Abstract. Dietary carbohydrate accentuation of endogenous triglyceride production has been studied in 33 patients. A broad and relatively continuous spectrum of steady-state plasma triglyceride concentrations was produced in 31 of the 33 subjects during 3 wk of a high carbohydrate (fat-free) liquid formula diet. Two patients developed plasma triglyceride concentrations in excess of 2000 mg/100 ml, and these were the only patients we have studied in which carbohydrate induction of hypertriglyceridemia seemed to be associated with a defect in endogenous plasma triglyceride removal mechanisms. In the remaining 31 patients the degree of hypertriglyceridemia was highly correlated with the insulin response elicited by the ingestion of the high carbohydrate formula (P < 0.005). No significant correlation existed between fasting plasma triglyceride concentration and either plasma glucose or free fatty acid concentrations after the high carbohydrate diet, nor was the degree of hypertriglyceridemia related to degree of obesity. It is suggested that hypertriglyceridemia in most subjects results from an increase in hepatic triglyceride secretion rate secondary to plasma insulin concentration.

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In order to evaluate the relation between insulin responses, glucose loads and glucose disappearance rate, normal subjects were given glucose doses from 0.5 to 40 g by rapid intravenous injection. A highly linear correlation was seen between dose and the rapidly attained peak plasma glucose level measured as either the mean of the 3-through 5-min (3-5') absolute (r=+.98) or 3-5' incremental (A) (r=+.98) glucose value, suggesting any of these parameters can be employed as an index of the glucose stimulus. Estimated from the 3-5' A plasma insulin levels, the early insulin response, which has been previously shown to be derived from a functional pool of stored insulin, increased in a nonlinear manner over the entire dosage range. In contrast, the total incremental insulin area increased linearly (r = +.85) with increasing glucose loads, suggesting that the total insulin output proportionally responds to the size of the glucose dose. Glucose tolerance measured as the glucose disappearance rate (KG) was also a nonlinear function of glucose dose and therefore was highly correlated (r = +.72) with the acute insulin response but less well with the total incremental insulin output. Furthermore, within the 20 g glucose dose, the KG was highly correlated with the acute insulin response (r= +.66) but not with total insulin output (r= +.04). These observations suggest that the storage pool of readily available insulin is small and finite and the magnitude of the response from this pool is an important determinant of intravenous glucose tolerance (KG). (J Clin Endocr 33: 409, 1971)

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Fasting plasma glucose levels and glycosuria were measured in untreated diabetic subjects on basal and on fat free, high carbohydrate diets. On the high carbohydrate diet the mean fasting plasma glucose was slightly, but not significantly, increased by 15 mg./100 ml. and the twenty-four hour excretion of glucose was increased by 56 gm./24 hr. (p &lt; .02). Five of these subjects were restudied following insulin or oral sulfonylurea therapy, and four similar patients were studied only while on this therapy. In these treated diabetic subjects receiving the high carbohydrate diet, fasting plasma glucose was significantly decreased by 22 mg./100 ml. plasma (p &lt; . 0 2); glycosuria did not change. Thus, among diabetics, only those who remain untreated have worsened glucose tolerance on fat free, high carbohydrate diets.