Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: EC:2.3.3.1 (citrate synthase)
 4,488 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The present study investigated whether recombinant human (rh) growth hormone (GH) combined with endurance training would have a larger effect on oxidative capacity, metabolism, and body fat than endurance training alone. Sixteen healthy, elderly women, aged 75 yr, performed closely monitored endurance training on a cycle ergometer over 12 wk. rhGH was given in a randomized, double-blinded, placebo-controlled design in addition to the training program. GH administration resulted in a doubling of serum insulin-like growth factor I levels. With endurance training, peak oxygen uptake increased by approximately 18% in both groups, whereas the marked increase in muscle citrate synthase activity was 50% larger in the GH group compared with the placebo group. In addition, only the GH group revealed an increase in muscle L-3-hydroxyacyl-CoA dehydrogenase activity. Body weight remained unchanged in both groups, but the GH group showed significant changes in body composition with a decrease in fat mass and an increase in lean body mass. Twenty-four-hour indirect calorimetry performed in four subjects showed a marked increase in energy expenditure with increased relative and absolute fat combustion in the two subjects receiving rhGH. In conclusion, rhGH adds to the effects of endurance training on muscle oxidative enzymes and causes a reduction in body fat in elderly women.
 ...
PMID:Growth hormone enhances effects of endurance training on oxidative muscle metabolism in elderly women. 1105 52

The transcriptome pattern of metabolic genes in vitamin A deficient (VAD) liver has been compared to the vitamin A-sufficient (VAS) state using the Mouse 32k oligonucleotide (70mer) array. In VAD liver there was a decrease in expression of genes encoding enzymes of mitochondrial fatty acid (FA) oxidation; these genes included fatty acyl CoA ligase, carnitine o-palmitoyl transferase 1, medium chain acyl-CoA dehydrogenase, 3-ketoacyl CoA thiolase, and citrate synthase. Particularly affected was peroxisome metabolism, as genes encoding enzymes of peroxisomal FA oxidation and transport proteins were differentially expressed. These genes included those encoding acyl-CoA oxidase 1, the peroxisomal bifunctional enzyme, peroxisomal thiolase, and carnitine o-octanoyl transferase, the enzyme involved in shuttling FAs from the peroxisome to the mitochondrion. Most genes that were differentially expressed with chronic vitamin A depletion were responsive to treatment with all-trans retinoic acid (RA). Consistent with the decreased expression of genes involved in FA oxidation, we found an increase in hepatic macrocytic lipid accumulation and triglyceride levels. The relevant nuclear receptor gene that was differentially expressed in the VAD liver was that encoding the peroxisome proliferator-activated receptor (PPAR) alpha, the mRNA levels for which were decreased in VAD liver and increased with all-trans RA treatment. Down regulation of the PPAR alpha gene is the likely cause of the altered expression pattern of the above metabolic genes in VAD liver.
 ...
PMID:Altered lipid catabolism in the vitamin A deficient liver. 1746 65