scholarly journals Peripheral signalling involved in energy homeostasis control

2012 ◽  
Vol 25 (2) ◽  
pp. 223-248 ◽  
Author(s):  
Andoni Lancha ◽  
Gema Frühbeck ◽  
Javier Gómez-Ambrosi
Keyword(s):  
Body Weight ◽  
Growth Factor ◽  
Weight Control ◽  
Energy Homeostasis ◽  
Molecular Mechanisms ◽  
Sex Hormone Binding Globulin ◽  
Fibroblast Growth Factor 21 ◽  
Peripheral Tissues ◽  
Body Weight Control

The alarming prevalence of obesity has led to a better understanding of the molecular mechanisms controlling energy homeostasis. Regulation of energy intake and expenditure is more complex than previously thought, being influenced by signals from many peripheral tissues. In this sense, a wide variety of peripheral signals derived from different organs contributes to the regulation of body weight and energy expenditure. Besides the well-known role of insulin and adipokines, such as leptin and adiponectin, in the regulation of energy homeostasis, signals from other tissues not previously thought to play a role in body weight regulation have emerged in recent years. The role of fibroblast growth factor 21 (FGF21), insulin-like growth factor 1 (IGF-I), and sex hormone-binding globulin (SHBG) produced by the liver in the regulation of body weight and insulin sensitivity has been recently described. Moreover, molecules expressed by skeletal muscle such as myostatin have also been involved in adipose tissue regulation. Better known is the involvement of ghrelin, cholecystokinin, glucagon-like peptide 1 (GLP-1) and PYY3–36, produced by the gut, in energy homeostasis. Even the kidney, through the production of renin, appears to regulate body weight, with mice lacking this hormone exhibiting resistance to diet-induced obesity. In addition, the skeleton has recently emerged as an endocrine organ, with effects on body weight control and glucose homeostasis through the actions of bone-derived factors such as osteocalcin and osteopontin. The comprehension of these signals will help in a better understanding of the aetiopathology of obesity, contributing to the potential development of new therapeutic targets aimed at tackling excess body fat accumulation.

Chronic intracerebroventricular infusion of MCH causes obesity in mice

2003 ◽  
Vol 284 (3) ◽  
pp. E583-E588 ◽  
Author(s):  
Akira Gomori ◽  
Akane Ishihara ◽  
Masahiko Ito ◽  
Satoshi Mashiko ◽  
Hiroko Matsushita ◽  
...  
Keyword(s):  
Body Weight ◽  
Weight Control ◽  
Energy Homeostasis ◽  
The Body ◽  
Intracerebroventricular Infusion ◽  
Melanin Concentrating Hormone ◽  
Important Regulator ◽  
Obesity In Mice ◽  
Body Weight Control

Melanin-concentrating hormone (MCH) is a cyclic amino acid neuropeptide localized in the lateral hypothalamus. Although MCH is thought to be an important regulator of feeding behavior, the involvement of this peptide in body weight control has been unclear. To examine the role of MCH in the development of obesity, we assessed the effect of chronic intracerebroventricular infusion of MCH in C57BL/6J mice that were fed with regular or moderately high-fat (MHF) diets. Intracerebroventricular infusion of MCH (10 μg/day for 14 days) caused a slight but significant increase in body weight in mice maintained on the regular diet. In the MHF diet-fed mice, MCH more clearly increased the body weight accompanied by a sustained hyperphagia and significant increase in fat and liver weights. Plasma glucose, insulin, and leptin levels were also increased in the MCH-treated mice fed the MHF diet. These results suggest that chronic stimulation of the brain MCH system causes obesity in mice and imply that MCH may have a major role in energy homeostasis.

scholarly journals The Short-Chain Fatty Acid Acetate in Body Weight Control and Insulin Sensitivity

Nutrients ◽  
2019 ◽  
Vol 11 (8) ◽  
pp. 1943 ◽  
Author(s):  
Hernández ◽  
Canfora ◽  
Jocken ◽  
Blaak
Keyword(s):  
Body Weight ◽  
Gut Microbiota ◽  
Weight Control ◽  
Peptide Yy ◽  
Short Chain ◽  
Whole Body ◽  
Peripheral Tissues ◽  
Substrate Metabolism ◽  
Human Data ◽  
Body Weight Control

The interplay of gut microbiota, host metabolism, and metabolic health has gained increased attention. Gut microbiota may play a regulatory role in gastrointestinal health, substrate metabolism, and peripheral tissues including adipose tissue, skeletal muscle, liver, and pancreas via its metabolites short-chain fatty acids (SCFA). Animal and human data demonstrated that, in particular, acetate beneficially affects host energy and substrate metabolism via secretion of the gut hormones like glucagon-like peptide-1 and peptide YY, which, thereby, affects appetite, via a reduction in whole-body lipolysis, systemic pro-inflammatory cytokine levels, and via an increase in energy expenditure and fat oxidation. Thus, potential therapies to increase gut microbial fermentation and acetate production have been under vigorous scientific scrutiny. In this review, the relevance of the colonically and systemically most abundant SCFA acetate and its effects on the previously mentioned tissues will be discussed in relation to body weight control and glucose homeostasis. We discuss in detail the differential effects of oral acetate administration (vinegar intake), colonic acetate infusions, acetogenic fiber, and acetogenic probiotic administrations as approaches to combat obesity and comorbidities. Notably, human data are scarce, which highlights the necessity for further human research to investigate acetate’s role in host physiology, metabolic, and cardiovascular health.

scholarly journals The Hypothalamic Preoptic Area and Body Weight Control

2017 ◽  
Vol 106 (2) ◽  
pp. 187-194 ◽  
Author(s):  
Sangho Yu ◽  
Marie François ◽  
Clara Huesing ◽  
Heike Münzberg
Keyword(s):  
Body Weight ◽  
Temperature Change ◽  
Weight Control ◽  
Energy Homeostasis ◽  
Preoptic Area ◽  
Scientific Basis ◽  
Main Function ◽  
Humoral Factors ◽  
Brown Adipose ◽  
Body Weight Control

The preoptic area (POA) of the hypothalamus is involved in many physiological and behavioral processes thanks to its interconnections to many brain areas and ability to respond to diverse humoral factors. One main function of the POA is to manage body temperature homeostasis, e.g. in response to ambient temperature change, which is achieved in part by controlling brown adipose tissue thermogenesis. The POA is also importantly involved in modulating food intake in response to temperature change, thus making it relevant for body weight homeostasis and obesity research. POA function in body weight control is highly unexplored, and a better understanding of POA circuits and their integration into classic hypothalamic circuits that regulate energy homeostasis is expected to provide new opportunities for the scientific basis and treatment of obesity and comorbidities.

scholarly journals Erratum

2002 ◽  
Vol 61 (2) ◽  
pp. 319-319
Author(s):  
Yves Schutz
Keyword(s):  
Body Weight ◽  
Weight Control ◽  
Substrate Utilization ◽  
Body Weight Control

Role of substrate utilization and thermogenesis on body-weight control with particular reference to alcohol By Yves Schutz Volume 59 (2000), Number 4 Figure 1, page 513

scholarly journals A Physiological Role of Breast Milk Leptin in Body Weight Control in Developing Infants*

Obesity ◽  
2006 ◽  
Vol 14 (8) ◽  
pp. 1371-1377 ◽  
Author(s):  
Olga Miralles ◽  
Juana Sánchez ◽  
Andreu Palou ◽  
Catalina Picó
Keyword(s):  
Body Weight ◽  
Breast Milk ◽  
Weight Control ◽  
Physiological Role ◽  
Body Weight Control

scholarly journals Role of substrate utilization and thermogenesis on body-weight control with particular reference to alcohol

2000 ◽  
Vol 59 (4) ◽  
pp. 511-517 ◽  
Author(s):  
Yves Schutz
Keyword(s):  
Weight Control ◽  
De Novo ◽  
Experimental Studies ◽  
Substrate Utilization ◽  
The Body ◽  
Energy Utilization ◽  
Peripheral Tissues ◽  
Intrinsic Factors ◽  
Body Weight Control

Alcohol (ethanol; EtOH) provides fuel energy to the body (29·7 kJ (7·1 kcal)/g, 23·4 kJ (5·6 kcal)/ml), as do other macronutrients, but no associated essential nutrients. The thermogenic effect of EtOH (on average 15 % of its metabolizable value) is much greater than that of the main substrates utilized by the body, i.e. fat and carbohydrates (CHO), suggesting a lower net efficiency of energy utilization for EtOH than for fat and CHO. EtOH cannot be stored in the body and is toxic, so that there is an obligatory continuous oxidation of EtOH and it becomes the priority fuel to be metabolized. In contrast to CHO, its rate of oxidation does not depend on the dose ingested. As with CHO intake, it engenders a shift in postprandial substrate utilization (decrease in fat oxidation), but by a non-insulin-mediated mechanism. A limited amount of EtOH can be converted to fatty acids by hepatic de novo lipogenesis (as occurs with high levels of CHO feeding) from acetate production, which inhibits lipolysis in peripheral tissues. There is no evidence that EtOH consumed under normoenergetic conditions (i.e. isoenergetically replacing CHO or fat) leads to greater body fat storage than fat or CHO. However, there is still a lack of experimental studies on the influence of EtOH on the level of spontaneous physical activity in man. This effect may well depend on the dose of EtOH consumed as well as other intrinsic factors.

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