ORCID Profile
0000-0002-9032-0862
Current Organisations
Institut universitaire de cardiologie et de pneumologie de Québec
,
Université Laval
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Animal Physiology - Systems | Zoology | Animal Behaviour | Cell Neurochemistry
Expanding Knowledge in the Biological Sciences | Expanding Knowledge in Technology |
Publisher: No publisher found
Date: 2020
Publisher: Wiley
Date: 07-2019
DOI: 10.1002/TRE.705
Publisher: Informa UK Limited
Date: 24-05-2021
Publisher: eLife Sciences Publications, Ltd
Date: 19-09-2018
DOI: 10.7554/ELIFE.38704
Abstract: Hypothalamic neurons respond to nutritional cues by altering gene expression and neuronal excitability. The mechanisms that control such adaptive processes remain unclear. Here we define populations of POMC neurons in mice that are activated or inhibited by insulin and thereby repress or inhibit hepatic glucose production (HGP). The proportion of POMC neurons activated by insulin was dependent on the regulation of insulin receptor signaling by the phosphatase TCPTP, which is increased by fasting, degraded after feeding and elevated in diet-induced obesity. TCPTP-deficiency enhanced insulin signaling and the proportion of POMC neurons activated by insulin to repress HGP. Elevated TCPTP in POMC neurons in obesity and/or after fasting repressed insulin signaling, the activation of POMC neurons by insulin and the insulin-induced and POMC-mediated repression of HGP. Our findings define a molecular mechanism for integrating POMC neural responses with feeding to control glucose metabolism.
Publisher: Elsevier BV
Date: 09-2022
DOI: 10.1016/J.BIOCHI.2022.09.006
Abstract: Coordinated detection of changes in metabolic state by the nervous system is fundamental for survival. Hypothalamic pro-opiomelanocortin (POMC) neurons play a critical role in integrating metabolic signals, including leptin levels. They also coordinate adaptative responses and thus represent an important relay in the regulation of energy balance. Despite a plethora of work documenting the effects of in idual hormones, nutrients, and neuropeptides on POMC neurons, the importance for crosstalk and additive effects between such signaling molecules is still underexplored. The ability of the metabolic state and the concentrations of nutrients, such as glucose, to influence leptin's effects on POMC neurons appears critical for understanding the function and complexity of this regulatory network. Here, we summarize the current knowledge on the effects of leptin on POMC neuron electrical excitability and discuss factors potentially contributing to variability in these effects, with a particular focus on the mouse models that have been developed and the importance of extracellular glucose levels. This review highlights the importance of the metabolic "environment" for determining hypothalamic neuronal responsiveness to metabolic cues and for determining the fundamental effects of leptin on the activity of hypothalamic POMC neurons.
Publisher: Wiley
Date: 08-02-2023
DOI: 10.1111/JNC.15765
Abstract: The discovery of leptin in 1994 was an “eureka moment” in the field of neurometabolism that provided new opportunities to better understand the central control of energy balance and glucose metabolism. Rapidly, a prevalent model in the field emerged that pro‐opiomelanocortin (POMC) neurons were key in promoting leptin's anorexigenic effects and that the arcuate nucleus of the hypothalamus (ARC) was a key region for the regulation of energy homeostasis. While this model inspired many important discoveries, a growing body of literature indicates that this model is now outdated. In this review, we re‐evaluate the hypothalamic leptin–melanocortin model in light of recent advances that directly tackle previous assumptions, with a particular focus on the ARC. We discuss how segregated and heterogeneous these neurons are, and examine how the development of modern approaches allowing spatiotemporal, intersectional, and chemogenetic manipulations of melanocortin neurons has allowed a better definition of the complexity of the leptin–melanocortin system. We review the importance of leptin in regulating glucose homeostasis, but not food intake, through direct actions on ARC POMC neurons. We further highlight how non‐POMC, GABAergic neurons mediate leptin's direct effects on energy balance and influence POMC neurons. image
Publisher: Informa UK Limited
Date: 12-05-2020
Publisher: The Endocrine Society
Date: 12-06-2021
Abstract: Obesity is a disease of the nervous system. While some will view this statement as provocative, others will take it as obvious. Whatever our side is, the pharmacology tells us that targeting the nervous system works for promoting weight loss. It works, but at what cost? Is the nervous system a safe target for sustainable treatment of obesity? What have we learned—and unlearned—about the central control of energy balance in the last few years? Herein we provide a thought-provoking exploration of obesity as a disorder of neurotransmission. We discuss the state of knowledge on the brain pathways regulating energy homeostasis that are commonly targeted in anti-obesity therapy and explore how medications affecting neurotransmission such as atypical antipsychotics, antidepressants, and antihistamines relate to body weight. Our goal is to provide the endocrine community with a conceptual framework that will help expending our understanding of the pathophysiology of obesity, a disease of the nervous system.
Publisher: Elsevier BV
Date: 05-2020
Publisher: Elsevier BV
Date: 12-2020
Publisher: Elsevier BV
Date: 09-2020
Publisher: Routledge
Date: 16-07-2021
Publisher: Informa UK Limited
Date: 05-09-2019
Publisher: Elsevier BV
Date: 09-2019
Publisher: Informa UK Limited
Date: 06-07-2017
Publisher: Springer Science and Business Media LLC
Date: 09-06-2008
DOI: 10.1007/S00213-008-1202-Z
Abstract: Caffeine is a well-known stimulant that can be used to increase alertness and performance especially in low arousal situations such as monotonous highway driving or after sleep deprivation. The effects of caffeine in rested, alert, participants are less clear, and this may be attributable to difficulties in objectively assessing small changes in alertness. The present study examined the effects of caffeine in non-sleep-deprived participants with methods that have previously been shown to be sensitive to changes in alertness. In order to avoid confounding results, low, or non-users of caffeine, were sought as participants. Twelve subjects participated in a within-subjects double-blind placebo-controlled design study and were administered either a capsule containing 200 mg of caffeine or placebo on two separate days. Ten-minute long tests of vigilance were performed at baseline and then at 30, 60, 120, 180, and 240 min after swallowing the capsule. During vigilance tests, eye blink variables were measured using infrared reflectance oculography and converted into a drowsiness score, Johns Drowsiness Scale (JDS). Caffeine significantly reduced JDS scores (drowsiness) and reaction times, and these changes persisted for 3 to 4 h. Self reports of sleepiness were not as sensitive, with Karolinska Sleepiness Scale scores only being significantly lower in the caffeine compared to placebo condition at 30 min post capsule administration. The results demonstrated that despite being well rested, administration of caffeine significantly increased alertness and enhanced performance, and these changes were able to be detected with the JDS.
Publisher: American Society for Clinical Investigation
Date: 17-08-2020
DOI: 10.1172/JCI140585
Publisher: Wiley
Date: 10-2017
DOI: 10.1111/JNE.12528
Abstract: Obesity and ageing are risk factors for diabetes. In the present study, we investigated the effects of ageing, obesity and fasting on central and peripheral glucose tolerance and on glucose-sensing neuronal function in the arcuate nucleus of rats, with a view to providing insight into the central mechanisms regulating glucose homeostasis and how they change or are subject to dysfunction with ageing and obesity. We show that, following a glucose load, central glucose tolerance at the level of the cerebrospinal fluid (CSF) and plasma is significantly reduced in rats maintained on a high-fat diet (HFD). With ageing, up to 2 years, central glucose tolerance was impaired in an age-dependent manner, whereas peripheral glucose tolerance remained unaffected. Ageing-induced peripheral glucose intolerance was improved by a 24-hour fast, whereas central glucose tolerance was not corrected. Pre-wean, immature animals have elevated basal plasma glucose levels and a delayed increase in central glucose levels following peripheral glucose injection compared to mature animals. Electrophysiological recording techniques revealed an energy-status-dependent role for glucose-excited, inhibited and adapting neurones, along with glucose-induced changes in synaptic transmission. We conclude that ageing affects central glucose tolerance, whereas HFD profoundly affects central and peripheral glucose tolerance and, in addition, glucose-sensing neurones adapt function in an energy-status-dependent manner.
Publisher: Routledge
Date: 12-10-2022
Publisher: eLife Sciences Publications, Ltd
Date: 12-09-2018
Publisher: American Physiological Society
Date: 06-2023
Publisher: Elsevier BV
Date: 10-2019
Publisher: Elsevier BV
Date: 10-2023
Publisher: Elsevier BV
Date: 10-2017
Publisher: Elsevier BV
Date: 08-2017
DOI: 10.1016/J.CMET.2017.07.013
Abstract: Beige adipocytes can interconvert between white and brown-like states and switch between energy storage versus expenditure. Here we report that beige adipocyte plasticity is important for feeding-associated changes in energy expenditure and is coordinated by the hypothalamus and the phosphatase TCPTP. A fasting-induced and glucocorticoid-mediated induction of TCPTP, inhibited insulin signaling in AgRP/NPY neurons, repressed the browning of white fat and decreased energy expenditure. Conversely feeding reduced hypothalamic TCPTP, to increase AgRP/NPY neuronal insulin signaling, white adipose tissue browning and energy expenditure. The feeding-induced repression of hypothalamic TCPTP was defective in obesity. Mice lacking TCPTP in AgRP/NPY neurons were resistant to diet-induced obesity and had increased beige fat activity and energy expenditure. The deletion of hypothalamic TCPTP in obesity restored feeding-induced browning and increased energy expenditure to promote weight loss. Our studies define a hypothalamic switch that coordinates energy expenditure with feeding for the maintenance of energy balance.
Publisher: Elsevier BV
Date: 09-2023
Publisher: Springer Science and Business Media LLC
Date: 11-07-2007
Publisher: American Physiological Society
Date: 07-2021
DOI: 10.1152/AJPENDO.00044.2021
Abstract: Cannabinoid 1 receptors (CB1Rs) regulate metabolic homeostasis, and CB1R inverse agonists reduce body weight and improve parameters of glucose metabolism. However, the cell populations expressing CB1Rs that regulate metabolic homeostasis remain unclear. CB1Rs are highly expressed in the ventromedial hypothalamic nucleus (VMH), which is a crucial node that regulates metabolism. With CRISPR/Cas9, we generated mice lacking CB1Rs specifically in VMH neurons and found that CB1Rs in VMH neurons are essential for the regulation of glucose metabolism independent of body weight regulation.
Location: Canada
Location: United States of America
Start Date: 2023
End Date: 12-2025
Amount: $600,000.00
Funder: Australian Research Council
View Funded Activity