Glucose intolerance in thyrotoxicosis roles of insulin, glucagon and somatostatin

Abstract

Abstract. The responses in plasma glucose, insulin, C-peptide, glucagon and somatostatin to an oral glucose load were studied in 10 thyrotoxic patients and 10 matched euthyroid controls. The thyrotoxic patients had higher mean fasting plasma glucose (P < 0.05) and responded to oral glucose with an earlier peak at 30 min which was higher than the corresponding glucose level in the controls (P < 0.05). Impaired glucose tolerance was found in 3 patients. Fasting insulin and C-peptide levels were normal in the thyrotoxic patients when corrected for the higher glucose levels. Following glucose ingestion, there was no significant difference between the areas under the insulin or C-peptide curves in patients and controls, but Seltzer's insulinogenic index was reduced in the patients (P < 0.01) suggesting an impaired pancreatic B-cell response to oral glucose. Mean basal glucagon was normal in the thyrotoxic patients. However, while in the controls plasma glucagon became suppressed following glucose ingestion (P < 0.0001), no significant suppression was found in the patients. In the thyrotoxic patients, mean basal somatostatin was normal, but the area under the somatostatin curve following glucose ingestion was significantly increased (P < 0.02). Our findings suggest that décreased glucagon suppression and impaired insulin response after glucose ingestion are involved in glucose intolerance in thyrotoxicosis. Enhanced somatostatin responses to oral glucose in thyrotoxicosis may have contributed to the observed impairment in pancreatic B-cell responsiveness.

Estimation of serum insulin, Homeostasis model assessment-insulin resistance and C-peptide can help identify possible cardiovascular disease risk in thyroid disorder patients

“…[3132] However, the serum C-peptide evaluation in the present study showed a highly significant association with the lipoprotein fractions in the hypothyroid patients[33] [Table 3a]. Thus, it may be deduced that the raised serum C-peptide levels [Figure 5] indicate a state of dyslipidemia and deteriorated CVD risk ratios.…”

Association of elevated insulin‐like growth factor binding protein‐1 with insulin resistance in hyperthyroidism

“…Glucose intolerance is known to be common in hyperthyroidism and our finding of impaired glucose tolerance in 66% of hyperthyroid subjects supports this. The aetiology of abnormal glucose homeostasis in hyperthyroidism is unclear with previous studies examining the roles of insulin and glucagon (Hales & Hyams, 1964; Kabadi & Eisenstein, 1980; AvRuskin et al ., 1985; Shen & Davidson, 1985; Müller et al ., 1986; Lam et al ., 1987; Gonzalo et al ., 1996). Strong evidence exists that IGFBP‐1 has an independent action in glucose homeostasis with increasing concentrations leading to glucose intolerance.…”