Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: EC:3.1.1.79 (hormone-sensitive lipase)
 2,163 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

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

The insulin-induced genes INSIG1 and INSIG2 (INSIG) are known to regulate adipogenesis in nonruminants. Although data in bovine mammary tissue underscore a role for INSIG1 during lactation, regulatory mechanisms of INSIG action in ruminant mammary lipid metabolism are not well known. In the present study, INSIG1 and INSIG2 were overexpressed or silenced through adenoviral transfection to evaluate their role in lipid metabolism in goat mammary epithelial cells (GMEC). The INSIG were overexpressed using an adenovirus system with recombinant green fluorescent protein as the control. Downregulation of INSIG was performed via small interfering RNA targeting INSIG with a scrambled small interfering RNA as a negative control. The GMEC were treated with these constructs for 48 h before analyses. Responses to overexpressing INSIG1 or INSIG2 included downregulation of SREBF1, ACACA, FASN, SCD1, GPAM, DGAT2, ATGL, and HSL coupled with a decrease in content of triacylglycerol (TAG), total cholesterol (TC), and lipid droplet accumulation. The marked decrease in content of TAG and TC in response to overexpression of INSIG2, along with a modest decrease in content of TAG when INSIG1 was overexpressed, suggested that TAG synthesis is mainly regulated by INSIG2, whereas TC synthesis is equally regulated by INSIG2 and INSIG1. The lack of difference in mRNA expression of genes related to lipid metabolism, content of TAG, and accumulation of lipids in response to interference alone of INSIG1 or INSIG2 indicated that INSIG proteins play a biological role in the maintenance of lipid homeostasis. However, in response to simultaneous interference of INSIG1 and INSIG2, the marked increase in content of TAG and TC and accumulation of lipids along with significant upregulation of SREBF1, ACACA, SCD1, AGPAT6, and DGAT2 suggested that INSIG1 and INSIG2 synergistically regulate milk fat synthesis in GMEC. These results highlight an essential role of INSIG in regulating lipid synthesis in dairy goat mammary cells and underscore the complexity of mammary lipid synthesis in ruminants.
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PMID:Insulin-induced gene 1 and 2 isoforms synergistically regulate triacylglycerol accumulation, lipid droplet formation, and lipogenic gene expression in goat mammary epithelial cells. 3059 61