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  • Title: Increased serum resistin concentration in patients with chronic pancreatitis: possible cause of pancreatic fibrosis.
    Author: Adrych K, Smoczynski M, Sledzinski T, Dettlaff-Pokora A, Goyke E, Swierczynski J.
    Journal: J Clin Gastroenterol; 2009 Jan; 43(1):63-8. PubMed ID: 18827713.
    Abstract:
    BACKGROUND: Resistin is an adipokine, which displays proinflammatory properties. Thus, it is likely that resistin can influence the course of chronic pancreatitis, and/or that chronic pancreatitis may affect the serum resistin concentration. GOALS: The aim of the present study was to determine the serum resistin concentration in patients with chronic pancreatitis and to analyze the relationship between serum resistin concentration and serum concentrations of leptin (proinflammatory adipokine) and adiponectin (anti-inflammatory adipokine). STUDY: A total of 23 male, nondiabetic patients with chronic pancreatitis of alcoholic origin and 16 healthy subjects were examined. Fasting blood samples were collected from patients in both groups. Serum resistin concentration was assayed by enzyme-linked immunosorbent assay. Serum adiponectin, leptin, and insulin concentrations were determined by radioimmunoassay. RESULTS: Serum resistin concentration was significantly higher in patients with chronic pancreatitis as compared with control subjects. In contrast, patients with chronic pancreatitis had lower serum leptin and insulin concentrations than healthy subjects. There were no statistically significant differences in serum adiponectin concentration between patients with pancreatitis and healthy subjects. CONCLUSIONS: The results presented in this paper indicate that chronic pancreatitis in human is associated with the increase in serum resistin concentration and with the decrease in serum leptin and insulin concentrations. It can be supposed that resistin, by stimulation of tumor necrosis factor-alpha synthesis in blood mononuclear cells and in macrophages, increases the concentration of tumor necrosis factor-alpha, which in turn activates stellate cells. Activated stellate cells can produce collagen, eventually resulting in the development of pancreatic fibrosis.
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