Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: EC:1.3.99.3 (acyl-CoA dehydrogenase)
 1,425 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Men with regular physical training habits voluntarily increased their dietary fat intake from 43 to 54% of energy (E%) for four weeks. This was followed by a low-fat (29 E%), high-carbohydrate diet for another four weeks. During the high-fat diet period, the muscle lipoprotein lipase activity (LPLA) increased from 59 +/- 8 to 106 +/- 12 mU/g (mean +/- SE) (P less than 0.05). After the high-carbohydrate diet, LPLA was 57 +/- 16 mU/g, and unchanged relative to the pre-trial value. The triglyceride content in m. vastus lateralis increased from 30 +/- 4 to 47 +/- 9 mmol/kg d.w. (P less than 0.05; mean +/- SE) following the high-fat diet and to 41 +/- 8 following the high-carbohydrate diet. Neither of the diets affected the serum triglyceride and insulin concentrations, nor glucose, glycerol, beta-hydroxybutyrate, citrate and lactate levels in the blood. Nor did they alter enzyme activities in muscle used as markers for the oxidative (citrate synthase, beta-hydroxy-acyl CoA dehydrogenase) and glycolytic (glyceraldehyde phosphate dehydrogenase, lactate dehydrogenase) capacity. It is concluded that one month's adaptation to a high-fat diet results in increased muscle-LPL activity indicating a higher capacity for uptake of fatty acids from circulating serum triglycerides into the muscle cell in association with a greater capacity for triglyceride storage in the muscle. Under these conditions serum triglycerides were not decreased despite the increased muscle LPLA, and serum insulin variations could not explain the change in muscle LPLA.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Lipoprotein lipase activity and intramuscular triglyceride stores after long-term high-fat and high-carbohydrate diets in physically trained men. 354 51

The VLDL (very low-density lipoprotein) receptor is a peripheral lipoprotein receptor expressing in fatty acid active tissues abundantly. In the Balb/c fasting mice, VLDL receptor as well as LPL (lipoprotein lipase), FAT (fatty acid translocase)/CD36, H-FABP (heart-type fatty acid-binding protein), ACS (acyl-CoA synthetase) and LCAD (long-chain acyl-CoA dehydrogenase) expressions increased. An electron microscopic examination indicated the lipid droplets that accumulated in the hearts of fasting Balb/c mice. During the development of SD (Sprague-Dawley) rats, VLDL receptor, LPL, FAT/CD36, H-FABP, ACS, and LCAD mRNAs concomitantly increased with growth. However, PK (pyruvate kinase) mRNA expression was negligible. In cultured neonatal rat cardiomyocytes, VLDL receptor expression increased with days in culture. Oil red-O staining showed that cardiomyocytes after 7 days in culture (when the VLDL receptor protein is present) accumulated beta-migrating VLDL. Thereby, we showed that the cardiac VLDL receptor pathway for delivery of remnant lipoprotein particles might be part of a cardiac fatty acid metabolism.
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PMID:Remnant lipoprotein particles are taken up into myocardium through VLDL receptor--a possible mechanism for cardiac fatty acid metabolism. 1205 60