scholarly journals Regulation of Body Weight in Humans

1999 ◽  
Vol 79 (2) ◽  
pp. 451-480 ◽  
Author(s):  
Eric Jéquier ◽  
Luc Tappy
Keyword(s):  
Body Weight ◽  
Adipose Tissue ◽  
Energy Expenditure ◽  
Weight Regulation ◽  
Body Weight Regulation ◽  
Human Obesity ◽  
Tissue Mass ◽  
Leptin Receptors ◽  
Adipose Tissue Mass ◽  
Plasma Leptin

The mechanisms involved in body weight regulation in humans include genetic, physiological, and behavioral factors. Stability of body weight and body composition requires that energy intake matches energy expenditure and that nutrient balance is achieved. Human obesity is usually associated with high rates of energy expenditure. In adult individuals, protein and carbohydrate stores vary relatively little, whereas adipose tissue mass may change markedly. A feedback regulatory loop with three distinct steps has been recently identified in rodents: 1) a sensor that monitors the size of adipose tissue mass is represented by the amount of leptin synthesized by adipose cells (a protein encoded by the ob gene) which determines the plasma leptin levels; 2) hypothalamic centers, with specific leptin receptors, which receive and integrate the intensity of the signal; and 3) effector systems that influence the two determinants of energy balance, i.e., energy intake and energy expenditure. With the exception of a few very rare cases, the majority of obese human subjects have high plasma leptin levels that are related to the size of their adipose tissue mass. However, the expected regulatory responses (reduction in food intake and increase in energy expenditure) are not observed in obese individuals. Thus obese humans are resistant to the effect of endogenous leptin, despite unaltered hypothalamic leptin receptors. Whether defects in the leptin signaling cascade play a role in the development of human obesity is a field of great actual interest that needs further research. Present evidences suggest that genetic and environmental factors influence eating behavior of people prone to obesity and that diets that are high in fat or energy dense undermine body weight regulation by promoting an overconsumption of energy relative to need.

Triazole GHS-R1a antagonists JMV4208 and JMV3002 attenuate food intake, body weight, and adipose tissue mass in mice

2014 ◽  
Vol 393 (1-2) ◽  
pp. 120-128 ◽  
Author(s):  
M. Holubová ◽  
V. Nagelová ◽  
Z. Lacinová ◽  
M. Haluzík ◽  
D. Sýkora ◽  
...  
Keyword(s):  
Body Weight ◽  
Adipose Tissue ◽  
Food Intake ◽  
Tissue Mass ◽  
Adipose Tissue Mass

scholarly journals Individual housing of male C57BL/6J mice after weaning impairs growth and predisposes for obesity

2019 ◽  
Author(s):  
Lidewij Schipper ◽  
Steffen van Heijningen ◽  
Giorgio Karapetsas ◽  
Eline M. van der Beek ◽  
Gertjan van Dijk
Keyword(s):  
Body Weight ◽  
Adipose Tissue ◽  
Weight Gain ◽  
Energy Intake ◽  
White Adipose Tissue ◽  
Body Weight Gain ◽  
Tissue Mass ◽  
Individual Housing ◽  
Adipose Tissue Mass ◽  
Obesogenic Diet

AbstractIndividual housing from weaning onwards resulted in reduced growth rate during adolescence in male C57Bl/6J mice that were housed individually, while energy intake and energy expenditure were increased compared to socially housed counterparts. At 6 weeks of age, these mice had reduced lean body mass, but significantly higher white adipose tissue mass compared to socially housed mice. Body weight gain of individually housed animals exceeded that of socially housed mice during adulthood, with elevations in both energy intake and expenditure. At 18 weeks of age, individually housed mice showed higher adiposity and higher mRNA expression of UCP-1 in inguinal white adipose tissue. Exposure to an obesogenic diet starting at 6 weeks of age further amplified body weight gain and adipose tissue deposition. This study shows that post-weaning individual housing of male mice results in impaired adolescent growth and higher susceptibility to obesity in adulthood. Mice are widely used to study obesity and cardiometabolic comorbidities. For (metabolic) research models using mice, (social) housing practices should be carefully considered and regarded as a potential confounder due to their modulating effect on metabolic health outcomes.

scholarly journals Energy Expenditure, Fat Oxidation, and Body Weight Regulation: A Study of Metabolic Adaptation to Long- Term Weight Change

2000 ◽  
Vol 85 (3) ◽  
pp. 1087-1094 ◽  
Author(s):  
Christian Weyer ◽  
Richard E. Pratley ◽  
Arline D. Salbe ◽  
Clifton Bogardus ◽  
Eric Ravussin ◽  
...  
Keyword(s):  
Body Weight ◽  
Energy Expenditure ◽  
Weight Change ◽  
Fat Oxidation ◽  
Metabolic Adaptation ◽  
Weight Regulation ◽  
Body Weight Regulation

scholarly journals Effect of VPAC1 Blockade on Adipose Tissue Formation and Composition in Mouse Models of Nutritionally Induced Obesity

2010 ◽  
Vol 2010 ◽  
pp. 1-5 ◽  
Author(s):  
H. Roger Lijnen ◽  
Kathleen Freson ◽  
Marc F. Hoylaerts
Keyword(s):  
Body Weight ◽  
Adipose Tissue ◽  
Mouse Models ◽  
Tissue Formation ◽  
Tissue Mass ◽  
Diet Induced Obesity ◽  
Pituitary Adenylate Cyclase ◽  
Adipose Tissue Mass ◽  
Adipocyte Hypertrophy ◽  
G Protein Coupled

Background. The pituitary adenylate cyclase activating polypeptide (PACAP) may affect adipogenesis and adipose tissue formation through interaction with its G-protein-coupled receptor VPAC1.Methods. We have used a monoclonal antibody (MAb 23A11) blocking VPAC1 in mouse models of nutritionally induced obesity.Results. Administration of MAb 23A11 (25 mg/kg body weight i.p. twice weekly) to 5-week old male C57Bl/6 mice kept on a high-fat diet for 15 weeks had no significant effect on weight gain, nor on subcutaneous (SC) or gonadal (GON) adipose tissue mass, as compared to the control MAb 1C8. However, adipocyte hypertrophy was observed in SC adipose tissue of MAb 23A11 treated mice. In a second study, 24 weeks old obese mice were treated for 5 weeks with MAb 23A11, without effect on body weight or fat mass, as compared to treatment with MAb 1C8. In addition, MAb 23A11 had no significant effect on glucose tolerance or insulin resistance in lean or obese C57Bl/6 mice.Conclusion. Blocking VPAC1 does not significantly affect adipose tissue formation in mouse models of diet-induced obesity, although it may be associated with mild adipocyte hypertrophy.

Brown adipose tissue thermogenesis in testosterone-treated rats

1992 ◽  
Vol 126 (5) ◽  
pp. 434-437 ◽  
Author(s):  
María Abelenda ◽  
Maria Paz Nava ◽  
Alberto Fernández ◽  
María Luisa Puerta
Keyword(s):  
Body Weight ◽  
Adipose Tissue ◽  
Food Intake ◽  
Brown Adipose Tissue ◽  
Male Rats ◽  
Weight Regulation ◽  
Body Weight Regulation ◽  
Sexual Hormones ◽  
Brown Adipose ◽  
Brown Adipose Tissue Thermogenesis

The participation of sexual hormones in body weight regulation is partly accomplished by altering food intake. Nonetheless, female sexual hormones also alter brown adipose tissue thermogenesis in females. This study was aimed to find out if male hormones could alter brown adipose tissue thermogenesis in male rats. Testosterone was administered by means of Silastic capsules in adult male rats acclimated either at 28°C (thermoneutrality) or at 6°C (cold), treatment lasting 15 days. Food intake and body weight gain were reduced by hormonal treatment. However, brown adipose tissue mass, protein content, mitochondrial mass and GDP-binding were unchanged at both environmental temperatures. Accordingly, testosterone participation in body weight regulation is thought to be carried out without altering brown adipose tissue thermogenesis. A reduction in the weight of the sex accessory glands was also observed after cold acclimation.

scholarly journals High Dietary Sodium Intake Increases White Adipose Tissue Mass and Plasma Leptin in Rats*

Obesity ◽  
2007 ◽  
Vol 15 (9) ◽  
pp. 2200-2208 ◽  
Author(s):  
Miriam H. Fonseca-Alaniz ◽  
Luciana C. Brito ◽  
Cristina N. Borges-Silva ◽  
Julie Takada ◽  
Sandra Andreotti ◽  
...  
Keyword(s):  
Adipose Tissue ◽  
White Adipose Tissue ◽  
Sodium Intake ◽  
Dietary Sodium ◽  
Tissue Mass ◽  
Adipose Tissue Mass ◽  
Plasma Leptin

scholarly journals Prophylactic and therapeutic effects of different doses of vitamin C on high-fat-diet-induced non-alcoholic fatty liver disease in mice

2020 ◽  
Author(s):  
Qingmin Zeng ◽  
Lili Zhao ◽  
Chao Meng ◽  
Xiaotong Zhao ◽  
Yonggang Liu ◽  
...  
Keyword(s):  
Body Weight ◽  
Adipose Tissue ◽  
Therapeutic Effects ◽  
High Fat ◽  
Tissue Mass ◽  
Alcoholic Fatty Liver ◽  
Perirenal Adipose Tissue ◽  
Adipose Tissue Mass ◽  
Lobular Inflammation ◽  
Different Doses

Abstract Background: Epidemiological studies support the association between inadequate vitamin C (Vc) intake and non-alcoholic fatty liver disease (NAFLD). However, the intervention dose of Vc and the mechanisms of its action in NAFLD are unclear. This study aimed to investigate the prophylactic and therapeutic effects of low, medium and high doses of Vc on NAFLD. Methods: C57BL/6 mice were randomly assigned to prophylactic groups or therapeutic groups. Each group had five subgroups: control subgroup (C), high-fat subgroup (HF), low-dose Vc subgroup (15 mg/kg per day, LVc), medium-dose Vc subgroup (30 mg/kg per day, MVc), and high-dose Vc subgroup (90 mg/kg per day, HVc). In prophylactic groups, mice received high-fat diet (HFD) and simultaneously supplied with different doses Vc for 12 weeks. In therapeutic groups, mice were fed HFD for 6 weeks to form NAFLD model, and then treated with different dose Vc for 12 weeks. Results: Prophylactic LVc and MVc administration reduced the risk of NAFLD development in HFD-fed mice, as evidenced by significantly lowered body weight, perirenal adipose tissue mass, and steatosis, whereas prophylactic HVc administration did not prevent HFD-induced NAFLD development. Furthermore, therapeutic MVc administration significantly ameliorated HFD-induced increase in body weight, perirenal adipose tissue mass and steatosis, whereas therapeutic LVc and HVc administration did not ameliorate NAFLD symptoms. In fact, therapeutic HVc administration significantly increased body weight, perirenal adipose tissue mass and lobular inflammation. Moreover, prophylactic LVc administration was more effective than therapeutic LVc administration as evidenced by significantly lower body weight, perirenal adipose tissue mass, steatosis, ballooned hepatocytes, and lobular inflammation in the prophylactic LVc subgroup. And same trends were observed between prophylactic HVc administration and therapeutic HVc administration. In addition, all Vc-administered mice exhibited low blood glucose, triglycerides, and homeostasis model assessment of insulin resistance values and high adiponectin levels compared to HF mice. Conclusion: MVc was beneficial for HFD-induced NAFLD prophylaxis and therapy. LVc prevented HFD-induced NAFLD development, while HVc for NAFLD management was risky. This study offers valuable insight into the effect of various Vc doses on NAFLD management.

scholarly journals GGEx regulates body weight gain, hyperphagia and adipose tissue mass in obese and diabetic Otsuka Long‐Evans Tokushima fatty (OLETF) rats.

2007 ◽  
Vol 21 (6) ◽  
Author(s):  
Yang Sam Jung ◽  
Pei Chin Tsung ◽  
Byoung Chul Kim ◽  
Jong Hoon Kim ◽  
Hoa Jun Seok ◽  
...  
Keyword(s):  
Body Weight ◽  
Adipose Tissue ◽  
Weight Gain ◽  
Body Weight Gain ◽  
Tissue Mass ◽  
Oletf Rats ◽  
Adipose Tissue Mass ◽  
Long Evans

2008 Robert Levy Memorial Lecture—Tissue-Specific Regulation of Lipoprotein Lipase and Energy Balance: The Story Gets Even More Interesting

Circulation ◽  
2008 ◽  
Vol 118 (suppl_18) ◽  
Author(s):  
Robert Eckel
Keyword(s):  
Insulin Resistance ◽  
Skeletal Muscle ◽  
Fatty Acids ◽  
Body Weight ◽  
Adipose Tissue ◽  
Weight Regulation ◽  
Body Weight Regulation ◽  
Tissue Specific ◽  
Specific Manner ◽  
The Brain

Lipoprotein lipase (LPL) is a multifunctional enzyme produced by and studied in many tissues, including adipose tissue, cardiac and skeletal muscle, islets, and macrophages. After synthesis by parenchymal cells, the lipase is transported to the capillary endothelium, where it is rate-limiting for the hydrolysis of the triglyceride (TG) core of the circulating TG-rich lipoproteins, chylomicrons, and very low density lipoproteins (VLDL). The reaction products, fatty acids and monoacylglycerol, are in part taken up by the tissues locally, where they are processed in a tissue-specific manner, e.g., stored as neutral lipids (TG > cholesteryl esters[CE]) in adipose tissue, oxidized or stored in muscle, or as CE/TG in foam cells in macrophages. LPL is regulated in a tissue-specific manner. In adipose tissue, LPL is increased by insulin and meals but decreased by fasting, whereas muscle LPL is decreased by insulin and increased by fasting. In obesity, adipose tissue LPL is increased; however, the insulin dose-response curve is shifted to the right. After weight reduction and stabilization of the reduced obese state, adipose tissue LPL is increased, as is the response of the enzyme to insulin and meals. In skeletal muscle, insulin does not stimulate LPL nor is the enzyme activity changed in obesity; however, after weight reduction, LPL in skeletal muscle is decreased by 70%. These tissue-specific changes in LPL set the stage for lipid partitioning to help explain the recidivism of obesity. To examine this divergent regulation further, transgenic and knockout murine models of tissue-specific LPL expression have been developed. Mice with overexpression of LPL in skeletal muscle develop TG accumulation in muscle, develop insulin resistance, are protected from excessive weight gain, and increase their metabolic rate in the cold. When placed onto the LPL knockout and leptin deficient background, overexpression of LPL using an MCK promoter reduces obesity. Alternatively, a deletion of LPL in skeletal muscle reduces TG accumulation and increases insulin-mediated glucose transport into muscle but leads to lipid partitioning to other tissues, insulin resistance, and obesity. In the heart, loss of LPL is associated with hypertriglyceridemia and a greater utilization of glucose, implying that free fatty acids are not a sufficient fuel for optimal cardiac function. LPL is also produced in the brain, and that’s where the “story gets even more interesting.” We have just created mice with a neuron-specific deletion of LPL (NEXLPL−/−) using cre recombinase driven by the helix-loop-helix nuclear transcription factor NEX promoter. By 6 months of age, NEXLPL−/− mice weigh 50% more than their litter mates. This phenotype provides convincing evidence that lipoprotein sensing occurs in the brain and is important to energy balance and body weight regulation. Overall, LPL is a fascinating enzyme that contributes in a pronounced way to normal lipoprotein metabolism, tissue-specific substrate delivery and utilization, and to the many aspects of metabolism that relate to cardiovascular disease, including energy metabolism, insulin action, body weight regulation, and atherosclerosis.

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