Search PubMed⌕ Search

Biomedical subjects

M Kadowaki

Publications and source records attributed to M Kadowaki.

At least 73 records · Page 4Linked to original sources
PubMed1984

Regulation of plasma amino acid levels by perfusion of hindquarters of rats.

To clarify the role of skeletal muscle in the regulation of plasma amino acid levels, we investigated the response of skeletal muscle to changes in plasma amino acid levels using the perfusion technique of rat hindquarters. The hindquarters of overnight-fasted rats were perfused with a medium containing no amino acids (0 X) and amino acids with plasma levels simulating normal (1 X) or 5 times the normal levels (5 X). Each amino acid level in the perfusate changed in various ways during a 2 h perfusion. The characteristics of amino acid flows in response to the changes in their perfusate levels were divided into four groups as follows: the amino acids which are always taken up irrespective of their plasma levels: glutamate and aspartate; those which are always released: alanine, glutamine and glycine; those which are taken up or released depending on their plasma levels: valine, leucine, isoleucine, serine and (threonine); and those which are released at lower, but neither taken up nor released, at higher plasma levels: tyrosine, phenylalanine, tryptophan, histidine, methionine, asparagine, arginine, lysine and proline. Comparing these results with the data of liver perfusion (Bloxam, D.L. (1971): Br. J. Nutr., 26, 393-422), we assumed that skeletal muscle plays a role complementary to liver in the regulation of plasma amino acid levels.

Amino Acids↗
PubMed1983

Effects of sodium ursodeoxycholate, hyodeoxycholate and dehydrocholate on cholesterol and bile acid metabolism in rats.

Effects of sodium ursodeoxycholate, hyodeoxycholate and dehydrocholate on serum and liver cholesterol levels, bile flow, biliary cholesterol, phospholipid and bile acid secretions, and fecal sterol and bile acid excretions were examined with Wistar strain male rats fed ordinary and 2% cholesterol supplemented diets. Dehydrocholate increased the liver cholesterol level, bile flow and biliary lipid secretion, but ursodeoxycholate and hyodeoxycholate did not. The serum cholesterol level was not changed by the treatments. Ursodeoxycholate and hyodeoxycholate increased their own secretion into the bile and decreased cholic acid secretion, while dehydrocholate increased deoxycholic acid and oxo bile acid secretion. Ursodeoxycholate increased but dehydrocholate decreased the fecal sterol excretion, and hyodeoxycholate caused no change. Dehydrocholate decreased the fecal coprostanol level. The total amounts of the fecal bile acids were similar in all the treated groups, but ursodeoxycholate increased lithocholic acid, alpha, beta- and omega-muricholic acids and ursodeoxycholic acid; hyodeoxycholate increased hyodeoxycholic acid, 3 alpha, 7 beta, 12 alpha-trihydroxy-5 beta-cholanoic acid and oxo bile acids; and dehydrocholate increased deoxycholic acid, cholic acid, omega-muricholic acid and oxo bile acids and decreased hyodeoxycholic acid. These data suggested that ursodeoxycholate was transformed into lithocholic and muricholic acids, and dehydrocholate into cholic and deoxycholic acids during the enterohepatic circulation, but hyodeoxycholate showed almost no change. Ursodeoxycholate and hyodeoxycholate caused neither accumulation of cholesterol in tissues nor increase in bile flow and biliary lipid secretion as well as chenodeoxycholate did. The biological effect of dehydrocholate was similar to that of cholate, and this was partially due to its conversion into cholic acid and deoxycholic acid.

Animals↗
PubMed1981

Effect of bile duct ligation on bile acid metabolism in rats.

The effect of bile duct ligation on the quantitative and qualitative changes of bile acids in serum, liver, urine, and feces, and the concentration of cholesterol and phospholipids in serum and liver were examined in male rats. The concentration of bile acids in serum increased over 100-fold on day 5 but was lower than the 5-day level on days 10 and 15. The concentration in the liver also increased about 10-fold. beta-Muricholic acid predominantly increased but the secondary bile acids, deoxycholic acid and hyodeoxycholic acid, decreased. The urinary excretion of bile acids increased to about 40 mg/day per rat on the first day of bile duct ligation but this increase was reduced on day 2 to about half and remained at that level until day 24. These values exceeded that of fecal bile acids, 12 mg/day per rat, before bile duct ligation. The amount of bile acid sulfates in the urine was as low as 1% of the total. The urinary non-sulfated bile acids consisted mainly of beta-muricholic acid (60%) and cholic acid (20%), while the sulfates contained a considerable amount of unidentified acidic substances (40%) in addition to cholic acid and beta-muricholic acid. The concentration of cholesterol and phospholipids in serum markedly increased on day 5 but declined gradually thereafter. The liver cholesterol concentration did not change but the phospholipid concentration decreased. Fecal sterols did not change in both the total amount and composition. These data indicated that daily synthesis of bile acids, especially beta-muricholic acid, was accelerated in bile duct-ligated rats.

Animals↗
PubMed1979

Altered bile acid metabolism in alloxan diabetic rats.

Changes of cholesterol, phospholipid, triglyceride or bile acid levels in serum liver, bile and feces after the treatment with alloxan were examined in Wistar strain male rats. Serum cholesterol, phospholipid and triglyceride levels and liver cholesterol level markedly increased but liver phospholipid and triglyceride levels remained unchanged. The lipid levels in serum very low density and low density lipoproteins were elevated but those in high density lipoprotein were not. Bile flow was not changed but biliary secretion of cholesterol, phospholipid and bile acids markedly increased. Among the biliary bile acid components, cholic acid markedly increased but the amount of chenodeoxycholic acid was similar to that of normal rats. Fecal excretion of deoxycholic acid increased but that of lithocholic and hyodeoxycholic acids decreased, and alpha, beta- and omega-muricholic acids did not change, thus, the total amount of fecal bile acids remained unchanged. Hepatic cholesterol synthesis was markedly depressed, while cholesterol 7 alpha-hydroxylase activity did not change and cytochrome P-450 content was elevated by about 40%. From such evidence, it was apparent that synthesis of cholic acid increased while that of chenodeoxycholic acid decreased and the total amount of bile acids synthesized did not change in the diabetic rats. Furthermore, marked increase of the pool size of cholic acid and hepatic secretion of cholic acid stimulated the absorption of lipids and produced a hyperlipidemia in the diabetic rats.

Alloxan↗