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BioMed Research International
Volume 2013, Article ID 617569, 19 pages
Research Article

Obesity, Insulin Resistance, and Metabolic Syndrome: A Study in WNIN/Ob Rats from a Pancreatic Perspective

1Department of Biochemistry/Stem Cell Research, National Institute of Nutrition, Indian Council of Medical Research, Jamai-Osmania (P.O), Hyderabad, Andhra Pradesh 500007, India
2Laboratory 12, National Center for Cell Sciences, NCCS Complex, Pune University Campus, Ganeshkhind, Pune, Maharashtra 411007, India
3Division of Community Studies, National Institute of Nutrition, Hyderabad, Andhra Pradesh 500007, India
4Manipal Institute of Regenerative Medicine, GKVK Post, Bellary Road, Allalasandra, Yelahanka, Bangalore, Karnataka 560065, India
5National Center for Laboratory Animal Sciences, National Institute of Nutrition, Hyderabad, Andhra Pradesh 500007, India

Received 16 July 2013; Revised 9 November 2013; Accepted 11 November 2013

Academic Editor: Oreste Gualillo

Copyright © 2013 Vijayalakshmi Venkatesan et al. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.


Alterations in pancreatic milieu to adapt to physiological shifts occurring in conditions of obesity and metabolic syndrome (MS) have been documented, though mechanisms leading to such a state have remained elusive so far. The data presented here tries to look at the gravity of metabolic insult during the early and prolonged phases of obesity/insulin resistance (IR) depicted in WNIN/Ob strain of rats—an obese euglycemic mutant rat model developed indigenously at our institute which is highly vulnerable for a variety of degenerative diseases. The present results in situ show the participation of several confounding factors in the pancreatic milieu that collectively coprecipitates for a state of profound inflammation in the pancreas (among Mutant compared to Lean/Control) which gets worsened with age. These include hypertrophy, macrophage infiltration (CD11b/TNF /IL6), apoptosis, -cell vacuolation, hyperinsulinemia (HI), and stress markers (RL-77/HSP104/TBARS) all of which correlated well with indices for obesity (2-3 fold), IR (1.5-3 fold), and HI (2-3 fold). Further, supportive data was also obtained from in vitro studies using islet cell cultures amongst phenotypes. Taken together, these results advocate that inflammation was the major precipitating factor to cause islet cell dysfunctions (in situ and in vitro) in these Mutant rats compared to their Lean littermates and parental Control.