Hypothalamic regulation of energy homeostasis

2002 ◽  
Vol 16 (4) ◽  
pp. 623-637 ◽  
Author(s):  
Amanda Sainsbury ◽  
Gregory J Cooney ◽  
Herbert Herzog
Keyword(s):  
Energy Homeostasis ◽  
Hypothalamic Regulation

Role of dopamine D2 receptor in hypothalamic regulation of energy homeostasis

2006 ◽  
Vol 27 (1) ◽  
pp. 88
Author(s):  
Sa Yong Kim ◽  
Kyu seok Kim ◽  
Seung Woo Shin ◽  
Min Sun Kim ◽  
Ja Hyun Baik
Keyword(s):  
Energy Homeostasis ◽  
Dopamine D2 Receptor ◽  
D2 Receptor ◽  
Dopamine D2 ◽  
Hypothalamic Regulation

scholarly journals Endocrine factors in the hypothalamic regulation of food intake in females: a review of the physiological roles and interactions of ghrelin, leptin, thyroid hormones, oestrogen and insulin

2011 ◽  
Vol 24 (1) ◽  
pp. 132-154 ◽  
Author(s):  
V. Somogyi ◽  
A. Gyorffy ◽  
T. J. Scalise ◽  
D. S. Kiss ◽  
G. Goszleth ◽  
...  
Keyword(s):  
Food Intake ◽  
Energy Expenditure ◽  
Thyroid Hormones ◽  
Energy Homeostasis ◽  
The Body ◽  
Feedback Information ◽  
Hypothalamic Regulation ◽  
The Individual ◽  
Desire To Eat ◽  
The Brain

Controlling energy homeostasis involves modulating the desire to eat and regulating energy expenditure. The controlling machinery includes a complex interplay of hormones secreted at various peripheral endocrine endpoints, such as the gastrointestinal tract, the adipose tissue, thyroid gland and thyroid hormone-exporting organs, the ovary and the pancreas, and, last but not least, the brain itself. The peripheral hormones that are the focus of the present review (ghrelin, leptin, thyroid hormones, oestrogen and insulin) play integrated regulatory roles in and provide feedback information on the nutritional and energetic status of the body. As peripheral signals, these hormones modulate central pathways in the brain, including the hypothalamus, to influence food intake, energy expenditure and to maintain energy homeostasis. Since the growth of the literature on the role of various hormones in the regulation of energy homeostasis shows a remarkable and dynamic expansion, it is now becoming increasingly difficult to understand the individual and interactive roles of hormonal mechanisms in their true complexity. Therefore, our goal is to review, in the context of general physiology, the roles of the five best-known peripheral trophic hormones (ghrelin, leptin, thyroid hormones, oestrogen and insulin, respectively) and discuss their interactions in the hypothalamic regulation of food intake.

060. OVER FEEDING EARLY IN LIFE AND RISK OF OBESITY: INSIGHT FROM THE RODENT

2009 ◽  
Vol 21 (9) ◽  
pp. 15
Author(s):  
M. J. Morris
Keyword(s):  
High Fat Diet ◽  
Animal Studies ◽  
Energy Homeostasis ◽  
Maternal Obesity ◽  
Obesity Risk ◽  
High Fat ◽  
Generational Effects ◽  
Hypothalamic Regulation ◽  
The Impact ◽  
Detrimental Impact

While adult lifestyle factors undoubtedly contribute to the incidence of obesity and its attendant disorders, mounting evidence suggests that programming of obesity may occur following over-nutrition during development. As hypothalamic control of appetite and energy expenditure is set early in life and can be perturbed by certain exposures such as under-nutrition and altered metabolic and hormonal signals, in utero exposure to maternal obesity related changes may contribute to programming of obesity in offspring. Data from animal studies indicate both intrauterine and postnatal environments are critical determinants of the development of pathways regulating energy homeostasis. Experimental evidence in rat studies from our laboratory points to an additive detrimental impact of high fat diet consumption after weaning in animals born of obese mothers. Deleterious effects of high fat diet during pregnancy on metabolic profile, adiposity and cardiac hypertrophy were enhanced by postnatal over consumption. Even modest early postnatal overfeeding induced by litter size reduction leads to increased adiposity. Studies are needed to determine to what extent the effect of maternal and early nutritional changes persist. This presentation summarizes recent evidence of the impact of maternal obesity on subsequent obesity risk, paying particular attention to the hypothalamic regulation of appetite, and markers of metabolic control. There is an urgent need to investigate the mechanisms underlying the trans-generational effects of maternal obesity due to an extraordinary rise in the rates of maternal obesity.

Obesity and Nutritional Disorders

2016 ◽  
pp. 185-190
Author(s):  
Ryan T. Hurt
Keyword(s):  
Environmental Factors ◽  
Energy Homeostasis ◽  
Caloric Intake ◽  
The United States ◽  
Overweight And Obesity ◽  
Prader Willi Syndrome ◽  
Gene Variants ◽  
Obesity Epidemic ◽  
Hypothalamic Regulation ◽  
Genetic And Environmental Factors

The prevalence of overweight and obesity has been increasing in the United States and the westernized world. The cause of the recent obesity epidemic involves a complex interplay between genetic and environmental factors. Specific, rare genetic disruptions of the hypothalamic regulation of energy homeostasis pathways can cause obesity (eg, Prader-Willi syndrome). Most cases of obesity result from a group of gene variants exposed to environmental factors. The 2 major environmental factors that contribute to overweight and obesity are excess caloric intake and low physical activity.

Cardiovascular effects of leptin and orexins

2003 ◽  
Vol 284 (3) ◽  
pp. R639-R651 ◽  
Author(s):  
Tetsuro Shirasaka ◽  
Mayumi Takasaki ◽  
Hiroshi Kannan
Keyword(s):  
Energy Homeostasis ◽  
Cardiovascular Effects ◽  
Autonomic Functions ◽  
Signaling Mechanism ◽  
Functional Studies ◽  
Hypothalamic Regulation ◽  
Sympathetic Regulation ◽  
The Brain

Leptin, the product of the obgene, is a satiety factor secreted mainly in adipose tissue and is part of a signaling mechanism regulating the content of body fat. It acts on leptin receptors, most of which are located in the hypothalamus, a region of the brain known to control body homeostasis. The fastest and strongest hypothalamic response to leptin in ob/ob mice occurs in the paraventricular nucleus, which is involved in neuroendocrine and autonomic functions. On the other hand, orexins (orexin-A and -B) or hypocretins (hypocretin-1 and -2) were recently discovered in the hypothalamus, in which a number of neuropeptides are known to stimulate or suppress food intake. These substances are considered important for the regulation of appetite and energy homeostasis. Orexins were initially thought to function in the hypothalamic regulation of feeding behavior, but orexin-containing fibers and their receptors are also distributed in parts of the brain closely associated with the regulation of cardiovascular and autonomic functions. Functional studies have shown that these peptides are involved in cardiovascular and sympathetic regulation. The objective of this article is to summarize evidence on the effects of leptin and orexins on cardiovascular function in vivo and in vitro and to discuss the pathophysiological relevance of these peptides and possible interactions.

scholarly journals New Insights of SF1 Neurons in Hypothalamic Regulation of Obesity and Diabetes

2021 ◽  
Vol 22 (12) ◽  
pp. 6186
Author(s):  
Anna Fosch ◽  
Sebastián Zagmutt ◽  
Núria Casals ◽  
Rosalía Rodríguez-Rodríguez
Keyword(s):  
Glucose Homeostasis ◽  
Energy Homeostasis ◽  
Ventromedial Hypothalamus ◽  
Whole Body ◽  
Metabolic Adaptation ◽  
Glucose Levels ◽  
Obesity And Diabetes ◽  
Hypothalamic Regulation ◽  
Feeding Control ◽  
Body Energy

Despite the substantial role played by the hypothalamus in the regulation of energy balance and glucose homeostasis, the exact mechanisms and neuronal circuits underlying this regulation remain poorly understood. In the last 15 years, investigations using transgenic models, optogenetic, and chemogenetic approaches have revealed that SF1 neurons in the ventromedial hypothalamus are a specific lead in the brain’s ability to sense glucose levels and conduct insulin and leptin signaling in energy expenditure and glucose homeostasis, with minor feeding control. Deletion of hormonal receptors, nutritional sensors, or synaptic receptors in SF1 neurons triggers metabolic alterations mostly appreciated under high-fat feeding, indicating that SF1 neurons are particularly important for metabolic adaptation in the early stages of obesity. Although these studies have provided exciting insight into the implications of hypothalamic SF1 neurons on whole-body energy homeostasis, new questions have arisen from these results. Particularly, the existence of neuronal sub-populations of SF1 neurons and the intricate neurocircuitry linking these neurons with other nuclei and with the periphery. In this review, we address the most relevant studies carried out in SF1 neurons to date, to provide a global view of the central role played by these neurons in the pathogenesis of obesity and diabetes.

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