Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0028754 (obesity)
 124,988 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Adipocyte fatty acid-binding protein (A-FABP) has been reported to be increased in obese adults and to be related to metabolic syndrome. Because studies concerning A-FABP in weight loss are limited and studies in obese children are missing, we analyzed A-FABP in obese children before and after weight loss. Fasting serum A-FABP, leptin, insulin, glucose, triglycerides, low-and high-density lipoprotein cholesterol, high-sensitivity C-reactive protein, and tumor necrosis factor alpha concentrations as markers of the metabolic syndrome, and weight status (body mass index and percentage body fat based on skinfold measurements) were determined in 30 obese children (median age, 11.9 years) before and after participating in a 1-year obesity intervention. Furthermore, A-FABP levels were measured in 10 nonobese children of similar age, sex, and pubertal stage. Obese children had significantly (P < .001) higher A-FABP concentrations compared with nonobese children. In backward multivariate linear regression analysis, A-FABP correlated significantly (P < .05) with percentage body fat and leptin, but not with any of the markers of the metabolic syndrome. Changes of A-FABP concentrations correlated significantly with changes of percentage body fat (r = 0.53, P = .001) and leptin (r = 0.55, P < .001), but not with any changes of parameters of the metabolic syndrome. Substantial weight loss in 10 children led to a significant (P < .05) decrease in A-FABP levels in contrast to the 20 children without change of weight status. In cross-sectional as well as longitudinal analyses, A-FABP levels were related to weight status and leptin levels. Further longitudinal studies are necessary to study the relationship between A-FABP concentrations and parameters of the metabolic syndrome.
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PMID:Adipocyte fatty acid-binding protein in obese children before and after weight loss. 1799 29

Body weight (BW) mainly depends on a balance between fat storage (lipogenesis) and fat mobilization (lipolysis) in adipocytes. BW changes play a role in insulin resistance (IR), the inability of insulin target tissue to respond to physiological levels of insulin. This results in inhibition of lipogenesis and stimulation of lipolysis. Weight gain leads to IR whereas, weight loss improves insulin sensitivity (IS). The aim of this study was to evaluate the effect of weight loss and recovery of IS on the expression of genes involved in lipogenesis and lipolysis in weight losing dogs. Gene expression was studied in both subcutaneous and visceral adipose tissue. Obese dogs received a hypoenergetic low fat high protein diet (0.6 x NRC recommendation). Before and after weight loss, IS was assessed using the euglycaemic hyperinsulinaemic clamp. Gene expression of IRS-2, SREBP, intracellular insulin effectors, ACC, FAS, FABP, ADRP, PEPCK, lipogenesis key proteins, perilipin and HSL, lipolysis key proteins were quantified using real-time RT-PCR in subcutaneous and visceral fat. BW decreased from 15.2 +/- 0.5 to 11.4 +/- 0.4 kg (p < 0.05) over 78 +/- 8 days. When obese, dogs were insulin resistant. After weight loss, IS was improved. In the subcutaneous adipose tissue, the expression of only the IRS-2 was increased. In the visceral adipose tissue, the expression of the genes involved in the lipogenesis was decreased whereas one of the genes implied in the lipolysis did not change. The expression profile of genes involved in lipid metabolism, as measured after weight loss, is indicative for a lower lipogenesis after weight loss than in obese dogs. Our results also confirm dramatic differences in the lipid metabolism of visceral and subcutaneous fat. They should be completed by comparing gene expression during weight losing and normal weight steady state.
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PMID:Adipose tissue gene expression in obese dogs after weight loss. 1847 22

Adipocyte-fatty acid binding protein (A-FABP) is a biomarker of adiposity and metabolic syndrome. The aim of our work was to investigate the effect of weight reduction on serum A-FABP value. In the study, we analyzed a group of 189 probands suffering from obesity (102 women and 87 men; aged 57.3+/-12 years) initially, after a 3-month low-fat diet and once again 3 months after the termination of the diet for serum A-FABP, insulin, glucose, total cholesterol, HDL-cholesterol, LDL-cholesterol, and triglycerides. Basal biomarker concentrations were typical of the metabolic syndrome, and moreover A-FABP correlated with Quicki and BMI. We observed a reduction in BMI in 145 subjects who were divided into two subgroups: A-with persistent BMI reduction even after 6 months, B-with BMI reduction after 3 months and its regress after 6 months. Individuals with rise or no BMI difference were signed as subgroup C. In subgroup A, A-FABP level increased and returned to the earlier level (42.3 vs 68.3 vs 37.1 microg/l) and correlated with the markers of the metabolic syndrome. In subgroup B, A-FABP level increased less significantly, however elevated A-FABP level persisted for 6 months (41.9 vs 53.6 vs 50.7 microg/l). Subgroup C (n=54) showed no difference in A-FABP after 3-month diet and after next 3 months. The A-FABP value correlated with the some components of the metabolic syndrome. In conclusion, we describe that serum A-FABP might be a prognostic marker of body weight loss suggesting a preventive therapeutic intervention.
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PMID:Serum adipocyte-fatty acid binding protein discriminates patients with permanent and temporary body weight loss. 1880 74

Previous work conducted in our laboratory suggested a role for liver fatty acid-binding protein (L-FABP) in obesity that develops in aging female L-FABP gene-ablated (-/-) mice. To examine this possibility in more detail, cohorts of wild-type (+/+) and L-FABP (-/-) female mice were fed a standard, low-fat, nonpurified rodent diet for up to 18 mo. Various obesity-related parameters were examined, including body weight and fat and lean tissue mass. Obesity in (-/-) mice was associated with increased expression of nuclear receptors that induce PPARalpha (e.g. hepatocyte nuclear factor 1alpha, genotype effect) and of PPARalpha-regulated proteins involved in uptake of free (lipoprotein lipase and fatty acid transport protein, genotype, and/or age effect) and esterified (scavenger receptor class B type 1, genotype effect) long-chain fatty acids (LCFA). Hepatic total lipid and neutral lipid levels were not affected by age or genotype, consistent with absence of gross and histologic steatosis. There was increased mRNA expression of liver proteins involved in LCFA oxidation [mitochondrial 3-oxoacyl-CoA thiolase (genotype effect) and butyryl-CoA dehydrogenase (genotype and/or age effect)], increased expression of LCFA esterification enzymes [glycerol-3-phosphate acyltransferase (age x genotype effect) and acyl-CoA:cholesterol acyltransferase-2 (genotype and/or age effect)], and increased expression of proteins involved in intracellular transfer and secretion of esterified LCFA [liver microsomal triacylglycerol transfer protein (genotype effect), serum apolipoprotein (apo) B (genotype or age effect), and liver apoB (age and age x genotype effect)]. The data support a working model in which obesity development in these mice results from shifts toward reduced energy expenditure and/or more efficient energy uptake in the gut.
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PMID:Liver fatty acid-binding protein gene-ablated female mice exhibit increased age-dependent obesity. 1880 93

We investigated the contribution of fatty acid-binding protein 3 (FABP3) to adaptive thermogenesis in brown adipose tissue (BAT) in rodents. The expression of FABP3 mRNA in BAT was regulated discriminatively in response to alteration of the ambient temperature, which regulation was similar and reciprocal to the regulation of uncoupling protein 1 (UCP1) and leptin, respectively. FABP3 expression in the BAT was significantly higher in the UCP1-knockout (KO) mice than in the wild-type ones, and these KO mice showed a higher clearance rate of free fatty acid from the plasma. In addition, FABP3 expression in the BAT was increased greatly with the development of diet-induced obesity in mice. These results indicate that the induction of FABP3 in BAT correlates with an increased demand for adaptive thermogenesis in rodents. FABP3 appears to be essential for accelerating fatty acid flux and its oxidation through UCP1 activity for non-shivering thermogenesis in BAT.
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PMID:Induction of fatty acid-binding protein 3 in brown adipose tissue correlates with increased demand for adaptive thermogenesis in rodents. 1893 35

Adipocyte/macrophage fatty acid binding protein (A-FABP) has been shown to be closely associated with metabolic syndrome, obesity and development of atherosclerosis. Moreover, A-FABP has been recently suggested as a potential therapeutic target of these abnormalities in animal models. The present review aims to summarize current knowledge on A-FABP functions and regulations both in animal models and humans, since the role of A-FABP in human physiology and disease has not been presently clarified.
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PMID:Fatty acid binding proteins in adipose tissue: a promising link between metabolic syndrome and atherosclerosis? 1897 52

Liver fatty acid binding protein (L-FABP) is highly expressed in both enterocytes and hepatocytes and binds multiple ligands, including saturated (SFA), unsaturated fatty acids (PUFA), and cholesterol. L-fabp (-/-) mice were protected against obesity and hepatic steatosis on a high saturated fat (SF), high cholesterol "Western" diet and manifested a similar phenotype when fed with a high SF, low cholesterol diet. There were no significant differences in fecal fat content or food consumption between the genotypes, and fatty acid (FA) oxidation was reduced, rather than increased, in SF-fed L-fabp (-/-) mice as evidenced by decreased heat production and serum ketones. In contrast to mice fed with a SF diet, L-fabp (-/-) mice fed with a high PUFA diet were not protected against obesity and hepatic steatosis. These observations together suggest that L-fabp (-/-) mice exhibit a specific defect in the metabolism of SFA, possibly reflecting altered kinetics of FA utilization. In support of this possibility, microarray analysis of muscle from Western diet-fed mice revealed alterations in genes regulating glucose uptake and FA synthesis. In addition, intestinal cholesterol absorption was decreased in L-fabp (-/-) mice. On the other hand, and in striking contrast to other reports, female L-fabp (-/-) mice fed with low fat, high cholesterol diets gained slightly less weight than control mice, with minor reductions in hepatic triglyceride content. Together these data indicate a role for L-FABP in intestinal trafficking of both SFA and cholesterol.
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PMID:Diet-induced alterations in intestinal and extrahepatic lipid metabolism in liver fatty acid binding protein knockout mice. 1911 76

Obstructive sleep apnoea (OSA) is associated with insulin resistance and metabolic syndrome. There is evidence that adipocyte-fatty acid binding protein (A-FABP) may be involved in the development of cardiometabolic dysfunction. The present authors hypothesise that A-FABP is upregulated in OSA. A total of 124 males without hypertension, diabetes mellitus, hyperlipidaemia or cardiovascular disease were recruited and underwent polysomnography. Serum A-FABP levels showed significant positive correlations with duration of oxygen desaturation and minimal oxygen saturation, fasting insulin and insulin resistance index by homeostasis model assessment. When subjects were divided into tertiles according to apnoea/hypopnoea index (AHI), serum A-FABP levels were significantly higher in the group with AHI >/=34.4 events.h(-1) than the groups with AHI 13.2-34.4 events.h(-1) or with AHI <13.2 events.h(-1). Serum A-FABP levels were significantly higher in the AHI >/=34.4 group than obesity-matched subjects with AHI <34.4 events.h(-1). Serum adipocyte-fatty acid binding protein levels correlated with obstructive sleep apnoea and insulin resistance, independently of obesity, and were significantly higher in severe obstructive sleep apnoea. Adipocyte-fatty acid binding protein may play a role in obstructive sleep apnoea and metabolic dysfunction.
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PMID:Serum adipocyte-fatty acid binding protein level is elevated in severe OSA and correlates with insulin resistance. 1918 13

The aim of the study was to evaluate human plasma circulating levels of adipocyte fatty acid-binding protein (A-FABP) and its relationship with proinflammatory adipocytokines and insulin resistance in a severely obese cohort, before and 1 year after a surgical gastric bypass. Plasmatic levels of A-FABP were measured in 77 morbid-obese women before and 1 year after bariatric surgery. Anthropometrical parameters and body composition by bioelectrical impedance analysis were determined. Circulating levels of soluble tumor necrosis factor receptor 2 (sTNFR2), Interleukin 18 (IL-18), adiponectin, and high-sensitive C-reactive protein (hsCRP) were also analyzed. Insulin resistance by homeostasis model assessment of insulin resistance (HOMA-IR) index was calculated. After massive weight loss, A-FABP plasmatic levels decreased significantly [7.6 (8.9) vs. 4.3 (5.1); P<0,001] but no association with circulating adipokines or proinflammatory cytokines, both at the beginning and at the end of follow-up, was observed. A decrease in sTNFR2, IL-18, hsCRP, and an increase in adiponectin levels (P<0.001 in all cases) were observed after the gastric bypass. HOMA-IR index improved 1 year after surgery and after multiple regression analysis remained associated with A-FABP after controlling for confounding variables (beta=0.322, P=0.014; R2 for the model 0.281). In morbid-obese women, plasma A-FABP concentrations were dramatically reduced after gastric bypass surgery. After weight loss this protein contributed to HOMA-IR index independently of proinflammatory/antinflammatory cytokine profile. Further studies are warranted to elucidate the role of A-FABP in the pathogenesis of insulin resistance in morbid obesity.
Obesity (Silver Spring) 2009 Jun
PMID:Adipocyte fatty acid-binding protein as a determinant of insulin sensitivity in morbid-obese women. 1919 57

Maternal nutrient restriction (NR) from early to midgestation has marked effects on endocrine sensitivity and organ function of the resulting offspring. We hypothesized that early NR may reset the expression profile of genes central to myocardial energy metabolism, influencing ectopic lipid deposition and cardiac function in the obese adult offspring. NR offspring were exposed to an "obesogenic" environment, and their cardiac function and molecular indexes of myocardial energy metabolism were assessed to explore the hypothesis that an obese individual's risk of heart disease may be modified after maternal NR. Pregnant sheep were fed 100% (control) or 50% (NR) energy requirement from days 30 to 80 of gestation and 100% energy requirement thereafter. At weaning, offspring were exposed to an obesogenic environment or remained lean. At approximately 1 yr of age, the hemodynamic response of these offspring to hypotension, together with left ventricular expression profiles of fatty acid-binding protein 3 (FABP3), peroxisome proliferator-activated receptor-gamma (PPARgamma) and its coactivator (PGC)-1alpha, acetyl-CoA carboxylase (ACC), AMP-activated protein kinase (AMPK)-alpha(2), and voltage-dependent anion channel 1 (VDAC1), was determined. Obesity produced left ventricular hypertrophy in all animals, with increased ectopic (myocardial) lipid in NR offspring. Obesity per se significantly reduced myocardial transcript expression of PGC-1alpha, AMPKalpha(2), VDAC1, and ACC and increased expression of PPARgamma and FABP3. However, although NR animals were similarly obese, their transcript expression of ACC, PPARgamma, and FABP3 was similar to that of lean animals, indicating altered cardiac energy metabolism. Indeed, blunted tachycardia and an amplified inotropic response to hypotension characterized cardiac function in obese NR offspring. The results suggest that maternal NR during early organogenesis can precipitate an altered myocardial response to hypotension and increased myocardial lipid deposition in the adult offspring after adolescent-onset obesity, potentially rendering these individuals more at risk of early heart failure as they age.
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PMID:Effect of maternal nutrient restriction from early to midgestation on cardiac function and metabolism after adolescent-onset obesity. 1924 82


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