Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: EC:1.3.1.8 (acyl-CoA dehydrogenase)
 785 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

We previously demonstrated that transgenic mice overexpressing mouse apolipoprotein A-II (apoA-II) exhibit several traits associated with the insulin resistance (IR) syndrome, including increased atherosclerosis, hypertriglyceridemia, obesity, and IR. The skeletal muscle appeared to be the insulin-resistant tissue in the apoA-II transgenic mice. We now demonstrate a decrease in FA oxidation in skeletal muscle of apoA-II transgenic mice, consistent with reports that decreased skeletal muscle FA oxidation is associated with increased skeletal muscle triglyceride accumulation, skeletal muscle IR, and obesity. The decrease in FA oxidation is not due to decreased carnitine palmitoyltransferase 1 activity, because oxidation of palmitate and octanoate were similarly decreased. Quantitative RT-PCR analysis of gene expression demonstrated that the decrease in FA oxidation may be explained by a decrease in medium chain acyl-CoA dehydrogenase. We previously demonstrated that HDLs from apoA-II transgenic mice exhibit reduced binding to CD36, a scavenger receptor involved in FA metabolism. However, studies of combined apoA-II transgenic and CD36 knockout mice suggest that the major effects of apoA-II are independent of CD36. Rosiglitazone treatment significantly ameliorated IR in the apoA-II transgenic mice, suggesting that the underlying mechanisms of IR in this animal model may share common features with certain types of human IR.
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PMID:Mechanisms mediating insulin resistance in transgenic mice overexpressing mouse apolipoprotein A-II. 1546 64

Leptin is a hormone secreted primarily by adipose tissue and its blood levels depend on the amount of fat stored in adipocytes. Leptin has a wide range of physiological effects. Acting directly or through the sympathetic nervous system it participates in the regulation of energy metabolism. Leptin inhibits synthesis of triacylglycerols in the liver, adipose tissue and skeletal muscles, thus reducing the intracellular lipid content in these tissues. In adipocytes, leptin down-regulates the expression of genes encoding fatty acid synthase (FAS) and acetyl-CoA carboxylase (ACC), the major enzymes of fatty acid synthesis, while it up-regulates the expression of the hormone-sensitive lipase (HSL) encoding gene, thus stimulating hydrolysis of triacylglycerols in adipose tissue. Moreover, leptin enhances fatty acid oxidation in adipocytes, and skeletal and cardiac muscle by increasing the expression of genes encoding key enzymes involved in this process, carnitine palmitoyltransferase 1 (CPT1) and medium chain acyl-CoA dehydrogenase (MCAD). It has also been demonstrated that this hormone improves insulin sensitivity and glucose tolerance by stimulating glucose transport and metabolism in many tissues. It is known that leptin is involved in the long-term regulation of food intake. However, increasing evidence suggests that it may also influence energy substrate utilization in peripheral tissues. Therefore, leptin can effectively control whole-body energy homeostasis by altering lipid and carbohydrate metabolism, especially in adipose tissue and muscles.
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PMID:[Role of leptin in the regulation of lipid and carbohydrate metabolism]. 2167 50

Reprogramming of cellular energy metabolism, such as lipid metabolism, is a hallmark of squamous cell carcinoma of the head and neck (SCCHN). However, whether protein expression related to fatty acid oxidation (FAO) affects survival in SCCHN remains unclear. We aimed to investigate FAO-related enzyme expression and determine its correlation with clinicopathological variables in SCCHN patients. Immunohistochemical analysis (IHC) of FAO-related protein expression, including carnitine palmitoyltransferase 1 (CPT1), the acyl-CoA dehydrogenase family, and fatty acid synthase (FAS), was performed using tissue microarrays from 102 resected SCCHN tumors. Expressions were categorized according to IHC scores, and the statistical association with clinicopathological factors was determined. Moderate-to-high expression of long-chain acyl-CoA dehydrogenase (LCAD) had a protective role against cancer-related death (adjusted hazard ratio (HR), 0.2; 95% confidence interval (CI), 0.05-0.87) after covariate adjustment. Age and clinical stage remained independent predictors of survival (adjusted HR, 1.75; 95% CI, 1.22-2.49 for age; adjusted HR, 14.33; 95% CI, 1.89-108.60 for stage III/IV disease). Overexpression of medium-chain acyl-CoA dehydrogenase and FAS correlated with advanced tumor stage (T3/T4); however, none of these factors were independent predictors of survival. Several FAO-related enzymes were upregulated and LCAD overexpression had a protective effect on overall survival in advanced SCCHN patients. FAO-related-enzyme expression might have a prognostic impact on survival outcomes in SCCHN.
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PMID:Prognostic Value of the Overexpression of Fatty Acid Metabolism-Related Enzymes in Squamous Cell Carcinoma of the Head and Neck. 3296 83