PC61 MATERNAL BODY COMPOSITION DETERMINES OFFSPRING REGIONAL ADIPOSE TISSUE MASS IRRESPECTIVE OF MATERNAL FOOD INTAKE DURING GESTATION

2004 ◽  
Vol 39 (Supplement 1) ◽  
pp. S535
Author(s):  
D. S. Gardner ◽  
G. S. Gopalakrishnan ◽  
T. Stephenson ◽  
M. Symonds
Keyword(s):  
Body Composition ◽  
Adipose Tissue ◽  
Food Intake ◽  
Maternal Body ◽  
Tissue Mass ◽  
Adipose Tissue Mass

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

Abstract P129: FTO Genotype and 2-year Change in Body Composition and Fat Distribution in Response to Weight-loss Diets: The Pounds Lost Trial

Circulation ◽  
2012 ◽  
Vol 125 (suppl_10) ◽  
Author(s):  
Xiaomin Zhang ◽  
Qibin Qi ◽  
Frank Hu ◽  
Frank Sacks ◽  
Lu Qi
Keyword(s):  
Weight Loss ◽  
Body Composition ◽  
Adipose Tissue ◽  
Risk Allele ◽  
High Protein Diet ◽  
Fat Distribution ◽  
High Protein ◽  
Protein Diet ◽  
Tissue Mass ◽  
Adipose Tissue Mass

OBJECTIVE The fat mass and obesity-associated gene (FTO) variant has shown the strongest association with obesity. Recent studies suggest that dietary intake may modify the genetic effects of FTO. We tested the effect of FTO variant on long-term weight loss and change in body composition in a 2-year randomized intervention trial. RESEARCH DESIGN AND METHODS FTO SNP rs1558902 was genotyped in 742 overweight or obese adults who were randomly assigned to one of four diets differing in the percentages of energy derived from fat, protein and carbohydrate (20, 15, and 65%; 20, 25, and 55%; 40, 15, and 45%; and 40, 25, and 35%) in the Pounds Lost Trial for 2 years. Body composition and fat distribution were measured in 424 and 195 participants by Dual-energy X-ray absorptiometry (DXA) and computed tomography (CT), respectively. RESULTS We found significant modification effects for diet intervention varying in protein (low vs high), but not in fat, on 2-year changes in total fat, fat free mass (FFM), fat mass% (FM%), trunk fat%, total adipose tissue mass (TAT), visceral adipose tissue mass (VAT) and superficial adipose tissue mass (SAT) (P for interactions=0.045, 0.036, 0.033, 0.048, 0.001, 0.008 and 0.002, respectively). Carriers of the risk allele (A allele) had a greater loss of weight and regional fat in response to high protein diet, while an opposite genetic effect was observed on changes in TAT and SAT in response to low protein diet at 2 years. Significant gene by diet interventions (low vs high protein) were also observed at 6 months of intervention, when the maximum of weight-loss was achieved, for changes in FFM, TAT, VAT and SAT (P for interactions=0.007, 0.019, 0.036 and 0.041, respectively). Patterns of change in body composition and fat distribution by diet intervention were similar at 6 month and 2 year. CONCLUSIONS Our data suggest that a high-protein diet may be beneficial for weight loss in individuals with the risk allele of the FTO variant rs1558902.

Acylation-stimulating protein/C5L2-neutralizing antibodies alter triglyceride metabolism in vitro and in vivo

2007 ◽  
Vol 293 (6) ◽  
pp. E1482-E1491 ◽  
Author(s):  
Wei Cui ◽  
Sabina Paglialunga ◽  
David Kalant ◽  
HuiLing Lu ◽  
Christian Roy ◽  
...  
Keyword(s):  
Adipose Tissue ◽  
Food Intake ◽  
Glucose Transport ◽  
Neutralizing Antibodies ◽  
Tissue Mass ◽  
Acylation Stimulating Protein ◽  
Adipose Tissue Mass ◽  
Ampk Activity

Acylation-stimulating protein (ASP), a lipogenic hormone, stimulates triglyceride (TG) synthesis and glucose transport upon activation of C5L2, a G protein-coupled receptor. ASP-deficient mice have reduced adipose tissue mass due to increased energy expenditure despite increased food intake. The objective of this study was to evaluate the blocking of ASP-C5L2 interaction via neutralizing antibodies (anti-ASP and anti-C5L2-L1 against C5L2 extracellular loop 1). In vitro, anti-ASP and anti-C5L2-L1 blocked ASP binding to C5L2 and efficiently inhibited ASP stimulation of TG synthesis and glucose transport. In vivo, neither anti-ASP nor anti-C5L2-L1 altered body weight, adipose tissue mass, food intake, or hormone levels (insulin, leptin, and adiponectin), but they did induce a significant delay in TG clearance [ P < 0.0001, 2-way repeated-measures (RM) ANOVA] and NEFA clearance ( P < 0.0001, 2-way RM ANOVA) after a fat load. After treatment with either anti-ASP or anti-C5L2-L1 antibody there was no change in adipose tissue AMPK activity, but neutralizing antibodies decreased perirenal TG mass (−38.4% anti-ASP, −18.8% anti-C5L2, P < 0.01–0.001) and perirenal LPL activity (−75.6% anti-ASP, −72.5% anti-C5L2, P < 0.05). In liver, anti-C5L2-L1 decreased TG mass (−42.8%, P < 0.05), whereas anti-ASP increased AMPK activity (+34.6%, P < 0.001). In the muscle, anti-C5L2-L1 significantly increased TG mass (+128.0%, P < 0.05), LPL activity (+226.1%, P < 0.001), and AMPK activity (+71.1%, P < 0.01). In addition, anti-ASP increased LPL activity (+164.4, P < 0.05) and AMPK activity (+53.9%, P < 0.05) in muscle. ASP/C5L2-neutralizing antibodies effectively block ASP-C5L2 interaction, altering lipid distribution and energy utilization.

scholarly journals Body Composition of Chronic Kidney Disease Patients

2021 ◽  
Vol 5 (1) ◽  
pp. 54-58
Author(s):  
Anjani Bakshi ◽  
Kalyani Singh ◽  
Anupa Siddhu
Keyword(s):  
Chronic Kidney Disease ◽  
Body Composition ◽  
Adipose Tissue ◽  
Kidney Disease ◽  
Fat Tissue ◽  
Lean Tissue ◽  
Tissue Mass ◽  
Lean Tissue Mass ◽  
Significant Difference ◽  
Adipose Tissue Mass

With accelerated muscle proteolysis, a decrease in muscle mass is evident in chronic kidney disease (CKD) patients. This eventually leads to nutritional disturbance that for a long has been mostly attributed to malnutrition. This predisposes patients to premature morbidity and mortality. Assessing body composition, thus, becomes vital. In this cross-sectional study, CKD patients (n = 47) of stages 2, 3a, 3b and 4 were assessed for their lean tissue mass, adipose tissue mass and overhydration by body composition monitor. Lean tissue index and fat tissue index were calculated as lean tissue mass and adipose tissue mass in kilogram divided by patients’ height in square meters. Patients were assessed for their handgrip strength (HGS) by Jamar hydraulic hand dynamometer, and also for their 7-day diet history. Mean lean tissue index of CKD patients was 11.73 ± 2.49 kg/m2. About 34 (72.3%) out of 47 patients were below the reference value of lean tissue index. A significant difference in lean tissue index (P = 0.03) was observed at various stages. Patients at stage 4 had the lowest lean tissue index. Lean tissue was significantly (P = 0.03) low in patients consuming protein <0.6 gm/kg/day. All 47 patients had less than normal HGS values. Patients’ mean fat tissue index was 14.86 ± 6.18 kg/m2 and had water retention with a mean overhydration of 1.47 ± 2.12 L. CKD patients were malnourished with a significant low lean tissue index. Dietary protein intake and HGS of these patients were positively associated with lean tissue index.

scholarly journals MED19 Regulates Adipogenesis and Maintenance of White Adipose Tissue Mass by Mediating PPARγ-Dependent Gene Expression

Cell Reports ◽  
2020 ◽  
Vol 33 (1) ◽  
pp. 108228 ◽  
Author(s):  
John M. Dean ◽  
Anyuan He ◽  
Min Tan ◽  
Jun Wang ◽  
Dongliang Lu ◽  
...  
Keyword(s):  
Gene Expression ◽  
Adipose Tissue ◽  
White Adipose Tissue ◽  
Tissue Mass ◽  
Adipose Tissue Mass

scholarly journals Chemotactic cytokines, obesity and type 2 diabetes:in vivoandin vitroevidence for a possible causal correlation?

2009 ◽  
Vol 68 (4) ◽  
pp. 378-384 ◽  
Author(s):  
Henrike Sell ◽  
Jürgen Eckel
Keyword(s):  
Insulin Resistance ◽  
Adipose Tissue ◽  
Low Grade ◽  
Obese Patients ◽  
Tissue Mass ◽  
Tissue Biology ◽  
Wide Range ◽  
Adipose Tissue Mass

A strong causal link between increased adipose tissue mass and insulin resistance in tissues such as liver and skeletal muscle exists in obesity-related disorders such as type 2 diabetes. Increased adipose tissue mass in obese patients and patients with diabetes is associated with altered secretion of adipokines, which also includes chemotactic proteins. Adipose tissue releases a wide range of chemotactic proteins including many chemokines and chemerin, which are interesting targets for adipose tissue biology and for biomedical research in obesity and obesity-related diseases. This class of adipokines may be directly linked to a chronic state of low-grade inflammation and macrophage infiltration in adipose tissue, a concept intensively studied in adipose tissue biology in recent years. The inflammatory state of adipose tissue in obese patients may be the most important factor linking increased adipose tissue mass to insulin resistance. Furthermore, chemoattractant adipokines may play an important role in this situation, as many of these proteins possess biological activity beyond the recruitment of immune cells including effects on adipogenesis and glucose homeostasis in insulin-sensitive tissues. The present review provides a summary of experimental evidence of the role of adipose tissue-derived chemotactic cytokines and their function in insulin resistancein vivoandin vitro.

Fibroblast growth factor receptor 1 is a key regulator of early adipogenic events in human preadipocytes

2009 ◽  
Vol 296 (1) ◽  
pp. E121-E131 ◽  
Author(s):  
C. H. Widberg ◽  
F. S. Newell ◽  
A. W. Bachmann ◽  
S. N. Ramnoruth ◽  
M. C. Spelta ◽  
...  
Keyword(s):  
Adipose Tissue ◽  
Growth Factor ◽  
Fibroblast Growth Factor ◽  
Tissue Expansion ◽  
Cell Number ◽  
Fibroblast Growth ◽  
Tissue Mass ◽  
Proliferation And Differentiation ◽  
Adipose Tissue Mass ◽  
Human Preadipocytes

Cell number is an important determinant of adipose tissue mass, and the coordinated proliferation and differentiation of preadipocytes into mature lipid-laden adipocytes underpins the increased adipose tissue mass associated with obesity. Despite this, the molecular cues governing such adipose tissue expansion are poorly understood. We previously reported that fibroblast growth factor-1 (FGF-1) promotes both proliferation and differentiation of human preadipocytes and that the major adipogenic effect of FGF-1 occurs during proliferation, priming the cells for adipose conversion. In the current study, we examined whether this effect was linked to the mitogenic action of FGF-1 by investigating the mitogenic and adipogenic potential of other growth factors, platelet-derived growth factor (PDGF; AA and BB) and vascular endothelial growth factor. Although PDGF-AA and PDGF-BB showed comparable mitogenic potential to FGF-1, only FGF-1 treatment resulted in priming and subsequent differentiation. Pharmacological inhibition of FGF receptor (FGFR) tyrosine kinase activity, using the FGFR-specific inhibitors PD-173074 and SU-5402, revealed an obligate requirement for FGFR activity in these processes. A combination of biochemical and genetic approaches revealed an important role for FGFR1. Knock down of FGFR1 expression by small-interfering RNA reduced FGF-1-stimulated signaling events, proliferation, and priming. Together these data highlight the unique nature of the role of FGF-1 during the earliest stages of adipogenesis and establish a role for FGFR1 in human adipogenesis, identifying FGFR1 as a potential therapeutic target to reduce obesity.

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