Inhibition of Insulin Secretion and Increase of Plasma Non-Esterified Fatty Acids Induced by Biotin Deficiency in Osteogenic Disorder Shionogi Rats.

Abstract

SummaryWe determined the changes in the sources of energy supply

Therapeutic Evaluation of the Effect of Biotin on Hyperglycemia in Patients with Non-Insulin Dependent Diabetes Mellitus.

“…Therefore we presume that the biotin depletion observed in diabetic patient may interfere with pyruvate catabolism as a consequence of reduced activity of the enzyme, resulting in an accumulation of pyruvate and subsequent hyperglycemia. Experimentally it has been shown that there is an impairment in glucose catabolism in biotin-deficient rats [4,[12][13][14][15] and that administration of a biotin supplement counteracts the defect in the oral glucose tolerance and in the insulin response to the oral glucose load in diabetic kk mice [1]. In the present patients, biotin administration decreased the serum levels of pyruvate and lactate.…”

“…Therefore, it seems unlikely that biotin directly stimulates the insulin release with a resultant decrease in the blood glucose level. On the other hand, we demonstrated that the plasma insulin level remarkably declined so that insulin synthesis or the excretion system of the rats may be impaired at an early stage during the course of development of biotin deficiency in osteogenic disorder Shionogi rats [4]. Furthermore, the plasma insulin secreted in response to the glucose load in the deficient rats was approximately one-third the concentration of that in the control rats.…”

“…Hyperglycemia is one of the common complications in the patients because of a diminished ability to utilize glucose by entry into the tricarboxylic acid cycle. We have recently shown that in biotindeficient rats, induced by the feeding of a diet containing raw egg white, the oral glucose tolerance and the plasma insulin level in response to an oral glucose load were lower than in rats with sufficient biotin [4]. Coggeshall et al demonstrated that a pharmacologic dose of biotin lowered the concentration of fasting blood glucose in insulin-dependent diabetic subjects during insulin withdrawal [5].…”

Effect of Biotin Treatment on Metabolic Abnormalities Occurring in Patients with Sternocostoclavicular Hyperostosis.

“…There are acetyl-CoA carboxylase involved in fatty acid synthesis, pyruvate carboxylase involved in glucose metabolism, and propionyl-CoA carboxylase and f3-methylcrotonyl-CoA carboxylase involved in the catabolism of amino acids. Biotin depletion, therefore, causes metabolic abnormalities such as an impairment of glucose utilization [14][15][16], a reduced synthesis of prostaglandins (PGs) [17] and of their precursor fatty acids [18][19][20][21], and an accumulation of abnormal catabolites derived from amino acids [22,23]. However, no information is available concerning the effect of biotin depletion on these metabolic abnormalities in patients with SCCH, nor is it known whether the metabolic abnormalities are associated with the pathogenesis of the disorder.…”

Effect of Biotin Deficiency on the Composition of Intestinal Microflora in Osteogenic Disorder Shionogi Rats.

“…All animals were fed a biotin-deficient diet (20% freeze-dried raw egg white as a protein source). The composition of the experimental diet was reported previously [15,16]. The rats were given free access to the semisynthetic diet and drinking water; and the control and the biotin-deficient groups were given an intraperitoneal injection of 0.5 ml of saline containing 1001ag of biotin and saline only, respectively, once a week.…”