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Altered insulin sensitivity, insulin secretion and lipid profile in non-diabetic prostate carcinoma.

Insulin can influence cancer risk through its effect on cell proliferation, differentiation and apoptosis. Although hyperinsulinemia is considered as a risk factor in the pathogenesis of various cancers, the data related to insulin sensitivity, insulin secretion and lipid profile is lacking in non-diabetic prostate carcinoma cases. The present study was undertaken to evaluate lipid profile parameters and insulin sensitivity and secretion using surrogate markers derived from the measurements of fasting glucose and fasting insulin. The study group comprises 27 prostate carcinoma cases and 27 controls having similar age. Fasting serum insulin, glucose and lipid profile parameters were estimated in both the groups. Insulin sensitivity was assessed by Homeostasis model assessment of insulin sensitivity and Quantitative insulin sensitivity check index. Insulin secretion was assessed by insulinogenic index. Fasting serum insulin, insulinogenic index and LDL-cholesterol were significantly increased (p < 0.05) and HOMA-IS, QUICKI and HDL-cholesterol was significantly decreased (p < 0.05) in carcinoma cases compared to controls. PSA level was significantly associated with fasting insulin (R2 = 0.150, beta = 0.387, p = 0.046) and QUICKI (R2 = 0.173, beta = -0.416, p = 0.031). Fasting insulin was significantly correlated with triglyceride (r = 0.404, p = 0.037) and HDL-cholesterol (r = -0.474, p = 0.013). The present study concludes that hyperinsulinemia associated with reduced insulin sensitivity may play a role in the pathogenesis of prostate carcinoma.