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 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.

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

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.

Genetic loci determining bone density in mice with diet-induced atherosclerosis

2001 ◽  
Vol 5 (4) ◽  
pp. 205-215 ◽  
Author(s):  
THOMAS A. DRAKE ◽  
ERIC SCHADT ◽  
KAMBIZ HANNANI ◽  
J. MICHAEL KABO ◽  
KELLY KRASS ◽  
...  
Keyword(s):  
Body Weight ◽  
Adipose Tissue ◽  
Bone Density ◽  
Bone Mass ◽  
Plasma Lipids ◽  
Statistical Tests ◽  
Genetic Relationships ◽  
Bone Mass Density ◽  
Tissue Mass ◽  
Adipose Tissue Mass

This study investigates the phenotypic and genetic relationships among bone-density-related traits and those of adipose tissue and plasma lipids in mice with diet-induced atherosclerosis. Sixteen-month-old female F2 progeny of a C57BL/6J and DBA/2J intercross, which had received an atherogenic diet for 4 mo, were examined for multiple measures of femoral bone mass, density, and biomechanical properties using both computerized tomographic and radiographic methods. In addition, body weight and length, adipose tissue mass, plasma lipids and insulin, and aortic fatty lesions were assessed. Bone mass was inversely correlated with extent of atherosclerosis and with a prooxidant lipid profile and directly correlated with body weight, length, and, most strongly, adipose tissue mass. Quantitative trait locus (QTL) analysis, using composite interval mapping (CIM) and multi-trait analysis, identified six loci with multi-trait CIM LOD scores > 5. Three of these coincided with loci linked with adipose tissue and plasma high-density lipoprotein. Application of statistical tests for distinguishing close linkage vs. pleiotropy supported the presence of a potential pleiotropic effect of two of the loci on these traits. This study shows that bone mass in older female mice with atherosclerosis has multiple genetic determinants and provides phenotypic and genetic evidence linking the regulation of bone density with adipose tissue and plasma lipids.

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