Dietary Myoinositol Results in Lower Urine Glucose and in Lower Postprandial Plasma Glucose in Obese Insulin Resistant Rhesus Monkeys.

In a previous study, D‐chiroinositol added to a meal (0.5 g/kg) resulted in significantly lower postprandial plasma glucose concentrations without an increase in insulin concentrations in obese insulin‐resistant monkeys. The present report describes the effects of another isomer of inositol, myoinositol, on postprandial plasma glucose and insulin concentrations and on urine glucose concentrations in 6 similarly insulin‐resistant monkeys. The three 5 day study periods included a control period (liquid diet ad libitum) and 2 experimental periods (liquid diet ad libitum with either 1.5 g/kg/day myoinositol or D‐chiroinositol added). Twenty‐four hour urine samples were collected during each 5 day period. On the sixth day of each period the monkeys were anesthetized 110 min after completing either the control meal (15 ml/kg) or the experimental meals (1.5 g/kg myoinositol or D‐chiroinositol) and plasma samples were obtained at 120, 150,180, 210, 240, 270 and 300 min. The plasma glucose concentration was lower after the meal with myoinositol compared to the control meal at 120, 150 and 180 min (p's<0.05). The plasma insulin concentration was lower after the meal with myoinositol compared to the control meal at 150 and 180 min (p's<0.05). In addition, 24 hour urine glucose concentrations were lower during the myoinositol diet compared to the control diet (p<0.001). The plasma glucose concentration was lower after the meal with D‐chiroinositol compared to the control meal at 150, 240, 270 and 300 min (p's≥0.05). In obese insulin‐resistant monkeys, myoinositol added to the diet lowers urine glucose concentrations and both myoinositol and D‐chiroinositol added to a meal lower postprandial plasma glucose concentrations without increasing postprandial insulin concentrations. Therefore, myoinositol, like D‐chiroinositol, may be a useful agent for reducing meal‐induced hyperglycemia without inducing hyperinsulinemia in insulin‐resistant subjects.