant effect was observed at either 10 μM or 1 μM memantine. Overall, these data suggest that memantine does block KATP channels, but at a much higher concentration than is therapeutically relevant.
Overall, this work provides new evidence that supplements our understanding of both the impacts of pharmacological treatment on KATP channel activity, as well as the role of KATP channel activity on cellular glucose metabolism. Furthermore, and most importantly, this work furthers our understanding of the effects of memantine on KATP mediated membrane conductance and its effectiveness, or lack thereof, as a novel treatment for NDM.

Abstract.

Robb J (2020). Characterisation of immunometabolic responses in astrocytes. Abstract.

MacDonald A (2020). Defining the contribution of dorsal vagal complex astrocytes to the regulation of food intake.

Food intake is controlled by the coordinated action of numerous brain regions but a complete understanding of the process remains elusive. The nucleus of the solitary tract (NTS), located in the brainstem dorsal vagal complex (DVC) is the first site for integration of visceral synaptic and hormonal cues that act to inhibit food intake. NTS neurons receive synaptic input from sensory neurons of the vagus nerve that relay signals of gastrointestinal stretch and nutrient content. In response to these signals of ingestion, NTS neurons signal to higher brain centres in the hypothalamus and midbrain to inhibit hunger and promote meal termination.
A role for astrocytes in brain circuits controlling food intake has begun to be
identified. Hypothalamic astrocyte signalling has been implicated in regulating energy homeostasis. Despite a wealth of evidence showing astrocytes in the NTS/DVC are involved in synaptic integration of vagal signals and control of autonomic physiology, the potential role of these cells in feeding control has not been investigated.
We hypothesised that NTS astrocytes, and those in the wider DVC, would be
responsive to increases in food intake and, in turn, their activation would act in concert with NTS neurons to drive a corresponding suppression of food intake.
To investigate this prospect we used dietary manipulation,
immunohistochemistry, selective chemogenetic manipulation of DVC astrocytes, behavioural assays and electrophysiology in mice. The key findings of these studies show that in response to acute nutrient excess
and gastric distention NTS astrocytes increase their expression of the
cytoskeletal glial fibrillary acidic protein and adopt a more ramified morphology, indicative of activation. We also show that selective activation of Gq-proteincoupled receptor signalling in DVC astrocytes suppresses nocturnal food intake and refeeding after a fast. These studies provide evidence that astrocytes may be integrators and effectors of satiety signals and appropriate feeding responses
in the DVC.

Abstract.

Cruz AM, Beall C (2020). Exogenous ATP promotes glucose uptake and utilisation in skeletal muscle cells but does not alter glucose clearance in vivo. Author URL.

MacDonald AJ, Holmes FE, Beall C, Pickering AE, Ellacott KLJ (2020). Regulation of food intake by astrocytes in the brainstem dorsal vagal complex. Glia, 68(6), 1241-1254.

Cruz AM (2020). The integrated physiology of glucose. homeostasis: regulation by extracellular. and intracellular nucleotide sensors.

Physiological glucose levels are maintained by the complex integration of neuroendocrine, hormonal and nutritional signals controlled by multiple tissues in the body. A dysregulation in these mechanisms leads to increasingly prevalent conditions characterised by an inability to regulate blood glucose levels, such as diabetes. Maintaining glycaemia within a target range remains a daily challenge for individuals with both Type 1 and Type 2 diabetes and a better understanding of the pathophysiology of impaired glucose homeostasis in these conditions is still required to identify more effective and targeted therapeutic approaches.
Work in this thesis focused on elucidating the mechanisms by which lipid overflow, be it from increasingly sedentary behaviour or overfeeding, leads to the development of insulin and anabolic resistance in skeletal muscle. Loss of insulin-stimulated glucose clearance by skeletal muscle is a main driver for impaired glucose disposal in Type 2 diabetes and a role for excessive lipid availability in this pathology is well established. Here, muscle cells were treated with high concentrations of a saturated fatty acid and data demonstrated that lipid overflow led to impaired anabolic sensitivity, inflammatory cytokine release and mitochondrial dysfunction. Furthermore, these experiments elucidated a novel role for adenosine tri-phosphate, acting as a signalling molecule, in the regulation of muscle glucose metabolism, identifying insulin and exercise mimetic roles of the nucleotide that could be therapeutically targetable.
This work was translated into humans, where the effect of lipid overflow by high-fat overfeeding was assessed in an experimental model of inactivity-induced insulin and anabolic resistance. Data suggested that two days of disuse (by forearm immobilisation) were sufficient to cause substantial muscle insulin resistance. After 7 days, muscle strength was significantly reduced and anabolic resistance was evident due to decreased forearm balance of potent anabolic amino acids such as leucine. Contrary to the hypothesis, high-fat overfeeding did not accelerate or exacerbate these impairments, suggesting that removal of contraction represents a potent stimulus for loss of substrate demand by muscle, irrespective of energy balance.

Insulin replacement therapy has been the cornerstone of treatment for Type 1 and advanced Type 2 diabetes for over 8 decades. A serious and inadvertent consequence of prolonged insulin therapy is the increased risk of hypoglycaemia. Hypoglycaemia can lead to impaired physiological defences against a decrease in blood glucose and loss of awareness of these changes. AMP-activated protein kinase activators, which are widely used (to target peripheral tissues) as anti-hyperglycaemic agents in Type 2 diabetes have demonstrated central effects that amplify the first defence against hypoglycaemia, or counterregulatory response. Data presented here demonstrated that peripheral administration of a brain permeable AMP-activated protein kinase activator amplified the counterregulatory response to hypoglycaemia by enhancing glucagon levels in healthy rats, without altering fasting blood glucose. This demonstrates important clinical implications for the pharmaceutical use of AMP-activated protein kinase activators as the central roles that regulate blood glucose may supersede the peripheral effects of these compounds, during hypoglycaemia.
Work presented here highlights the complexity of the regulation of glycaemia and discusses the contribution of extracellular and intracellular nucleotides/nucleotide sensors to glucose homeostasis. It can be concluded from this work that strategies to manage or treat diabetes in future should consider the importance of tissue-specific or metabolic status specific actions of the targets of interest.

Abstract.

2019

Robb JL, Hammad NA, Beall C, Ellacott KL (2019). A role for translocator protein 18kDa (TSPO) in immunometabolic regulation in astrocytes. Author URL.

MacDonald AJ, Robb JL, Morrissey NA, Beall C, Ellacott KLJ (2019). Astrocytes in neuroendocrine systems: an overview. J Neuroendocrinol, 31(5). Abstract. Author URL.

Weightman Potter P (2019). The impact of glucose variation on human astrocytes.

Diabetes is a metabolic disorder dysregulating glucose homeostasis. The role of astrocytes in central glucose sensing is poorly understood. But it is recognised they take part in whole-body energy homeostasis, specifically as glucose sensors necessary for the counterregulatory response (CRR) to hypoglycaemia. Iatrogenic hypoglycaemia is the limiting factor to glycaemic control in people with type 1 or type 2 diabetes. Severe hypoglycaemia occurs approximately once per year, whereas, the incidence of minor hypoglycaemia is much greater. Hypoglycaemia impairs awareness of future hypoglycaemia and blunts the CRR, eventually causing hypoglycaemia-associated autonomic failure. The mechanisms of this process are poorly understood.
This thesis utilised isolated human astrocytes exposed to acute or recurrent low glucose (RLG) in vitro to mimic glucose variation in diabetes. Cellular responses were characterised of three key astrocyte functions. Firstly, is astrocyte metabolism altered by acute and RLG treatment? Secondly, do isolated human astrocytes become activated by low glucose treatment, and is this affected by RLG? Thirdly, are astrocytic inflammatory pathways altered by acute or RLG?
The key findings from this thesis shows for the first time that astrocytic mitochondrial oxidation is increased following RLG, with a concurrent increase in fatty acid dependency but decreased coupling efficiency; glycolytic function is also enhanced. Together, this indicates that astrocytes successfully adapt to low glucose to sustain intracellular nucleotide ratios. Contrary to previous work, these human astrocytes do not respond to low glucose by Ca2+-dependent activation. However, the astrocytes do increase inflammatory cytokine release following acute and RLG. Lastly, for the first time an RNA-sequencing approach has been used to identify low glucose-induced differential gene expression. Together these findings support the argument that astrocytes are sensitive to low glucose and may be important in glucose sensation and the CRR.

Abstract.

2018

Logie L, Beall C, Rena G (2018). Effect of metformin but not AICAR on total adenosine triphosphate (ATP) levels in primary hepatocytes. Author URL.

Robb J, Hammad N, Beall C, Ellacott K (2018). The 18-kDa translocator protein (TSPO) regulates cellular metabolism in astrocytes. Author URL.

2017

Beall C, Hanna L, Ellacott KLJ (2017). CNS Targets of Adipokines. Compr Physiol, 7(4), 1359-1406. Abstract. Author URL.

Walker JMV, Potter PGW, Robb J, Ellacott KLJ, Beall C (2017). Exposure of Astrocytes to Recurrent Hypoglycemia in Vitro Alters Gliotransmission and Purinergic Signaling. Author URL.

2016

Walker JMV, Malhi A, Hardy H, Chilton J, Beall C (2016). A769662 regulates intracellular calcium and extracellular ATP independent of AMPK. Author URL.

Abstract. Author URL.

2015

Cameron A, Forteath C, Beall C, Rena G (2015). Anti-inflammatory effects of metformin and their relationship to the therapeutic action of the drug. Endocrine Abstracts

Walker JV, Ashford M, McCrimmon R, Beall C (2015). Characterisation of the astrocytic response to acute and recurrent hypoglycaemia. Endocrine Abstracts

2014

2013

2012

Ashford M, Beall C, McCrimmon R (2012). Hypoglycaemia: exercise for the brain?. J Neuroendocrinol, 24(10), 1365-1366. Abstract. Author URL.

Abstract. Author URL.

2010

Craig_Beall Details from cache as at 2023-03-30 20:40:46

Refresh publications

External Engagement and Impact

Administrative responsibilities

Co-chair University of Exeter Neuroscience Seminar Series

Committee/panel activities

May 2018-2022: JDRF Scientific Advisory Committee

January 2017- present: Diabetes Research Steering Group (DRSG5; Diabetes UK): Long term self-management & glycaemic control

2017-2018 University of Exeter Medical School Senate Representative (elected)

Society for Endocrinology Endocrine Ambassador

2019-2023 Society for Endocrinology Neuroendocrinology network co-convenor and scientific committee member

2019-2020 Socety for Endocrinology Leadership and Development Awards selection committee

International recognition, such as international research collaborations, visiting research posts in overseas institutions, involvement at senior levels in international research associations, acting as referee for national and international research councils.

March 2017: JDRF Strategies to Prevent and Treat Hypoglycemia Unawareness Workshop; New York.
Sept 2018: Mouse Metabolic Phenotyping Course: Glucose clamping in the conscious mouse

Workshops organised

January 2017: Agilent Seahorse users workshop - University of Exeter

September 2017: Exeter Neuroscience Seminar Series: Causes and Consequences of Dementia

Teaching

Modules

2022/23

Supervision / Group

Postdoctoral researchers

Ana Miguel cruz Cruz
Alastair MacDonald
Paul Weightman Potter Postdoctoral Research Associate

Postgraduate researchers

Katie Partridge
Jiping Zhang

Alumni

Jennie Gabriel (University of Dundee; 2014)
Cristina Lumbreras
Aman Malhi
Ashley Nicholls
Josephine Robb

Back | Edit Profile

Profile

Dr Craig Beall

Senior Lecturer

Overview

Qualifications

Career

Links

Research

Research interests

Research projects

Grants/Funding

Research networks

Research grants

Links

Publications

Key publications

Abstract:Brain Permeable AMP-Activated Protein Kinase Activator R481 Raises Glycaemia by Autonomic Nervous System Activation and Amplifies the Counterregulatory Response to Hypoglycaemia in Rats

Abstract:Brain-Body Control of Glucose Homeostasis—Insights from Model Organisms

Publications by category

Journal articles

Abstract:Analysis of the transcriptome and DNA methylome in response to acute and recurrent low glucose in human primary astrocytes

Abstract:Brain permeable AMPK activator R481 raises glycemia by autonomic nervous system activation and amplifies the counterregulatory response to hypoglycemia in rats

Abstract:Human primary astrocytes increase basal fatty acid oxidation following recurrent low glucose to maintain intracellular nucleotide levels

Abstract:Regulation of food intake by astrocytes in the brainstem dorsal vagal complex

Abstract:Glutamate Prevents Altered Mitochondrial Function Following Recurrent Low Glucose in Hypothalamic but Not Cortical Primary Rat Astrocytes

Abstract:Brain Permeable AMP-Activated Protein Kinase Activator R481 Raises Glycaemia by Autonomic Nervous System Activation and Amplifies the Counterregulatory Response to Hypoglycaemia in Rats

Abstract:Brain-Body Control of Glucose Homeostasis—Insights from Model Organisms

Abstract:Astrocytes in neuroendocrine systems: an overview.

Abstract:AMP-activated protein kinase (AMPK) activator A-769662 increases intracellular calcium and ATP release from astrocytes in an AMPK-independent manner

Abstract:CNS Targets of Adipokines.

Abstract:Anti-Inflammatory Effects of Metformin Irrespective of Diabetes Status.

Abstract:Chronic Activation of γ2 AMPK Induces Obesity and Reduces β Cell Function.

Abstract:Kv1.3 inhibitors have differential effects on glucose uptake and AMPK activity in skeletal muscle cell lines and mouse ex vivo skeletal muscle.

Abstract:AMPK modulates glucose-sensing in insulin-secreting cells by altered phosphotransfer to KATP channels.

Abstract:Continuous hypothalamic K(ATP) activation blunts glucose counter-regulation in vivo in rats and suppresses K(ATP) conductance in vitro.

Abstract:Hypoglycaemia: exercise for the brain?

Abstract:Mouse hypothalamic GT1-7 cells demonstrate AMPK-dependent intrinsic glucose-sensing behaviour.

Abstract:The physiology and pathophysiology of the neural control of the counterregulatory response.

Abstract:Loss of AMP-activated protein kinase alpha2 subunit in mouse beta-cells impairs glucose-stimulated insulin secretion and inhibits their sensitivity to hypoglycaemia.

Conferences

Abstract:Amplified Glucagon Response to Hypoglycemia following AMP-Activated Protein Kinase (AMPK) Activator R481 Treatment in Healthy Rats

Publications by year

In Press

Abstract:Analysis of the transcriptome and DNA methylome in response to acute and recurrent low glucose in human primary astrocytes

Abstract:Brain permeable AMPK activator R481 raises glycemia by autonomic nervous system activation and amplifies the counterregulatory response to hypoglycemia in rats

Abstract:Human primary astrocytes increase basal fatty acid oxidation following recurrent low glucose to maintain intracellular nucleotide levels

Abstract:Regulation of food intake by astrocytes in the brainstem dorsal vagal complex

2022

Abstract:Glutamate Prevents Altered Mitochondrial Function Following Recurrent Low Glucose in Hypothalamic but Not Cortical Primary Rat Astrocytes

2021

Abstract:Brain Permeable AMP-Activated Protein Kinase Activator R481 Raises Glycaemia by Autonomic Nervous System Activation and Amplifies the Counterregulatory Response to Hypoglycaemia in Rats

Abstract:Brain-Body Control of Glucose Homeostasis—Insights from Model Organisms

2020

Abstract:An investigation into the effect of acute and chronic KATP channel modulation on membrane conductance and cellular metabolism.

Abstract:Characterisation of immunometabolic responses in astrocytes

Abstract:Defining the contribution of dorsal vagal complex astrocytes to the regulation of food intake

Abstract:The integrated physiology of glucose. homeostasis: regulation by extracellular. and intracellular nucleotide sensors

2019

Abstract:Amplified Glucagon Response to Hypoglycemia following AMP-Activated Protein Kinase (AMPK) Activator R481 Treatment in Healthy Rats

Abstract:Astrocytes in neuroendocrine systems: an overview.

Abstract:The impact of glucose variation on human astrocytes

2018

2017

Abstract:AMP-activated protein kinase (AMPK) activator A-769662 increases intracellular calcium and ATP release from astrocytes in an AMPK-independent manner

Abstract:CNS Targets of Adipokines.

2016

Abstract:Anti-Inflammatory Effects of Metformin Irrespective of Diabetes Status.

Abstract:Chronic Activation of γ2 AMPK Induces Obesity and Reduces β Cell Function.

2015

2014

Abstract:Kv1.3 inhibitors have differential effects on glucose uptake and AMPK activity in skeletal muscle cell lines and mouse ex vivo skeletal muscle.

2013

Abstract:AMPK modulates glucose-sensing in insulin-secreting cells by altered phosphotransfer to KATP channels.

Abstract:Continuous hypothalamic K(ATP) activation blunts glucose counter-regulation in vivo in rats and suppresses K(ATP) conductance in vitro.

2012

Abstract:Hypoglycaemia: exercise for the brain?

Abstract:Mouse hypothalamic GT1-7 cells demonstrate AMPK-dependent intrinsic glucose-sensing behaviour.

Abstract:The physiology and pathophysiology of the neural control of the counterregulatory response.

2010

Abstract:Loss of AMP-activated protein kinase alpha2 subunit in mouse beta-cells impairs glucose-stimulated insulin secretion and inhibits their sensitivity to hypoglycaemia.

Abstract:
Brain Permeable AMP-Activated Protein Kinase Activator R481 Raises Glycaemia by Autonomic Nervous System Activation and Amplifies the Counterregulatory Response to Hypoglycaemia in Rats

Abstract:
Brain-Body Control of Glucose Homeostasis—Insights from Model Organisms

Abstract:
Analysis of the transcriptome and DNA methylome in response to acute and recurrent low glucose in human primary astrocytes

Abstract:
Brain permeable AMPK activator R481 raises glycemia by autonomic nervous system activation and amplifies the counterregulatory response to hypoglycemia in rats

Abstract:
Human primary astrocytes increase basal fatty acid oxidation following recurrent low glucose to maintain intracellular nucleotide levels

Abstract:
Regulation of food intake by astrocytes in the brainstem dorsal vagal complex

Abstract:
Glutamate Prevents Altered Mitochondrial Function Following Recurrent Low Glucose in Hypothalamic but Not Cortical Primary Rat Astrocytes

Abstract:
Brain Permeable AMP-Activated Protein Kinase Activator R481 Raises Glycaemia by Autonomic Nervous System Activation and Amplifies the Counterregulatory Response to Hypoglycaemia in Rats

Abstract:
Brain-Body Control of Glucose Homeostasis—Insights from Model Organisms

Abstract:
Astrocytes in neuroendocrine systems: an overview.

Abstract:
AMP-activated protein kinase (AMPK) activator A-769662 increases intracellular calcium and ATP release from astrocytes in an AMPK-independent manner

Abstract:
CNS Targets of Adipokines.

Abstract:
Anti-Inflammatory Effects of Metformin Irrespective of Diabetes Status.

Abstract:
Chronic Activation of γ2 AMPK Induces Obesity and Reduces β Cell Function.

Abstract:
Kv1.3 inhibitors have differential effects on glucose uptake and AMPK activity in skeletal muscle cell lines and mouse ex vivo skeletal muscle.

Abstract:
AMPK modulates glucose-sensing in insulin-secreting cells by altered phosphotransfer to KATP channels.

Abstract:
Continuous hypothalamic K(ATP) activation blunts glucose counter-regulation in vivo in rats and suppresses K(ATP) conductance in vitro.

Abstract:
Hypoglycaemia: exercise for the brain?

Abstract:
Mouse hypothalamic GT1-7 cells demonstrate AMPK-dependent intrinsic glucose-sensing behaviour.

Abstract:
The physiology and pathophysiology of the neural control of the counterregulatory response.

Abstract:
Loss of AMP-activated protein kinase alpha2 subunit in mouse beta-cells impairs glucose-stimulated insulin secretion and inhibits their sensitivity to hypoglycaemia.

Abstract:
Amplified Glucagon Response to Hypoglycemia following AMP-Activated Protein Kinase (AMPK) Activator R481 Treatment in Healthy Rats

Abstract:
Analysis of the transcriptome and DNA methylome in response to acute and recurrent low glucose in human primary astrocytes

Abstract:
Brain permeable AMPK activator R481 raises glycemia by autonomic nervous system activation and amplifies the counterregulatory response to hypoglycemia in rats

Abstract:
Human primary astrocytes increase basal fatty acid oxidation following recurrent low glucose to maintain intracellular nucleotide levels

Abstract:
Regulation of food intake by astrocytes in the brainstem dorsal vagal complex

Abstract:
Glutamate Prevents Altered Mitochondrial Function Following Recurrent Low Glucose in Hypothalamic but Not Cortical Primary Rat Astrocytes

Abstract:
Brain Permeable AMP-Activated Protein Kinase Activator R481 Raises Glycaemia by Autonomic Nervous System Activation and Amplifies the Counterregulatory Response to Hypoglycaemia in Rats

Abstract:
Brain-Body Control of Glucose Homeostasis—Insights from Model Organisms

Abstract:
An investigation into the effect of acute and chronic KATP channel modulation on membrane conductance and cellular metabolism.

Abstract:
Characterisation of immunometabolic responses in astrocytes

Abstract:
Defining the contribution of dorsal vagal complex astrocytes to the regulation of food intake

Abstract:
The integrated physiology of glucose. homeostasis: regulation by extracellular. and intracellular nucleotide sensors

Abstract:
Amplified Glucagon Response to Hypoglycemia following AMP-Activated Protein Kinase (AMPK) Activator R481 Treatment in Healthy Rats

Abstract:
Astrocytes in neuroendocrine systems: an overview.

Abstract:
The impact of glucose variation on human astrocytes

Abstract:
AMP-activated protein kinase (AMPK) activator A-769662 increases intracellular calcium and ATP release from astrocytes in an AMPK-independent manner

Abstract:
CNS Targets of Adipokines.

Abstract:
Anti-Inflammatory Effects of Metformin Irrespective of Diabetes Status.

Abstract:
Chronic Activation of γ2 AMPK Induces Obesity and Reduces β Cell Function.

Abstract:
Kv1.3 inhibitors have differential effects on glucose uptake and AMPK activity in skeletal muscle cell lines and mouse ex vivo skeletal muscle.

Abstract:
AMPK modulates glucose-sensing in insulin-secreting cells by altered phosphotransfer to KATP channels.

Abstract:
Continuous hypothalamic K(ATP) activation blunts glucose counter-regulation in vivo in rats and suppresses K(ATP) conductance in vitro.

Abstract:
Hypoglycaemia: exercise for the brain?

Abstract:
Mouse hypothalamic GT1-7 cells demonstrate AMPK-dependent intrinsic glucose-sensing behaviour.

Abstract:
The physiology and pathophysiology of the neural control of the counterregulatory response.

Abstract:
Loss of AMP-activated protein kinase alpha2 subunit in mouse beta-cells impairs glucose-stimulated insulin secretion and inhibits their sensitivity to hypoglycaemia.