Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: EC:2.3.1.21 (CPT)
 4,580 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Cadmium is an environmental toxic metal implicated in human prostate carcinogenesis. The mechanism of its toxicity is not fully understood. Previously, we showed that cadmium exposure induces oxidative stress, especially lipid peroxidation. This study evaluates the effect of chronic exposure to 0.886 mM of cadmium (Cd) per liter in the drinking water on prostate lipid content and metabolism in Wistar rats. We determined the lipid profile and measured the expression of lipogenic enzymes: FAS, GPAT, LPL, DGAT-1, DGAT-2, ACO, CPT-1 and CT, and of certain factors involved in lipid regulation and fatty acid transporters: FAT/CD36, E-FABP, SREBP-2, PPAR-gamma and PPAR-alpha by RT-PCR. Ultrastructure was analyzed by electron microscopy and, as prostate is an androgen controlled gland, AR expression was measured by RT-PCR and Western blot. Cd altered the prostatic lipid profile. Triglycerides (TG) and esterified cholesterol (EC) decreased, free cholesterol (FC) and phospholipids (PL) increased and total cholesterol (TC) did not change. FAS, MDH and IDH activities did not vary but G6PDH decreased significantly in Cd group. Regarding TG synthesis, DGAT-1 decreased while GPAT increased and FAS, LPL and DGAT-2 remained unchanged. Regarding beta oxidation, CPT-1 increased while ACO expression decreased in Cd group. In the PL pathway, CT expression was increased. All these results would justify the decrease of TG in Cd group when compared to control. In the cholesterol metabolic pathway, HMGCoAR and SREBP-2 increased. PPAR-alpha increased but PPAR-gamma did not change. Regarding fatty acid transporters, FAT/CD36 decreased, while E-FABP increased. AR mRNA and protein expression decreased. Ultrastructural analysis showed a decrease in lipid droplets and signs of cellular damage in the Cd group. Cadmium exposure induces important changes in prostatic lipid profile and metabolism, confirmed by the morphology analyses, which also showed signs of cellular damage. These results could be important to further understanding the complex mechanism of cadmium toxicity in prostate and in the development of better treatments for people and animals exposed to the heavy metal.
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PMID:Effects of chronic exposure to cadmium on prostate lipids and morphology. 1706 26

GPAT1, one of four known glycerol-3-phosphate acyltransferase isoforms, is located on the mitochondrial outer membrane, allowing reciprocal regulation with carnitine palmitoyltransferase-1. GPAT1 is upregulated transcriptionally by insulin and SREBP-1c and downregulated acutely by AMP-activated protein kinase, consistent with a role in triacylglycerol synthesis. Knockout and overexpression studies suggest that GPAT1 is critical for the development of hepatic steatosis and that steatosis initiated by overexpression of GPAT1 causes hepatic, and perhaps also peripheral, insulin resistance. Future questions include the function of GPAT1 in relation to the other GPAT isoforms and whether the lipid intermediates synthesized by GPAT and downstream enzymes in the pathway of glycerolipid biosynthesis participate in intracellular signaling pathways.
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PMID:Regulation of Triglyceride Metabolism. II. Function of mitochondrial GPAT1 in the regulation of triacylglycerol biosynthesis and insulin action. 1715 53

The aim of this study was to analyze regional differences in the time-course response to fasting and refeeding in the expression of genes involved in lipid metabolism in retroperitoneal, mesenteric and inguinal adipose tissue. Rats were studied under different feeding conditions: feeding state; after 4, 8 or 24 h of fasting; and after 3 h of refeeding following 8 h of fasting. The expression of lipogenesis-related genes decreased by fasting in adipose tissue, and the retroperitoneal depot showed the fastest response: mRNA levels of peroxisome proliferator-activated receptor gamma 2 (PPARgamma2) decreased after 4 h of fasting and those of sterol regulatory element binding protein 1c (SREBP1c), fatty acid synthase (FAS), GPAT and glucose transporter 4 (GLUT4) decreased after 8 h. In the inguinal depot, mRNA levels of SREBP1c, acetyl-coenzyme A carboxylase alpha, FAS and lipoprotein lipase decreased after 8 h of fasting, while in the mesenteric depot, only GLUT4 and FAS mRNA levels decreased after 8 and 24 h, respectively. Concerning lipolytic and fatty acid oxidation genes, only adipose triglyceride lipase and carnitine palmitoyltransferase 1a expression increased after 24 h of fasting in the retroperitoneal depot. Three hours of refeeding restored the expression of the lipogenic transcription factors PPARgamma2 and SREBP1c in the retroperitoneal depot and of PPARgamma2 in the inguinal depot. This period of refeeding was ineffective in changing the expression of genes related with lipid mobilization and fatty acid oxidation, except hormone-sensitive lipase, whose expression decreased in the mesenteric depot. It is suggested that different regulations of the expression of genes related with lipid metabolism between internal and subcutaneous depots to feeding and fasting conditions are site-specific metabolic features of white adipose tissue.
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PMID:Regional differences in the expression of genes involved in lipid metabolism in adipose tissue in response to short- and medium-term fasting and refeeding. 1915 23