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Elucidating the basic neurocircuitry of energy homeostasis is paramount in the prevention and treatment of obesity and type 2 diabetes. My laboratory attempts to delineate how the brain affects appetite, body weight, and insulin action by examining the basic neurocircuitry of neurotransmitter and neuropeptide systems, and further, how these systems interact. Using complementary genetic, pharmacological, and neuroanatomical approaches, we also investigate how perturbation or stimulation of components of these pathways affects energy homeostasis in an effort to identify new treatments for obesity and type 2 diabetes.
 | Mr. Dan Lam
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 | Hypothalamic cells co-stained to identify melanocortin neurons (red) expressing 5-HT2C receptors
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Dan Lam, PhD student
Recently, substantial support for central melanocortin pathways, through the melanocortin-4 receptors (MC4-Rs), in the regulation of metabolic-hormonal, neuroendocrine, and behavioral parameters associated with energy balance and type 2 diabetes has been reported in genetic and drug studies. However, relatively little is known about brain MC4-R expression and pathways regulating these effects. Our data suggest that the central serotonin (5-hydroytryptamine; 5-HT) system modulates melanocortin pathways. Dan is investigating the hypothesis that melanocortin-containing cell bodies express different serotonin receptors, and that these neurons innervate key nuclei in the hypothalamus and brainstem involved in feeding, body weight, energy expenditure, and insulin and glucose regulation.
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Ms. Sarah Scholfield
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 | Nociceptin/orphanin FQ (red) expression in N1E-115 neuroblastoma cells
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Ms Sarah Schofield, Student
Sarah is investigating an exciting new peptide which is structurally related to the opioid family. This peptide, nociceptin/orphanin FQ (N/OFQ), acting through its receptor opioid receptor-like-1 (ORL-1), potently modulates food intake. However, it has not yet been determined how this endogenous peptide acts in the brain via its receptor to affect appetite. Sarah is characterizing brain pathways employed by N/OFQ and ORL-1 to stimulate and suppress appetite. We hypothesize that a more complete understanding of the central systems involved in the initiation and termination of feeding will aid in the prevention and treatment of aberrant feeding behaviour.
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 | Mr. Stephen Moore
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 | Nissl stained hippocampal cells
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Stephen Moore, PhD student
Stephen, co-supervised by Dr. Mark Evans in the Department of Medicine, is examining how different nutritional states, such as hypoglycemia and hyperglycemia affect cortical and hippocampal cells associated with learning and memory. These basic science studies have broader application to our understanding of how the types and amounts of food we consume affects our cognitive performance at school and work.
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 | Dr. Al Garfield
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Dr Alastair Garfield, Postdoctoral fellow
The central serotonergic system has been heavily implicated in the modulation of appetite and the related physiological indices of obesity and glucose metabolism. Previous studies by our lab have identified specific roles for both the serotonin 5-HT1B and 5-HT2C receptor subtypes in regulating food intake, and the latter more recently in glucose homeostasis; functions attributable to the expression of these receptors on spatially distinct neuronal populations within the brain. Al is further defining the functional relationship between the 5-HT1B and 5-HT2C receptors in regard to their concerted regulation of appetite and glucose homeostasis, roles of clinical salience to the increasing incidence of obesity and type II diabetes.
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 | Dr. Ollie Marston
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Dr Oliver Marston, Postdoctoral fellow
Ollie's experiments focus primarily on the how the pathways and neuropeptides in the brain stimulate appetite, such as the orexin/hypocretin, neuropeptide-Y and nociceptin/orphanin-FQ neurosignalling pathways. Utilizing immunohistochemical, electrophysiological, and pharmacological techniques he is examining how these neuropeptides interact within the hypothalamus to influence feeding processes.
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Mr. Paul Hurst
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Paul Hurst, PhD student
Paul is investigating how the brain detects changes in blood glucose and
how such neuronal glucose sensing mechanisms may become perturbed in
pathological states such as, Diabetes, Obesity and Hypoglycaemia Associated
Autonomic Failure (HAAF). In particular, Paul's work focuses on the role of glucokinase, a key enzyme
responsible for the metabolism of glucose inside the cell, in such
processes
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Neurocircuitry modulating appetite, body weight and type 2 diabetes
