Pro-inflammatory cytokine-induced lipolysis after an episode of acute pancreatitis.

Context: Pro-inflammatory cytokine-stimulated lipolysis is one of the mechanisms underlying the pathogenesis of type 2 diabetes. However, whether it plays a role in the pathogenesis of post-pancreatitis diabetes mellitus (PPDM) remains unknown.
Objective: To investigate the associations between markers of lipid metabolism and pro-inflammatory cytokines in individuals after acute pancreatitis (AP) in general, and in individuals with abnormal glucose metabolism (AGM) following AP in particular.
Methods: Fasting blood samples were collected to measure markers of lipid metabolism (apolipoprotein-B, cholesterol, free fatty acids (FFA), glycerol, high and low-density lipoproteins, triglycerides) and cytokines (interleukin (IL)-6, monocyte chemoattractant protein (MCP)-1, and tumour necrosis factor (TNF) α). Linear regression analysis was conducted. Four statistical models were used to adjust for patient- and pancreatitis-related characteristics.
Results: A total of 83 patients were recruited. IL-6 was significantly associated with glycerol in all models (p < .05), with glycerol levels increasing by 106% in individuals with AGM after AP (p <.05) compared to a 30.3% increase in individuals with normal glucose metabolism (NGM) (p >.05). TNFα was significantly associated with FFA (p = .015) in individuals with AGM after AP in the most adjusted model, with FFA levels increasing by 314% in these individuals compared to a 162% decrease in individuals with NGM after AP (p >.05).
Conclusions: Lipolysis appears to be an important pathogenetic mechanism in glucose derangements after diseases of the exocrine pancreas. IL-6 and TNFα are the driving forces behind lipolysis in individuals with AGM after AP. Modulation of lipolysis may be a promising therapeutic modality.