scholarly journals Antagonistic modulation of NPY/AgRP and POMC neurons in the arcuate nucleus by noradrenalin

eLife ◽  
2017 ◽  
Vol 6 ◽  
Author(s):  
Lars Paeger ◽  
Ismene Karakasilioti ◽  
Janine Altmüller ◽  
Peter Frommolt ◽  
Jens Brüning ◽  
...  
Keyword(s):  
Adrenergic Receptors ◽  
Energy Homeostasis ◽  
Arcuate Nucleus ◽  
Differential Modulation ◽  
Control Food ◽  
Cell Type Specific ◽  
Control Food Intake ◽  
Perforated Patch Clamp ◽  
Β Adrenergic Receptors ◽  
Opposing Effect

In the arcuate nucleus of the hypothalamus (ARH) satiety signaling (anorexigenic) pro-opiomelanocortin (POMC)-expressing and hunger signaling (orexigenic) agouti-related peptide (AgRP)-expressing neurons are key components of the neuronal circuits that control food intake and energy homeostasis. Here, we assessed whether the catecholamine noradrenalin directly modulates the activity of these neurons in mice. Perforated patch clamp recordings showed that noradrenalin changes the activity of these functionally antagonistic neurons in opposite ways, increasing the activity of the orexigenic NPY/AgRP neurons and decreasing the activity of the anorexigenic POMC neurons. Cell type-specific transcriptomics and pharmacological experiments revealed that the opposing effect on these neurons is mediated by the activation of excitatory α1A - and β- adrenergic receptors in NPY/AgRP neurons, while POMC neurons are inhibited via α2A – adrenergic receptors. Thus, the coordinated differential modulation of the key hypothalamic neurons in control of energy homeostasis assigns noradrenalin an important role to promote feeding.

scholarly journals The Function of Gastrointestinal Hormones in Obesity—Implications for the Regulation of Energy Intake

Nutrients ◽  
2021 ◽  
Vol 13 (6) ◽  
pp. 1839
Author(s):  
Mona Farhadipour ◽  
Inge Depoortere
Keyword(s):  
Energy Homeostasis ◽  
Gastric Bypass Surgery ◽  
Gastrointestinal Hormones ◽  
Enteroendocrine Cells ◽  
Hormone Balance ◽  
Gut Hormone ◽  
Control Food ◽  
Induce Weight Loss ◽  
Novel Strategy ◽  
Control Food Intake

The global burden of obesity and the challenges of prevention prompted researchers to investigate the mechanisms that control food intake. Food ingestion triggers several physiological responses in the digestive system, including the release of gastrointestinal hormones from enteroendocrine cells that are involved in appetite signalling. Disturbed regulation of gut hormone release may affect energy homeostasis and contribute to obesity. In this review, we summarize the changes that occur in the gut hormone balance during the pre- and postprandial state in obesity and the alterations in the diurnal dynamics of their plasma levels. We further discuss how obesity may affect nutrient sensors on enteroendocrine cells that sense the luminal content and provoke alterations in their secretory profile. Gastric bypass surgery elicits one of the most favorable metabolic outcomes in obese patients. We summarize the effect of different strategies to induce weight loss on gut enteroendocrine function. Although the mechanisms underlying obesity are not fully understood, restoring the gut hormone balance in obesity by targeting nutrient sensors or by combination therapy with gut peptide mimetics represents a novel strategy to ameliorate obesity.

Neurobiology of food choices-between energy homeostasis, reward system, and neuroeconomics

e-Neuroforum ◽  
2016 ◽  
Vol 22 (1) ◽  
Author(s):  
Laura Enax ◽  
Bernd Weber
Keyword(s):  
Energy Homeostasis ◽  
Health Care Systems ◽  
Reward System ◽  
Feeding Regulation ◽  
Control Food ◽  
Care Systems ◽  
Food Decisions ◽  
Short And Long Term ◽  
Control Food Intake ◽  
Internal And External Factors

AbstractThe rate of patients with obesity has been rapidly increasing, and this imposes a heavy economic burden on health-care systems. Food decisions, under the influence of different internal and external factors, lie at the core of this increasing health problem. Due to the biological necessity to consume sufficient amounts of food and to correctly regulate energy expenditure, there are different systems that control food intake. This article first focuses on neurobiological and hormonal foundations and explains various metabolic short- and long-term signals, such as leptin, insulin, and ghrelin. We then also present genetic factors, which directly or indirectly (via other genes or environmental influences) may affect nutritional status. Since the consumption of high-caloric foods is accompanied by dopamine release and the activation of the brain’s reward system, we will then present the interdependence of metabolic and reward systems. Last, we will present a neuroeconomic perspective that complements research on metabolic and hedonic feeding regulation.

scholarly journals Leptin and Beyond: Actors in Cancer

Biomolecules ◽  
2021 ◽  
Vol 11 (12) ◽  
pp. 1836
Author(s):  
Ines Barone ◽  
Cinzia Giordano
Keyword(s):  
Immune Response ◽  
Adipose Tissue ◽  
Energy Homeostasis ◽  
Peptide Hormone ◽  
Tissue Mass ◽  
Adipose Tissue Mass ◽  
Control Food ◽  
Total Adipose Tissue ◽  
Control Food Intake ◽  
Reproductive Processes

Leptin is a 16-kDa multifunctional, neuroendocrine peptide hormone secreted by adipocytes in proportion to total adipose tissue mass, known to control food intake, energy homeostasis, immune response, and reproductive processes [...]

scholarly journals Obesity and Appetite Control

2012 ◽  
Vol 2012 ◽  
pp. 1-19 ◽  
Author(s):  
Keisuke Suzuki ◽  
Channa N. Jayasena ◽  
Stephen R. Bloom
Keyword(s):  
Food Intake ◽  
Energy Homeostasis ◽  
Peptide Yy ◽  
Gut Hormones ◽  
Appetite Control ◽  
Control Food ◽  
Adiposity Signals ◽  
Term Energy ◽  
Glucagon Like Peptide 1 ◽  
Control Food Intake

Obesity is one of the major challenges to human health worldwide; however, there are currently no effective pharmacological interventions for obesity. Recent studies have improved our understanding of energy homeostasis by identifying sophisticated neurohumoral networks which convey signals between the brain and gut in order to control food intake. The hypothalamus is a key region which possesses reciprocal connections between the higher cortical centres such as reward-related limbic pathways, and the brainstem. Furthermore, the hypothalamus integrates a number of peripheral signals which modulate food intake and energy expenditure. Gut hormones, such as peptide YY, pancreatic polypeptide, glucagon-like peptide-1, oxyntomodulin, and ghrelin, are modulated by acute food ingestion. In contrast, adiposity signals such as leptin and insulin are implicated in both short- and long-term energy homeostasis. In this paper, we focus on the role of gut hormones and their related neuronal networks (the gut-brain axis) in appetite control, and their potentials as novel therapies for obesity.

Mechanisms behind GLP-1 induced weight loss

2008 ◽  
Vol 8 (2_suppl) ◽  
pp. S34-S41 ◽  
Author(s):  
Philip J Larsen
Keyword(s):  
Energy Homeostasis ◽  
Caloric Intake ◽  
Underlying Mechanism ◽  
Negative Energy ◽  
Incretin Hormone ◽  
Dipeptidyl Peptidase 4 ◽  
Control Food ◽  
The Central Nervous System ◽  
Glucagon Like Peptide 1 ◽  
Control Food Intake

Endogenous glucagon-like peptide-1 (GLP-1) is an incretin hormone that plays an important role in maintaining pancreatic function as well as caloric intake. Since the advent of GLP-1 receptor agonists resistant to dipeptidyl peptidase-4 (DPP-4) (degradation, it has become clear that their chronic use promotes negative energy balance. With regard to their effects on body weight, the principal action of GLP-1 agonists is mediated via their inhibition of eating. In searching for the underlying mechanism of GLP-1 receptor agonist-induced anorexic effect, scientists have discovered pathways in the central nervous system, as well as in the periphery. This review describes emerging knowledge of a peripheral endocrine GLP-1 system mediating its activity through a central ascending GLP-1 pathway and targeting hypothalamic sites involved in the regulation of energy homeostasis. Thus peripheral and central GLP-1 sensitive pathways appear to be organised to co-operatively help control food intake and body weight.Br J Diabetes Vasc Dis 2008;8 (Suppl 2): S34—S41

scholarly journals Role of β-adrenergic receptors in the hyperphagic and hypermetabolic responses to dietary methionine restriction

2010 ◽  
Vol 299 (3) ◽  
pp. R740-R750 ◽  
Author(s):  
Eric P. Plaisance ◽  
Tara M. Henagan ◽  
Haley Echlin ◽  
Anik Boudreau ◽  
Kasey L. Hill ◽  
...  
Keyword(s):  
Adipose Tissue ◽  
Adrenergic Receptors ◽  
Energy Homeostasis ◽  
Uncoupling Protein ◽  
Control Diet ◽  
Fat Deposition ◽  
Plasma Adiponectin ◽  
Methionine Restriction ◽  
Plasma Leptin ◽  
Β Adrenergic Receptors

Dietary methionine restriction (MR) limits fat deposition and decreases plasma leptin, while increasing food consumption, total energy expenditure (EE), plasma adiponectin, and expression of uncoupling protein 1 (UCP1) in brown and white adipose tissue (BAT and WAT). β-adrenergic receptors (β-AR) serve as conduits for sympathetic input to adipose tissue, but their role in mediating the effects of MR on energy homeostasis is unclear. Energy intake, weight, and adiposity were modestly higher in β3-AR−/− mice on the Control diet compared with wild-type (WT) mice, but the hyperphagic response to the MR diet and the reduction in fat deposition did not differ between the genotypes. The absence of β3-ARs also did not diminish the ability of MR to increase total EE and plasma adiponectin or decrease leptin mRNA, but it did block the MR-dependent increase in UCP1 mRNA in BAT but not WAT. In a further study, propranolol was used to antagonize remaining β-adrenergic input (β1- and β2-ARs) in β3-AR−/− mice, and this treatment blocked >50% of the MR-induced increase in total EE and UCP1 induction in both BAT and WAT. We conclude that signaling through β-adrenergic receptors is a component of the mechanism used by dietary MR to increase EE, and that β1- and β2-ARs are able to substitute for β3-ARs in mediating the effect of dietary MR on EE. These findings are consistent with the involvement of both UCP1-dependent and -independent mechanisms in the physiological responses affecting energy balance that are produced by dietary MR.

scholarly journals Brain adiponectin signaling controls peripheral insulin response in Drosophila

2021 ◽  
Vol 12 (1) ◽  
Author(s):  
Nathalie Arquier ◽  
Marianne Bjordal ◽  
Philippe Hammann ◽  
Lauriane Kuhn ◽  
Pierre Léopold
Keyword(s):  
Insulin Signaling ◽  
Energy Homeostasis ◽  
Insulin Response ◽  
Larval Brain ◽  
Control Food ◽  
Dietary Sugar ◽  
Neuroendocrine Axis ◽  
Control Food Intake ◽  
The Brain ◽  
Glucose Regulated Protein

AbstractThe brain plays a key role in energy homeostasis, detecting nutrients, metabolites and circulating hormones from peripheral organs and integrating this information to control food intake and energy expenditure. Here, we show that a group of neurons in the Drosophila larval brain expresses the adiponectin receptor (AdipoR) and controls systemic growth and metabolism through insulin signaling. We identify glucose-regulated protein 78 (Grp78) as a circulating antagonist of AdipoR function produced by fat cells in response to dietary sugar. We further show that central AdipoR signaling inhibits peripheral Juvenile Hormone (JH) response, promoting insulin signaling. In conclusion, we identify a neuroendocrine axis whereby AdipoR-positive neurons control systemic insulin response.

Ghrelin: Structure and Function

2005 ◽  
Vol 85 (2) ◽  
pp. 495-522 ◽  
Author(s):  
Masayasu Kojima ◽  
Kenji Kangawa
Keyword(s):  
Growth Hormone ◽  
Energy Homeostasis ◽  
Peptide Hormone ◽  
Stable Cell Line ◽  
Growth Hormone Secretagogues ◽  
European Languages ◽  
Control Food ◽  
Control Food Intake ◽  
And Function ◽  
Hunger Signal

Small synthetic molecules called growth hormone secretagogues (GHSs) stimulate the release of growth hormone (GH) from the pituitary. They act through the GHS-R, a G protein-coupled receptor whose ligand has only been discovered recently. Using a reverse pharmacology paradigm with a stable cell line expressing GHS-R, we purified an endogenous ligand for GHS-R from rat stomach and named it “ghrelin,” after a word root (“ghre”) in Proto-Indo-European languages meaning “grow.” Ghrelin is a peptide hormone in which the third amino acid, usually a serine but in some species a threonine, is modified by a fatty acid; this modification is essential for ghrelin's activity. The discovery of ghrelin indicates that the release of GH from the pituitary might be regulated not only by hypothalamic GH-releasing hormone, but also by ghrelin derived from the stomach. In addition, ghrelin stimulates appetite by acting on the hypothalamic arcuate nucleus, a region known to control food intake. Ghrelin is orexigenic; it is secreted from the stomach and circulates in the bloodstream under fasting conditions, indicating that it transmits a hunger signal from the periphery to the central nervous system. Taking into account all these activities, ghrelin plays important roles for maintaining GH release and energy homeostasis in vertebrates.

scholarly journals Interleukin-6 Expression by Hypothalamic Microglia in Multiple Inflammatory Contexts: A Systematic Review

2019 ◽  
Vol 2019 ◽  
pp. 1-11 ◽  
Author(s):  
Vanessa C. D. Bobbo ◽  
Carlos P. Jara ◽  
Natália F. Mendes ◽  
Joseane Morari ◽  
Lício A. Velloso ◽  
...  
Keyword(s):  
Systematic Review ◽  
Interleukin 6 ◽  
Energy Homeostasis ◽  
Metabolic Diseases ◽  
Whole Body ◽  
Positive Energy ◽  
Anatomical Site ◽  
Control Food ◽  
Control Food Intake

Interleukin-6 (IL-6) is a unique cytokine that can play both pro- and anti-inflammatory roles depending on the anatomical site and conditions under which it has been induced. Specific neurons of the hypothalamus provide important signals to control food intake and energy expenditure. In individuals with obesity, a microglia-dependent inflammatory response damages the neural circuits responsible for maintaining whole-body energy homeostasis, resulting in a positive energy balance. However, little is known about the role of IL-6 in the regulation of hypothalamic microglia. In this systematic review, we asked what types of conditions and stimuli could modulate microglial IL-6 expression in murine model. We searched the PubMed and Web of Science databases and analyzed 13 articles that evaluated diverse contexts and study models focused on IL-6 expression and microglia activation, including the effects of stress, hypoxia, infection, neonatal overfeeding and nicotine exposure, lipopolysaccharide stimulus, hormones, exercise protocols, and aging. The results presented in this review emphasized the role of “injury-like” stimuli, under which IL-6 acts as a proinflammatory cytokine, concomitant with marked microglial activation, which drive hypothalamic neuroinflammation. Emerging evidence indicates an important correlation of basal IL-6 levels and microglial function with the maintenance of hypothalamic homeostasis. Advances in our understanding of these different contexts will lead to the development of more specific pharmacological approaches for the management of acute and chronic conditions, like obesity and metabolic diseases, without disturbing the homeostatic functions of IL-6 and microglia in the hypothalamus.

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