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Biomedical subjects

S Takase

Publications and source records attributed to S Takase.

At least 325 records · Page 18Linked to original sources

Long-term effect of medium-chain triglyceride on hepatic enzymes catalyzing lipogenesis and cholesterogenesis in rats.

This study was conducted to investigate the long-term effect of dietary medium-chain triglyceride (MCT) as compared with that of corn oil feeding on lipid metabolism in rats. Both serum cholesterol and triglyceride levels in MCT-fed rats showed significant decrease during the experimental period of eight weeks, although liver cholesterol and triglyceride contents were not distinguishable between the two groups. Significant elevation of the activity of lipogenic enzymes, such as fatty acid synthetase (FAS) and malic enzyme (ME) of the liver, was observed in MCT-fed rats without any fat accumulation of the liver (fatty liver). The increase of lipogenic enzyme activity was accompanied by a significant reduction of essential fatty acids (EFA) such as 18:2 (omega6) and 20:4 (omega6) in total liver lipid. In contrast, hepatic beta-hydroxy-beta-methylglutaryl CoA(HMG-CoA) reductase activity was significantly decreased in MCT-fed rats, that would play an important role in achieving hypocholesterolemia. From these results obtained in a long-term experiment, it is concluded that exogenous MCT depresses the key enzyme catalyzing cholesterol synthesis with a concomitant elevation of lipogenic enzyme activity in the rat liver.

Animals↗

Characterization of sterol carrier protein binding with 7-dehydrocholesterol and vitamin D3.

The interaction of rat liver sterol carrier protein (SCP) and 7-dehydrocholesterol or vitamin D3 was analyzed by the method of Scatchard plots and gel filtration on Sephadex G-100. Scatchard plots of binding data revealed that the binding behavior for 7-dehydrocholesterol was monophasic, while that for vitamin D3 was biphasic. In 7-dehydrocholesterol, the apparent number of binding sites and the apparent assocation constant K were 0.72 nmoles/mg protein and 8.75 X 10-7M-1, respectively. On the other hand, vitamin D3 showed two types of binding sites differing in affinity. The apparent number of binding sites and the K for high affinity binding were 0.65 nmoles/mg protein and 7.08 X 10-7M-1, those for low affinity binding were 1.51 nmoles/mg protein and 0.36 X 10-7M-1, respectively. Gel filtration of SCP on Sephadex G-100 column gave three protein peaks (peaks I, II and III protein according to the elution orders; Ve/Vo=1.0, 1.56 and 2.29, respectively). 7-Dehydrocholesterol was able to bind with peak III protein, while vitamin D3 was bound peaks II and III protein, respectively. The molecular weight of peak II protein was estimated to be 44,000 and that of peak III protein was 16,000. From these results, it was clearly demonstrated that SCP was involved in the transformation of 7-dehydrocholesterol to cholesterol and could also bind vitamin D3.

Animals↗

Isolated corticotrophin-deficiency found through alcohol-induced hypoglycemic coma.

A case of hypoglycemic coma after alcohol ingestion was observed in a chronic alcoholic. Upon close examination isolated corticotrophin-deficiency was found. It is suggested that ethanol-induced hypoglycemia may be consistent with dysfunction of mitochondria in hepatic cells and that there may be disorder of the hypothalamus in the chronic drinker.

Adrenocorticotropic Hormone↗

Binding of 7-dehydrocholesterol to sterol carrier protein and vitamin D3 effect.

It was confirmed that delta 5,7-sterol delta 7-reductase activity was suppressed by cholecalciferol (vitamin D3) in the enzyme system consisted of microsomes and sterol carrier protein (SCP). The enzyme activity was significantly decreased in the combination with microsomes obtained from either vitamin D-deficient or vitamin D3-treated rat liver and with SCP obtained from vitamin D3-treated rat. It was also demonstrated by the binding assay of the dextran-charcoal technique that 7-dehydrocholesterol binding to SCP could be specifically displaced by vitamin D3. The inhibition of cholecalciferol on 7-dehydrocholesterol binding to liver SCP was confirmed to be non-competitive inhibition.

Animals↗