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Biomedical subjects

G Boden

Publications and source records attributed to G Boden.

170 records · Page 10Linked to original sources
PubMed1968

Elevated serum human growth hormone and decreased serum insulin in prediabetic males after intravenous tolbutamide and glucose.

Serum human growth hormone (HGH), serum immunoreactive insulin (IRI), plasma free fatty acids, and blood glucose were measured during intravenous glucose and intravenous tolbutamide tolerance tests in 13 normal and 13 prediabetic (offspring of two diabetic parents) males, closely matched for weight and age. Only prediabetics with normal glucose tolerance during oral, intravenous, and cortisone-primed glucose tolerance tests were evaluated. Mean serum HGH levels were significantly higher in prediabetics in response to intravenous tolbutamide and at the end of the 3-hr intravenous glucose tolerance tests (IVGTT). This is interpreted as a hyperresponsiveness of the growth hormone-releasing mechanisms in prediabetic subjects. The insulin response during the first 10 min of an IVGTT was significantly reduced in prediabetic males as compared to normal controls, whereas the insulin response to intravenous tolbutamide was not significantly different at the same time intervals in the same subjects.It appears, therefore, that measuring IRI during an IVGTT can be valuable in detecting the earliest signs of diabetes even before any disturbance of blood glucose homeostasis is seen. The possibility that growth hormone hypersecretion in prediabetics might play a role in the pathogenesis of human diabetes mellitus is discussed.

Adult↗
PubMedDate not supplied

The role of growth hormone in the glucose intolerance of uremia.

The fasting plasma growth hormone (GH) concentration and the plasma growth hormone response to sustained hyperglycemia was examined in 8 chronically uremic subjects before and after hemodialysis employing the hyperglycemia clamp technique. The plasma glucose concentration was acutely raised and maintained at +125 mg/100 ml above basal levels. Since the glucose concentration was held constant, the glucose infusion rate is an index of glucose metabolism (M) and M divided by the plasma insulin response (I) is a measure of tissue sensitivity to insulin. Predialysis, the fasting GH concentration, 4.0 +/- 1.0 ng/ml, was significantly greater than controls, 0.3 +/- 0.1 ng/ml (p less than 0.01), and failed to suppress normally following sustained hyperglycemia. Both M, 4.23 +/- 0.36 mg/kg x min, and M/I, 5.05 +/- 0.79 mg/kg x min per microU/ml, were significantly reduced compared to controls (p less than 0.001). There was no correlation between either the fasting GH concentration or the GH response to sustained hyperglycemia and either M or M/I. Following dialysis both M, 6.30 +/- 0.64 mg/kg x min, and M/I, 8.39 +/- 1.06 mg/kg x min per microU/ml, increased (p less than 0.01) without significant change in either the fasting GH level, 4.0 +/- 1.2 ng/ml, or the plasma GH response to hyperglycemia. It is concluded that while deranged GH physiology is a common accompaniment of the uremic state, it is not responsible for the glucose intolerance and tissue insensitivity to insulin observed in uremia.

Adult↗
PubMedDate not supplied

Free fatty acids, insulin resistance, and type 2 diabetes mellitus.

Evidence is presented that shows that free fatty acids (FFA) are one important link between obesity, insulin resistance, and type 2 diabetes. Plasma FFA levels are elevated in most obese subjects, and physiological elevations of plasma FFA inhibit insulin-stimulated glucose uptake into muscle. This peripheral insulin resistance is caused by an FFA-induced defect, which develops 3-4 hr after raising plasma FFA, in insulin-stimulated glucose transport or phosphorylation, or both. This resistance is also caused by a second defect, which develops after 4-6 hr, consisting of inhibition of glycogen synthase activity. Whether elevated plasma FFA levels inhibit insulin action on endogenous glucose production (EGP), that is, cause central insulin resistance, is more difficult to demonstrate. On the one hand, FFA increase gluconeogenesis, which enhances EGP; on the other hand, FFA increase insulin secretion, which decreases EGP. Basal plasma FFA support approximately one third of basal insulin secretion in diabetic and nondiabetic subjects and, hence, are responsible for some of the hyperinsulinemia in obese, normoglycemic patients. In addition, elevated plasma FFA levels potentiate glucose-stimulated insulin secretion acutely and during prolonged exposure (48 hr). It is hypothesized that obese subjects who are genetically predisposed to develop type 2 diabetes will become partially "lipid blind," that is, unable to compensate for their FFA-induced insulin resistance with FFA-induced insulin oversecretion. The resulting insulin resistance/secretion deficit will then have to be compensated for with glucose-induced insulin secretion, which, because of their partial "glucose blindness," will result in hyperglycemia and eventually in type 2 diabetes.

Diabetes Mellitus, Type 2↗
PubMedDate not supplied

Free fatty acids-the link between obesity and insulin resistance.

OBJECTIVE: To present evidence that free fatty acids (FFA) are an important link between obesity and insulin resistance. METHODS: The role of FFA in peripheral insulin resistance, hepatic insulin resistance, insulin secretion, and type 2 diabetes is discussed. RESULTS: Obesity is invariably associated with insulin resistance. In most obese subjects, plasma FFA levels are increased. Physiologic increases in plasma FFA levels cause insulin resistance in both diabetic and nondiabetic subjects by producing several metabolic defects: (1) FFA inhibit insulin-stimulated glucose uptake at the level of glucose transport or phosphorylation (or both); (2) FFA inhibit insulin-stimulated glycogen synthesis; and (3) FFA inhibit insulin-stimulated glucose oxidation. (This last-mentioned defect probably does not contribute to insulin resistance.) FFA probably also cause hepatic insulin resistance, which results in increased rates of endogenous glucose production in relationship to the prevailing degree of hyperinsulinemia. Lastly, FFA support between 30 and 50% of basal insulin secretion and potentiate glucose-stimulated insulin secretion in short-term and long-term settings. The stimulatory action of FFA on b-cells enables obese individuals who do not have a genetic predisposition to develop type 2 diabetes mellitus to compensate for their FFA-potentiated insulin resistance with an increase in FFA-mediated insulin secretion. In contrast, subjects who are genetically predisposed to develop type 2 diabetes may be unable to secrete sufficient amounts of insulin to compensate for their FFA-induced insulin resistance. This situation will lead to an increase in blood glucose concentration and eventually to type 2 diabetes. CONCLUSION: FFA have been shown to have an important contributing role in the pathogenesis of insulin resistance in human obesity.

Blood Glucose↗