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)

Maternal diabetes can cause fetal macrosomia and increased risk of obesity, diabetes, and cardiovascular disease in adulthood of the offspring. Although increased transplacental lipid transport could be involved, the impact of maternal type 1 diabetes on molecular mechanisms for lipid transport in placenta is largely unknown. To examine whether maternal type 1 diabetes affects placental lipid metabolism, we measured lipids and mRNA expression of lipase-encoding genes in placentas from women with type 1 diabetes (n = 27) and a control group (n = 21). The placental triglyceride (TG) concentration and mRNA expression of endothelial lipase (EL) and hormone-sensitive lipase (HSL) were increased in placentas from women with diabetes. The differences were more pronounced in women with diabetes and suboptimal metabolic control than in women with diabetes and good metabolic control. Placental mRNA expression of lipoprotein lipase and lysosomal lipase were similar in women with diabetes and the control group. Immunohistochemistry showed EL protein in syncytiotrophoblasts facing the maternal blood and endothelial cells facing the fetal blood in placentas from both normal women and women with diabetes. These results suggest that maternal type 1 diabetes is associated with TG accumulation and increased EL and HSL gene expression in placenta and that optimal metabolic control reduces these effects.
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PMID:Placental triglyceride accumulation in maternal type 1 diabetes is associated with increased lipase gene expression. 1694 May 51

Perilipins are the proteins associating with the lipid droplets in adipocytes and steroidogenic cells. Unphosphorylated perilipins coat the surface of intracellular lipid droplets to form a barrier that prevents lipase from accessing to triacylglycerol core, thus suppressing lipolysis. Upon activation of protein kinase A (PKA), two proteins, hormone-sensitive lipase (HSL) and perilipins, are phosphorylated. The phosphorylated perilipin is required for inducing the translocation of HSL from the cytosol to the lipid droplets of adipocytes and is essential for the initiation of lipolytic reaction. It is proposed that phosphorylation of perilipin is a key step for the activation of lipolytic cascade via PKA and ERK signaling pathways. Dysregulation of perilipin involves in the pathogenesis of obesity, diabetes and atherosclerosis.
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PMID:[Perilipin associated with lipid droplets regulates lipolysis]. 1700 29

The effects of oral treatment with Aralox phytopreparation containing Aralia mandshurica (Araliaceae) and Engelhardtia chrysolepis (Juglandaceae) extracts on some parameters of lipid metabolism was studied in women with nondiabetic obesity receiving low-caloric diet. Our randomized placebo-controlled study comprising 32 volunteers showed that aralox treatment led to a decrease in total body weight and fat weight, reduced perilipin content in adipocytes and plasma triglyceride content, and stimulated activity of hormone-sensitive lipase.
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PMID:Effects of Aralia mandshurica and Engelhardtia chrysolepis extracts on some parameters of lipid metabolism in women with nondiabetic obesity. 1707 56

Prp19p is an integral component of the heteromeric protein complex (the NineTeen complex) in the nucleus, and it is essential for the structural integrity of NineTeen complex and its subsequent activation of the spliceosome. We identified Prp19p, which has never been reported in relation to any function outside of the nucleus, as a member of proteins associated with lipid droplets. Down-regulation of Prp19p expression with RNA interference in 3T3-L1 cells repressed lipid droplet formation with the reduction in the level of expression of perilipin and S3-12. The levels of expression of SCD1 (stearoyl-CoA desaturase-1), DGAT-1 (acyl-CoA diacylglycerol acyltransferase-1), and glycerol-3-phosphate acyltransferase were also reduced in Prp19p down-regulated cells, and a significant decrease in triglycerides was observed. Unlike perilipin, which is one of the most extensively studied lipid droplet-associated proteins, Prp19p is not essential for cAMP- and hormone-sensitive lipase-dependent lipolysis pathways, even though Prp19p is a component of the lipid droplet phospholipid monolayer, and down-regulation of Prp19p represses fat accretion significantly. These results suggest that Prp19p or Prp19-interacting proteins during lipid droplet biogenesis in adipocytes may be considered as another class of potential targets for attacking obesity and obesity-related problems.
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PMID:Identification of mouse Prp19p as a lipid droplet-associated protein and its possible involvement in the biogenesis of lipid droplets. 1711 36

We investigated the lipolytic effects of L-carnitine in 3T3-L1 adipocytes. L-carnitine at 10-S100 nM suppressed lipid accumulation. The release of glycerol and free fatty acid into the medium was significantly increased by 1.5- and 1.7- fold, respectively, by the addition of 100 nM L-carnitine compared with the control (P < .05). The mRNA levels of hormone-sensitive lipase, carnitine palmitoyltransferase I-a, and acyl-coenzyme A oxidase, all of which participate in lipid catabolism, were increased in the presence of 100 nM L-carnitine by 2.8-, 2.2-, and 1.6-fold, respectively (P < .05). However, the expression of peroxisome proliferator-activated receptor-gamma and adipose-specific fatty acid-binding protein, which are involved in adipogenesis, were down-regulated by L-carnitine in 3T3-L1 adipocytes (P < .05). These results suggest an anti-obesity action of L-carnitine. L-carnitine may modulate lipid metabolism by stimulation of lipolysis and beta-oxidation accompanied by corresponding changes in gene expression and suppression of adipogenic gene expression.
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PMID:L-carnitine stimulates lipolysis via induction of the lipolytic gene expression and suppression of the adipogenic gene expression in 3T3-L1 adipocytes. 1720 31

Although antipsychotics are established drugs in schizophrenia treatment, they are admittedly known to induce side effects favoring the onset of obesity and worsening its complications. Despite potential involvement of histamine receptor antagonism, or of other neurotransmitter systems, the mechanism by which antipsychotic drugs increase body weight is not elucidated. The aim of the present study was to investigate whether chronic antipsychotic treatments can directly alter the regulation of two main functions of white adipose tissue: lipolysis and glucose utilization. The influence of a classical antipsychotic (haloperidol) was compared to that of two atypical antipsychotics, one known to favor weight gain (olanzapine), the other not (ziprasidone). Cell size, lipolytic capacity and glucose transport activity were determined in white adipocytes of rats subjected to 5-week oral treatment with these antipsychotics. Gene expression of adipocyte proteins involved in glucose transport or fat storage and mobilization, such as glucose transporters (GLUT1 and GLUT4), leptin, matrix metallo-proteinase-9 (MMP9), hormone-sensitive lipase (HSL) and fatty acid synthase (FAS) was also evaluated. Adipocytes from chronic olanzapine-treated rats exhibited decreased lipolytic activity, lowered HSL expression and increased FAS expression. These changes were concomitant to enlarged fat deposition and adipocyte size. Alterations were observed in adipocytes from olanzapine-treated rats whereas the other antipsychotics did not induce any notable disorder. Our results therefore show evidence of an effect of chronic antipsychotic treatment on rat adipocyte metabolism. Thus, impairment of fat cell lipolysis should be considered as a side effect of certain antipsychotics, leading, along with the already documented hyperphagia, to the excessive weight gain observed in patients under prolonged treatment..
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PMID:Alterations of lipid metabolism and gene expression in rat adipocytes during chronic olanzapine treatment. 1721 38

The effect of early feed restriction on metabolic programming and compensatory growth was studied in broiler chickens. A total of 480 female 1-d-old broiler birds (Aconred) were randomly allocated to ad libitum and feed-restricted groups, each of which was replicated 6 times with 40 birds per replicate. Broilers were provided commercial diets. Feed-restricted broilers were deprived of feed for 4 h per day from 1 to 21 d of age. Effects of treatments were determined at 21 and 63 d of age. In feed-restricted birds at 21 d of age, BW, average daily gain and average daily feed intake, breast muscle (P < 0.01), carcass yield (P < 0.05), and abdominal fat (P < 0.05) were decreased. Ether extract content in breast muscle was increased (P < 0.01), whereas CP content was slightly decreased. Triiodothyronine (P < 0.01) and thyroxine (P < 0.05) were decreased in serum. Free fatty acid and very low density lipoprotein were slightly increased in serum, whereas triglyceride and glucose were decreased (P < 0.01). Activities of NADPH-generating enzymes in liver including malic dehydrogenase, isocitrate dehydrogenase, and glucose-6-phosphate remained unchanged in ad libitum birds, whereas hormone-sensitive lipase activity was increased (P < 0.01). In feed-restricted birds at 63 d of age, BW, average daily gain, average daily feed intake, carcass yield, breast muscle yield, and serum triiodothyronine and thyroxine remained as ad libitum birds, whereas abdominal fat yield was increased (P < 0.05). Ether extract content in breast muscle was decreased (P < 0.01), whereas CP content was increased (P < 0.05). Activities of NADPH-generating enzymes were significantly increased, except abdominal malic dehydrogenase and hormone-sensitive lipase activity was decreased (P < 0.01) in liver and abdominal fat. Lipoprotein lipase activity was increased (P < 0.05) in abdominal fat. In summary, feed restriction severely affected growth performance and lipid metabolism in broilers in the early period. Because there was no statistical difference among the final BW, near full compensatory growth was achieved. In addition, early feed restriction might have induced prolonged metabolic programming in chicks and led to adult obesity.
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PMID:Effect of early feed restriction on metabolic programming and compensatory growth in broiler chickens. 1736 35

Obesity is the result of an imbalance between food intake and energy expenditure resulting in the storing of energy as fat. Adipose tissue contains the largest store of energy in the body and plays important roles in regulating energy partitioning. Developments in genomics, in particular microarray-based expression profiling, have provided scientists with a number of new candidate genes whose expression in adipose tissue is regulated by obesity. Integrating expression profiles with genome-wide linkage and/or association analyses is a promising strategy to identify new genes underlying susceptibility to obesity. This article provides a comprehensive review of adipose-tissue-expressed genes implicated in predisposition to human obesity. The authors consider the following genes of particular interest: peroxisome proliferator-activated receptor gamma and, potentially, INSIG2 acting in adipogenesis; the adrenoreceptors beta 2 and 3, as well as hormone-sensitive lipase acting on lipolysis; uncoupling protein 2 acting in mitochondria energy expenditure; and among secreted molecules the cytokine tumor necrosis factor alpha and the hormone leptin. With the rapid development in genome research, we predict that additional alleles in genes regulating adipose tissue function will be established as risk factors for common obesity in the coming years. This has important implications for the prevention of obesity and may also offer new therapeutic targets.
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PMID:Obesity and polymorphisms in genes regulating human adipose tissue. 1756 63

We investigated the rs9939609 single nucleotide polymorphism of the FTO gene in relation to fat cell function and adipose tissue gene expression in 306 healthy women with a wide range in body mass index (18-53 kg/m(2)). Subcutaneous adipose tissue biopsies were taken for fat cell metabolism studies and in a subgroup (n = 90) for gene expression analyses. In homozygous carriers of the T-allele, the in vitro basal (spontaneous) adipocyte glycerol release was increased by 22% (P = 0.007) and the in vivo plasma glycerol level was increased by approximately 30% (P = 0.037) compared with carriers of the A allele. In contrast, there were no genotype effects on catecholamine-stimulated lipolysis or basal or insulin-induced lipogenesis. We found no difference between genotypes for adipose tissue mRNA levels of FTO, hormone-sensitive lipase, adipose triglyceride lipase, perilipin, or CGI-58. Finally, the adipose tissue level of FTO mRNA was increased in obesity (P = 0.002), was similar in subcutaneous and omental adipose tissue, was higher in fat cells than in fat tissue (P = 0.0007), and was induced at an early stage in the differentiation process (P = 0.004). These data suggest a role of the FTO gene in fat cell lipolysis, which may be important in explaining why the gene is implicated in body weight regulation.
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PMID:The common rs9939609 gene variant of the fat mass- and obesity-associated gene FTO is related to fat cell lipolysis. 1804 38

In comparison to subcutaneous (SC) fat, visceral adipose tissue is more sensitive to catecholamine-induced lipolysis and less sensitive to the antilipolytic effects of insulin. Variation in the expression of lipoprotein lipase (LPL) and hormone-sensitive lipase (HSL) have been reported. We therefore hypothesized that expression of adipose triglyceride lipase (ATGL) is different in visceral and SC depot and investigated whether ATGL mRNA expression is related to obesity, fat distribution and insulin sensitivity. ATGL, LPL, and HSL mRNA expression was measured in 85 paired samples of omental and subcutaneous adipose tissue in normal glucose tolerant lean and obese individuals. In addition, we included a subgroup of obese (BMI >30 kg/m2) individuals with either impaired or preserved insulin sensitivity determined by euglycemic-hyperinsulinemic clamps. ATGL mRNA levels are significantly decreased in insulin resistant obese subjects. Independently of body fat mass, omental ATGL mRNA correlates with fasting insulin concentration, glucose uptake during the steady state of the clamp and HSL mRNA expression. In obese, but not in lean subjects, LPL and HSL mRNA expression was significantly higher in omental compared to SC fat. In both depots, HSL mRNA was significantly lower in obese individuals. Visceral HSL mRNA expression is closely related to adipocyte size and fasting plasma insulin concentrations, whereas visceral fat area significantly predicts visceral LPL mRNA expression. ATGL mRNA expression is not significantly different between omental and SC fat. HSL, but not ATGL mRNA expression is closely related to individual and regional differences in adipocyte size. Impaired insulin sensitivity was associated with decreased ATGL and HSL mRNA expression, independently of body fat mass and fat distribution.
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PMID:Adipose triglyceride lipase gene expression in human visceral obesity. 1807 17


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