18 research outputs found
Effect of prolonged overnight fasting on energy metabolism in non-insulin-dependent diabetic and non-diabetic subjects
The effect on energy metabolism of a 6-h prolongation of the conventional 12-h overnight fast was examined in 9 healthy subjects and in 7 patients with non-insulin-dependent diabetes mellitus. Plasma glucose concentration decreased by 7 and 23%, in control and diabetic subjects, respectively. In control subjects, the fall in plasma glucose was associated with a slight but significant fall in plasma insulin and a rise in plasma free fatty acid concentrations. During this same period, the rates of plasma free fatty acid oxidation, measured by infusion of [14C]palmitate, and net lipid oxidation, measured by indirect calorimetry, increased in normal subjects by 55 and 76%, respectively; the rate of glucose oxidation measured by indirect calorimetry decreased by 37%. In the diabetic patients, the free fatty acid oxidation rate was enhanced already after 12 h of fasting compared with controls (2.06 vs 1.30 mumol.kg-1.min-1; p less than 0.05) and did not change significantly during the 6-h observation period. After 18 h of fasting, the rate of plasma free fatty acid oxidation was similar in control and diabetic subjects. The data thus emphasize the need for strict standardization of the overnight fasting period for metabolic studies, and demonstrate the difficulties in comparing basal rates of substrate oxidation between healthy and diabetic subjects
Effect of prolonged overnight fasting on energy metabolism in non-insulin-dependent diabetic and non-diabetic subjects
The effect on energy metabolism of a 6-h prolongation of the conventional 12-h overnight fast was examined in 9 healthy subjects and in 7 patients with non-insulin-dependent diabetes mellitus. Plasma glucose concentration decreased by 7 and 23%, in control and diabetic subjects, respectively. In control subjects, the fall in plasma glucose was associated with a slight but significant fall in plasma insulin and a rise in plasma free fatty acid concentrations. During this same period, the rates of plasma free fatty acid oxidation, measured by infusion of [14C]palmitate, and net lipid oxidation, measured by indirect calorimetry, increased in normal subjects by 55 and 76%, respectively; the rate of glucose oxidation measured by indirect calorimetry decreased by 37%. In the diabetic patients, the free fatty acid oxidation rate was enhanced already after 12 h of fasting compared with controls (2.06 vs 1.30 mumol.kg-1.min-1; p less than 0.05) and did not change significantly during the 6-h observation period. After 18 h of fasting, the rate of plasma free fatty acid oxidation was similar in control and diabetic subjects. The data thus emphasize the need for strict standardization of the overnight fasting period for metabolic studies, and demonstrate the difficulties in comparing basal rates of substrate oxidation between healthy and diabetic subjects
Effect of prolonged overnight fasting on energy metabolism in non-insulin-dependent diabetic and non-diabetic subjects
The effect on energy metabolism of a 6-h prolongation of the conventional 12-h overnight fast was examined in 9 healthy subjects and in 7 patients with non-insulin-dependent diabetes mellitus. Plasma glucose concentration decreased by 7 and 23%, in control and diabetic subjects, respectively. In control subjects, the fall in plasma glucose was associated with a slight but significant fall in plasma insulin and a rise in plasma free fatty acid concentrations. During this same period, the rates of plasma free fatty acid oxidation, measured by infusion of [14C]palmitate, and net lipid oxidation, measured by indirect calorimetry, increased in normal subjects by 55 and 76%, respectively; the rate of glucose oxidation measured by indirect calorimetry decreased by 37%. In the diabetic patients, the free fatty acid oxidation rate was enhanced already after 12 h of fasting compared with controls (2.06 vs 1.30 mumol.kg-1.min-1; p less than 0.05) and did not change significantly during the 6-h observation period. After 18 h of fasting, the rate of plasma free fatty acid oxidation was similar in control and diabetic subjects. The data thus emphasize the need for strict standardization of the overnight fasting period for metabolic studies, and demonstrate the difficulties in comparing basal rates of substrate oxidation between healthy and diabetic subjects
Effect of sulphonylurea on glucose-stimulated insulin secretion in healthy and non-insulin dependent diabetic subjects: a dose-response study
The effect of a rapid-acting sulphonylurea, glipizide, on the dose-response
relationship between the beta-cell response (insulin and C-peptide secretion) and
the ambient plasma glucose concentration was examined in 12 healthy and 6
non-insulin-dependent diabetic subjects. The subjects participated in two sets of
experiments which were performed in random order: (A) four hyperglycaemic clamp
studies, during which the plasma glucose concentration was raised for 120 min by
1 (only in healthy subjects), 3, 7, and 17 mmol/l; and (B) the same four
hyperglycaemic clamp studies preceded by ingestion of 5 mg glipizide. All
subjects participated in a further study, in which glipizide was ingested and the
plasma glucose concentration was maintained at the basal level. In control
subjects in the absence of glipizide, the first-phase plasma insulin response
(0-10 min) increased progressively with increasing plasma glucose concentration
up to 10 mmol/l, above which it tended to plateau. Glipizide augmented the
first-phase insulin response without changing the slope of the regression line
relating plasma insulin to glucose concentrations. The second-phase plasma
insulin response (20-120 min) increased linearly with increasing hyperglycaemia
(r = 0.997). Glipizide alone increased the plasma insulin response by 180 pmol/l.
A similar increase in plasma insulin response following glipizide was observed at
each hyperglycaemic step, indicating that glipizide did not affect the
sensitivity of the beta-cell to glucose. First-phase insulin secretion was
reduced in the type 2 (non-insulin-dependent) diabetic patients, and was not
influenced by glipizide
Effect of sulphonylurea on glucose-stimulated insulin secretion in healthy and non-insulin dependent diabetic subjects: a dose-response study
The effect of a rapid-acting sulphonylurea, glipizide, on the dose-response
relationship between the beta-cell response (insulin and C-peptide secretion) and
the ambient plasma glucose concentration was examined in 12 healthy and 6
non-insulin-dependent diabetic subjects. The subjects participated in two sets of
experiments which were performed in random order: (A) four hyperglycaemic clamp
studies, during which the plasma glucose concentration was raised for 120 min by
1 (only in healthy subjects), 3, 7, and 17 mmol/l; and (B) the same four
hyperglycaemic clamp studies preceded by ingestion of 5 mg glipizide. All
subjects participated in a further study, in which glipizide was ingested and the
plasma glucose concentration was maintained at the basal level. In control
subjects in the absence of glipizide, the first-phase plasma insulin response
(0-10 min) increased progressively with increasing plasma glucose concentration
up to 10 mmol/l, above which it tended to plateau. Glipizide augmented the
first-phase insulin response without changing the slope of the regression line
relating plasma insulin to glucose concentrations. The second-phase plasma
insulin response (20-120 min) increased linearly with increasing hyperglycaemia
(r = 0.997). Glipizide alone increased the plasma insulin response by 180 pmol/l.
A similar increase in plasma insulin response following glipizide was observed at
each hyperglycaemic step, indicating that glipizide did not affect the
sensitivity of the beta-cell to glucose. First-phase insulin secretion was
reduced in the type 2 (non-insulin-dependent) diabetic patients, and was not
influenced by glipizide