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Biomedical subjects

M Ukai

Publications and source records attributed to M Ukai.

At least 127 records · Page 7Linked to original sources
PubMed1979

The release and metabolism of pancreatic hormones after major hepatectomy in the dog.

Major hepatectomy in the dog induced a 50% decrease in peripheral serum glucose, a 11-fold increase in portal plasma glucagon and a 36-fold increase in the portal glucagon/insulin ratio 3 hr after operation. Peripheral serum glucose levels were inversely correlated to the logarithmic value of portal plasma glucagon (r = -0.50, p less than 0.01) and that of the portal glucagon/insulin ratio (r = -0.85, p less than 0.01) for 1-6 hr after operation. The ratio of peripheral to portal plasma glucagon was also inversely correlated to the logarithmic value of portal plasma glucagon (r = -0.59, p less than 0.01). In case of glucose infusion, plasma glucagon levels were not elevated after major hepatectomy. The data suggest that glucose deficiency after major hepatectomy in the dog may cause hyperglucagonemia with an enhanced glucagon requirement.

Animals↗
PubMed1977

Effect of somatostatin on neurotensin-induced glucagon release and hyperglycemia.

Administration of neurotensin to dogs resulted in rises in circulating blood glucose, glucagon and insulin levels, the rise in glucagon being more pronounced than that in insulin. Infusion of somatostatin along with neurotensin suppressed glucagon and insulin responses to neurotensin and prevented the rise in blood glucose levels. These results suggest that the hyperglycemia seen after neurotensin is due to neurotensin stimulation of glucagon release over insulin release.

Animals↗
PubMed1976

The histochemistry of mucosaccharides in some organs of germfree rats.

In order to study the histochemical nature of mucosaccharides in germfree animals, the organs in natural contact with bacteria (stomach, small and large intestine) and those naturally remote from bacteria (tracheal and ear cartilage and aorta) were studied by means of light microscopic methods for mucosaccharides in germfree and conventional rats. In the stomach (surface and foveolar cells) of germfree rats the histochemical reactions for acid and neutral mucosaccharides were apparently less intense than in that of conventional rats, whereas in the small and large intestine (goblet cells) of germfree rats the reactions were significantly more intense than in those of conventional rats. In the cartilage (intercellular matrix, lacunar border and chondrocyte cytoplasm) and aorta (interelastic spaces) of germfree animals the reactions were less intense than in those of conventional animals. In addition, some differences in the histochemical nature of mucosaccharides between the organs of germfree and conventional rats were noted, as revealed by the effects of chemical modifications and digestions with enzymes upon the histochemical reactions studied.

Animals↗
PubMed1976

Cholesterol synthesis in germfree and conventional rats.

The synthesis of cholesterol from labeled acetate and mevalonate by the liver and intestinal tract was investigated in germfree and conventional rats. When a low cholesterol diet was fed, the rates of in vitro synthesis from acetate by the liver, ileum and cecum of germfree rats were 13%, 11% and 25% of those of conventional rats, respectively. Cholesterol feeding markedly inhibited hepatic cholesterol synthesis from acetate in both germfree and conventional rats. Such inhibitions were released by additional cholestyramine feeding. The rate of hepatic cholesterol synthesis was greater and the liver cholesterol level was less after cholestyramine feeding in germfree rats than in conventional rats, suggesting an importance of bile acids in the regulation of cholesterol metabolism in the germfree rat. There was an inverse proportionality between the logarithmic rate of hepatic cholesterol synthesis and the liver cholesterol level in the germfree rat. Data indicate that endogenous cholesterol synthesis in the germfree rat may not be responsible for the high cholesterol level in plasma or liver and that the liver cholesterol level may play a major role in the regulation of hepatic cholesterogenesis in the germfree rat by a mechanism similar to that in the conventional rat.

Acetates↗