Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0002895 (sickle cell disease)
 11,747 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The importance of insulin for the in vivo effects of growth hormone (GH) on lipid and lipoprotein metabolism was investigated by examining the effects of GH treatment of hypophysectomized (Hx) female rats with and without concomitant insulin treatment. Hypophysectomy-induced changes of HDL, apolipoprotein (apo)E, LDL, and apoB levels were normalized by GH treatment but not affected by insulin treatment. The hepatic triglyceride secretion rate was lower in Hx rats than in normal rats and increased by GH treatment. This effect of GH was blunted by insulin treatment. The triglyceride content in the liver changed in parallel with the changes in triglyceride secretion rate, indicating that the effect of the hormones on triglyceride secretion was dependent on changed availability of triglycerides for VLDL assembly. GH and insulin independently increased editing of apoB mRNA, but the effects were not additive. The expression of fatty-acid synthase (FAS), stearoyl-CoA desaturase-1 (SCD-1), and sterol regulatory element-binding protein-1c (SREBP-1c) was increased by GH treatment. Insulin and GH had no additive effects on these genes; instead, insulin blunted the effect of GH on SREBP-1c mRNA. In contrast to the liver, adipose tissue expression of SREBP-1c, FAS, or SCD-1 mRNA was not influenced by GH. In conclusion, the increased hepatic expression of lipogenic enzymes after GH treatment may be explained by increased expression of SREBP-1c. Insulin does not mediate the effects of GH but inhibits the stimulatory effect of GH on hepatic SREBP-1c expression and triglyceride secretion rate.
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PMID:Interaction between growth hormone and insulin in the regulation of lipoprotein metabolism in the rat. 1237 31

We have previously reported that plasma levels of remnant-like lipoprotein particles (RLP) significantly increased in sudden cardiac death cases with and without coronary atherosclerosis. In this study we have elucidated the major subset of proatherogenic RLP, containing both apoB-48 and apoB-100-carrying remnants, in plasma of SCD and control death cases. One hundred and sixty seven Japanese cases of sudden cardiac death and 78 cases of control death underwent autopsy within 12h after death were studied. Heart weight was 9.2% higher in SCD cases than controls (P<0.05). Moreover 57.5% or 96/167 of the cases had more than grade (2+) coronary atherosclerosis versus 21.8% or 17 of 78 controls (P<0.01). Approximately 2/3 of the cases had full stomach, reflecting the postprandial state at the time of death. Plasma TC, TG, VLDL-C, LDL-C were significantly elevated (P<0.001) together with RLP-C (P<0.01), RLP-TG (P<0.005) in SCD cases. Plasma RLP-apoB-100 levels were significantly elevated in SCD (P<-0.001), but apoB-48 levels were not. The median ratio of apoB-100/apoB-48 in RLP was 7.1 in SCD. The median RLP-TG/RLP-C ratio was 4.7, which suggested a large VLDL size. When apoB-48 and apoB-100 in RLP were divided into two groups, above and below the median level, respectively, apoB-48 inversely correlated with RLP-C (P<0.05) and RLP-TG (P<0.01), while apoB-100 in RLP positively correlated with RLP-C (P<0.01) in SCD cases. In conclusion, these results indicated that apoB-100 carrying lipoproteins, not apoB-48 carrying lipoproteins, were the major subset of RLP associated with sudden cardiac death in the postprandial state, regardless to the severity of coronary atherosclerosis.
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PMID:ApoB-100 carrying lipoprotein, but not apoB-48, is the major subset of proatherogenic remnant-like lipoprotein particles detected in plasma of sudden cardiac death cases. 1704 70