Poster Topical Area: Dietary Bioactive Components
Location: Hall D
Poster Board Number: 256
Objective: Obesity is a major human health problem and its systemic effects extend to the pancreas. For example, obesity promotes insulin resistance, has a significant negative impact on the course of acute pancreatitis and is associated with an increased risk for developing pancreatic cancer. However, the cellular mechanisms that mediate these responses are incompletely understood. The objective of our study was to identify pancreatic proteins that are differentially expressed in normal mice and mice fed a high fat diet. Moreover, we evaluated the effects of (-)-Epicatechin (EC) supplementation in the regulation of pancreatic protein expression induced by high fat diet.
Methods: Male C57BL/6J mice (5 mice/group) were fed diets containing either 10% total calories from fat (control), 60% total calories from fat (lard) (HFD), or a HFD supplemented with EC (20mg/kg body weight) (HFE). After 15 weeks of dietary intervention, mice were euthanized, pancreata were collected and subjected to a proteomics analysis. Briefly, pancreatic proteins were extracted and subjected to TMT/iTRAQ profiling. Data were analyzed with iPathwayGuide (Impact analysis method).
Results: The proteomics analysis detected the expression of around 2,000 pancreatic proteins. When compared to control, HFD led to 1166 proteins that were differentially expressed. Among multiple biological processes/pathways that were found to be the significantly altered, proteins that regulate pancreatic secretion, such as Carboxyl Ester Lipase, Carboxypeptidase A1 and Protease, Serine 2, and proteins involved in the regulation of reactive oxygen species (ROS) including Glutathione S-Transferase Pi 1, Peroxiredoxin 2 and Voltage Dependent Anion Channel 1, were the most significantly affected by HFD. Interestingly, HFE mitigated, in part, the expression of pancreatic secretion proteins and ROS generating proteins affected by HFD.
Conclusion: Consumption of HFD alters pancreatic protein expression and EC supplementation partly mitigates against the HFD-induced effect. These data provide a valuable resource of candidate proteins and pathways that may be altered in obesity, and suggests the benefit of EC supplementation. Additional studies on mouse pancreas sections are warranted to validate these proteomics data.
University of California, Davis