A high biotin diet improves the impaired glucose tolerance of long-term spontaneously hyperglycemic rats with non-insulin-dependent diabetes mellitus
Zhang H.; Osada K.; Maebashi M.; Ito M.; Komai M.; Furukawa Y.
H. Zhang, Laboratory of Nutrition, Dept. Applied Biological Chemistry,
Faculty of Agriculture, Sendai 981 Japan
Journal of Nutritional Science and Vitaminology (Japan) , 1996, 42/6
The Otsuka Long-Evans Tokushima Fatty (OLETF) rat, serving as a spontaneously diabetic model with non-insulin-dependent diabetes mellitus (NIDDM),exhibits impaired glucose tolerance (IGT) at about 16 weeks of age. In this study, we investigated whether or not biotin, a water-soluble vitamin, improved the IGT of OLETF rats. To this end, we administered diets containing one of three levels of biotin, a high-biotin diet (BH), a normal-biotin diet (BN) and a basal-biotin diet (BB), to OLETF rats up to 24 weeks of age. An oral glucose tolerance test (OGTT) was performed four times between 13 and 22 weeks of age. The administration of a BH corrected the IGT of OLETF rats. Upon further investigation, we found that insulin secretion in the OLETF-BH rats was decreased to a significant extent, signaling that the hyperinsulinemia typical to the OLETF-BH rats had clearly improved. Body weights were significantly lower in the OLETF-BH group than in the other OLETF groups, even though the OLETF-BH rats showed a significantly higher average daily food intake. The body weight gain of the OLETF-BH rats followed the same tendency as the control-LETO (Long Evans Tokushima Otsuka) rats (LETO-BB and LETO-BN). These results demonstrate that a high-level biotin diet can improve the glucose handicap in NIDDM rats.
Oral glucose tolerance test after high-dose i.v. biotin administration in normoglucemic hemodialysis patients
Koutsikos D.; Fourtounas C.; Kapetanaki A.; Agroyannis B.; Tzanatos H.;
Rammos G.; Kopelias I.; Bosiolis B.; Bovoleti O.; Darema M.; Sallum G.
Aretaieon University Hospital, 76, Vas. Sofias AVE, 115 28 Athens Greece
Renal Failure (USA) , 1996, 18/1 (131-137)
Abnormal glucose metabolism in uremia may result from a complex interplay between decreased insulin secretion and insulin resistance. Recent studies report beneficial effect of biotin administration in glucose metabolism in diabetic animals and in a small number of patients with diabetes mellitus. The aim of the present study was to evaluate the response of oral glucose tolerance test (OGTT) to the i.v. administration of large doses of biotin in hemodialysis patients. Eleven hemodialysis patients aged 56.90 plus or minus 11.20 (32- 76) years on regular hemodialysis thrice a week for 2.72 plus or minus 1.79 (1-7) years were studied. Fasting venous plasma glucose, glucosylated hemoglobin (%GH), and plasma glucose concentration 2 h after the administration of a 75-g glucose load were measured before, and 2 weeks and 2 months after administration of 50 mg of biotin i.v. postdialysis, and after a 2-month washout period. During the study, dialysis schedule and patients' medication, diet, and dry weight were kept unchanged. OGTT was abnormal in 4 patients before biotin administration and became normal in 3 patients (75%). Our results offer support to the findings of other studies about the beneficial effect of biotin in experimental or clinical diabetes mellitus, and argue for the involvement of biotin in glucose metabolism.
Transcriptional regulation of liver phosphoenolpyruvate carboxykinase by biotin in diabetic rats
Dakshinamurti K.; Li W. Biochemistry/Molecular Biology Dept., University of Manitoba, Winnipeg,
Man. R3E OW3 Canada
MOL. CELL. BIOCHEM. (USA) , 1994, 132/2 (127-132)
Rat liver phosphoenolpyruvate carboxykinase (PEPCK) activity was followed over a time period of 5 h following administration of biotin to streptozotocin-induced diabetic rats. In parallel with the decrease in enzyme activity liver PEPCK mRNA decreased by 85% at 3 h after injection of biotin to diabetic rats. There was no significant change in the accumulation of kidney PEPCK mRNA. Parallel studies with insulin indicated that biotin had a regulatory effect similar to that of insulin on liver PEPCK mRNA. The administration of biotin did not change the insulin status of the diabetic rat indicating that biotin did not act via insulin. The transcriptional activity of the hepatic PEPCK gene, as measured by nuclear run-on assay; was decreased by 57% within 30 min of biotin administration. The results suggest that biotin regulates hepatic, but not renal, PEPCK mRNA concentration at the transcriptional level in diabetic rats.
Effect of biotin on the regulation of glucokinase in the intact rat
Hsieh Y.T.L.; Mistry S.P.
Department of Poultry/Avian Sciences, Institute of Food Science, Cornell
University, Ithaca, NY 14853-5601 USA
NUTR. RES. (USA) , 1992, 12/6 (787-799)
Glucokinase activity was affected by hormones, dietary state, and dietary sources (e.g., glucose). Therefore, various factors (such as glucose, insulin, and biotin) affecting glucokinase activity in the rat liver were investigated. The activity of glucokinase was low in diabetic, fasting, and/or biotin-deficient rats. In the present study, the de novo synthesis of the glucokinase induced by the insulin and biotin in the intact rat was proposed. The first induction of glucokinase was activated by insulin. The second phase of enzyme activity could be induced by biotin. In addition, supplementation of cGMP with glucose and insulin to biotin deficient rats fully restored the enzyme activity as did biotin, showing that cGMP induction of glucokinase was dependent on the biotin status of the animal.
Biotin supplementation improves glucose and insulin tolerances in genetically diabetic KK mice
Reddi A.; DeAngelis B.; Frank O.; Lasker N.; Baker H.
Department of Medicine, Division of Nephrology, University of Medicine
and Dentistry of New Jersey-New Jersey Medical School, Newark, NJ
LIFE SCI. (USA) , 1988, 42/13 (1323-1330)
Because biotin treatment may lower blood glucose in insulin-dependent diabetes, we chose to study such an effect in non-insulin dependent diabetes. Twenty-six diabetic KK mice, moderately hyperglycemic and insulin resistant, were treated for 10 weeks: 9 animals with 2 mg of biotin/Kg, 8 with 4 mg of biotin/Kg, and 9 with saline (controls). Blood glucose levels, oral glucose tolerance, insulin response to oral glucose, and blood glucose decrease in response to insulin were quantitated. Compared to controls, biotin treatment lowered post-prandial glucose levels, and improved tolerance to glucose and insulin resistance. Serum immunoreactive insulin levels in biotin-treated mice were like the controls.