Biotin as an Essential Factor for Normal Glucose-induced Insulin Secretory Response in Rats

Abstract

We studied the effect of biotin deficiency on insulin secretion from pancreas in rats with varying degrees of biotin-deficiency: moderate biotin deficiency (MBD), biotin deficiency (BD), and severe biotin deficiency (SBD). The plasma insulin levels were reduced with the severity of the deficiency. There was a significant positive correlation between the plasma insulin and plasma biotin levels. (r = 0.723, p < 0.001). To investigate the insulin secretion from pancreas, the isolated pancreas was perfused with 20 mM glucose or 10 mM arginine, which is a non-metabolic stimulus for insulin secretion. Compared to the control, the levels of insulin response to glucose in MBD, BD, and SBD rats were approximately 43 %, 35 %, and 22 %, respectively (p < 0.01). However, in MBD rats, the insulin content of the pancreas did not decrease significantly as compared with the control, and no retrogressive pathological change was observed in pancreas. In contrast, the level of insulin response to 10 mM arginine in MBD rats was approximately 76 % of the control (not significant). These results indicate that biotin directly acts in the glucose metabolic pathway for ATP production, which is a key mediator of nutrient-induced insulin secretion. Our study suggests that biotin is an essential factor and plays a pivotal role in the normal glucose-induced insulin secretory response.