Leptin and its correlation with exocrine and endocrine pancreatic function in idiopathic chronic pancreatitis - Implications for pathophysiology

Objectives: Leptin alters pancreatic exocrine and beta-cell secretion in animal studies. We hypothesized that leptin might be important in the pathogenesis of idiopathic chronic pancreatitis (ICP) and/or the development of diabetes in ICP. Methods: Fifty patients with ICP (25 with diabetes, 25 without diabetes) and 25 healthy controls were included in a prospective, case-control study. Fasting plasma leptin concentration was measured by enzyme-linked immunosorbent assay. Exocrine and endocrine pancreatic functions were assessed by fecal chymotrypsin and serum C-peptide, respectively. Anthropometric parameters and body fat mass (FM) were measured. Results: Patients with ICP (mean age, 30 years; 33 men) had significantly lower body mass index (19.5+/-2.6 kg/m(2)) and FM (10.6+/-4.2 kg) as compared with controls (body mass index, 21.7+/-4.1 kg/m(2); FM, 19.0+/-16.6 kg; P<0.01). Fecal chymotrypsin (median, 5.2 [range, 0.3-42.6] U/kg) and C-peptide (median, 1.7 [range, 0.2-9.5] ng/mL) were significantly lower in patients than in controls (12.9 [range, 2.5-33.0] U/kg and 3.5 [range, 0.3-10.3] ng/mL; P<0.01). Plasma leptin concentration was slightly lower but statistically insignificant in patients with ICP (median, 4.0 [range, 2.0-62.5] ng/mL) as compared with controls (median, 5.0 [range, 2.0-63.0] ng/mL). Patients with and those without diabetes were also comparable with regard to their leptin concentration, pancreatic functions, and anthropometric parameters. Conclusions: Leptin does not seem to have a pathophysiological role in either ICP or the development of diabetes in ICP.