Abstract
Chronic pancreatitis predisposes to diabetes. Loss of endocrine function by beta-cells in the Langerhans islets is considered to be the main causative factor, although several studies have also suggested insulin resistance as a possible additional mechanism. The aim of the study was to estimate insulin sensitivity in chronic pancreatitis in view of the coexisting meta bolic syndrome components. The study involved 30 patients (mean age 50.83 +/-6.61 years; 23.33% women, 76.66% men) diagnosed with chronic pancreatitis (using imaging tests). Insulin sensitivity with regard to the coexistent obesity, dyslipidemia, and arterial hypertension was measured using the euglycemic clamp method. Diabetes was present in 22 patients, impaired glucose tolerance in 4, and no carbohydrate metabolism disturbances in 4. Insulin resistance was present in 22 patients (73.33%), in whom a higher prevalence of diabetes (77.27% vs. 62.5%) and prediabetes (13.63% vs. 12.5%) was observed. The analysis of anthropometric para meters revealed that individuals with a high index of central obesity had a statistically significantly lower tissue glucose utilization (TGU) (3.23 vs. 4.89 mg/kg/min; P = 0.02), although there were no obese patients in the study group according to the body mass index. No statistically significant differences in TGU were observed in relation to lipid disorders (total cholesterol, low- and high-density lipoprotein cholesterol, triglycerides) and arterial hypertension. In patients with chronic pancreatitis, lack of correlation between insulin sensitivity and meta bolic syndrome components may indicate that insulin resistance is related to primary disease or that an additional mechanism underlying pancreatic diabetes operates.
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