Morvarid Kabir, PhD
Research Scientist, Diabetes & Obesity Rsrch Inst
|Assistant Professor, Biomedical Sciences|
There is an abundance of evidence demonstrating the association of obesity, in particular central or intra-abdominal obesity, with a cluster of metabolic disorders, such as insulin resistance, type 2 diabetes, dyslipidemia, hypertension and nonalcoholic steatohepatitis. The research goal of our laboratory is to understand the molecular regulation of adipose tissue from different anatomical depots, and why intra-abdominal obesity is associated with the whole body and hepatic insulin resistance. In our laboratory, we utilize molecular and cellular techniques to examine the interplay between adipose tissue and the liver during insulin resistance and obesity using interventions such as fat feeding and insulin sensitizing drugs such as a selective endocannabinoid receptor antagonist. We are particularly interested in the role of adipose tissue as an endocrine organ, especially the regulation of adiponectin and inflammatory cytokines.
We recently examined longitudinal changes in adipocyte size and distribution in visceral and subcutaneous fat in obesity-induced insulin resistance. We provided direct evidence that large adipocytes and their distribution in the visceral fat depot are critical predictors of insulin resistance.
Current investigations include:
The current major project is focused on separation of different subfamilies of adipocytes (small vs large) and evaluating the biochemical and molecular characteristic of these cells in insulin resistant animal model.
More recently we have begun to investigate in hepatoprotective role of a selective endocannabinoid receptor antagonist. We demonstrated that an increased delivery of adiponectin from visceral fat to the liver acts on its own receptors adiponectin 1 and 2, thereby improving fat oxidation and reducing inflammatory cytokine expression. We are currently interested in studying the liver transcriptome during fat feeding and endocannabinoid receptor antagonist treatment.
- Kabir M, Stefanovski D, Hsu IR, Iyer M, Woolcott OO, Zheng D, Catalano KJ, Chiu JD, Kim SP, Harrison LN, Ionut V, Lottati M, Bergman RN, Richey JM: Large size cells in the visceral adipose depot predict insulin resistance in the canine model. Obesity (Silver Spring), 19(11): 2121-9, 2011
- Kabir M, Catalano KJ, Ananthnarayan S, Kim SP, Van Citters GW, Dea MK, Bergman RN: Molecular evidence supporting the portal theory: a causative link between visceral adiposity and hepatic insulin resistance. Am. J. Physiol. Endocrinol. Metab., 288(2): E454-61, 2004
- Richey JM, Woolcott OO, Stefanovski D, Harrison LN, Zheng D, Lottati M, Hsu IR, Kim SP, Kabir M, Catalano KJ, Chiu JD, Ionut V, Kolka C, Mooradian V, Bergman RN: Rimonabant prevents additional accumulation of visceral and subcutaneous fat during high-fat feeding in dogs. Am. J. Physiol. Endocrinol. Metab., 296(6): E1311-8, 2009
- van Citters GW, Kabir M, Kim SP, Mittelman SD, Dea MK, Brubaker PL, Bergman RN: Elevated glucagon-like peptide-1-(7-36)-amide, but not glucose, associated with hyperinsulinemic compensation for fat feeding. J. Clin. Endocrinol. Metab., 87(11): 5191-8, 2002
- Kabir M, Skurnik G, Naour N, Pechtner V, Meugnier E, Rome S, Quignard-Boulangé A, Vidal H, Slama G, Clément K, Guerre-Millo M, Rizkalla SW: Treatment for 2 mo with n 3 polyunsaturated fatty acids reduces adiposity and some atherogenic factors but does not improve insulin sensitivity in women with type 2 diabetes: a randomized controlled study. Am. J. Clin. Nutr., 86(6): 1670-9, 2007
- Kabir M, Oppert JM, Vidal H, Bruzzo F, Fiquet C, Wursch P, Slama G, Rizkalla SW: Four-week low-glycemic index breakfast with a modest amount of soluble fibers in type 2 diabetic men. Metab. Clin. Exp., 51(7): 819-26, 2002