Peripheral Glucose Metabolism in Human Hyperthyroidism

Abstract

The present study was designed to determine the effect of spontaneous hyperthyroidism on the forearm muscle glucose uptake and oxidation during the postabsorptive state and after an oral glucose challenge. Ten normal subjects and 11 hyperthyroid patients were studied after an overnight fast (12-14 h) and for 3 h after ingestion of 75 g glucose. Peripheral glucose metabolism was analyzed by the forearm technique to estimate muscle exchange of substrate combined with indirect calorimetry. Increased forearm glucose uptake was observed in the hyperthyroid patients compared to that in the normal subjects (1286 +/- 212 vs. 677 +/- 88 mumol/100 mL forearm.3 h) with enhanced glucose oxidation (443 +/- 40 vs. 147 +/- 29 mumol/100 mL forearm.3 h). Nonoxidative glucose metabolism was also greater in hyperthyroid patients than in normal subjects (842 +/- 234 vs. 529 +/- 90 mumol/100 mL forearm.3 h). Basal serum FFA levels were significantly higher in hyperthyroid than in normal subjects (0.252 +/- 0.025 vs. 0.182 +/- 0.022 g/L), as were the basal lipid oxidation rates in the forearm muscles of the thyrotoxic individuals (0.290 +/- 0.066 vs. 0.088 +/- 0.016 mg/100 mL forearm.min). After glucose ingestion, serum FFA levels and lipid oxidation rates declined significantly to equivalent values in both groups of subjects, and the similar basal insulin concentrations increased to significantly higher levels in the hyperthyroid patients. In conclusion, spontaneous human hyperthyroidism increases glucose uptake by the forearm muscles in the postabsorptive state and during an oral glucose challenge, with augmented fluxes of glucose through the oxidative and nonoxidative pathways.

Insulin Resistance in the Third Trimester of Pregnancy Suffering from Gestational Diabetes Mellitus or Impaired Glucose Tolerance

“…Hypersomatotropism is associated with disturbance of glucose tolerance and insulin resistance. Hyperprolactinaemia, like hypersomatotropism, is associated with decreased insulin sensitivity (Foss et al, 1995). The present study (on control group) demonstrated that prolactin increases progressively from the first trimester through till third trimester.…”

Increased insulin sensitivity and upregulation of insulin receptor, insulin receptor substrate (IRS)-1 and IRS-2 in liver of Ames dwarf mice

“…Although GH has been established to have a primary role in this phenomenon (Davidson 1987), several studies indicate that PRL is also capable of antagonizing insulin action (Landgraf et al 1977, Schernthaner et al 1985, Foss et al 1995, Reis et al 1997. Increased responsiveness of plasma glucose to insulin in Ames dwarf mice, which are deficient in these hormones, is consistent with the diabetogenic effect of GH and PRL (Borg et al 1995).…”

“…In humans and animals, glucose intolerance, insulin resistance and hyperinsulinemia are associated with excess of GH (Rizza et al 1982, Ader et al 1987, Davidson 1987 or PRL (Landgraf et al 1977, Schernthaner et al 1985, Foss et al 1995, Reis et al 1997, while deficiency of these hormones leads to increased insulin sensitivity, decreased insulin secretion and hypoglycemia (Hopwood et al 1975, Bougneres et al 1985, Daugaard et al 1999. GH and PRL have been shown to promote tyrosine phosphorylation of IRS-1 and IRS-2 and their association with PI 3-kinase both in vitro (Souza et al 1994, Argetsinger et al 1995, Ridderstråle et al 1995, Berlanga et al 1997 and in vivo (Yamauchi et al 1998, Thirone et al 1999.…”

Neuroprotective Effects of Piracetam Versus Peroxisome Proliferator-Activated Receptor-Gamma Agonist Pioglitazone in Drug-Induced Parkinsonism

“…Our results agree with previous studies, on patients treated with atypical antipsychotics drugs like haloperidol and showed that they are more likely to develop diabetes and hyperglycemia (22) . Hyperglycemia could be related to the hyperprolactinemia caused by the typical antipsychotics drugs as causing an increased insulin resistance (23) . Haloperidol antagonizes dopamine D2 receptors, and the activation of these receptors enhances insulin secretion (24) .…”