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Mesenteric and omental depot differences in fat tissue inflammatory markers and signaling from type 2 diabetic (T2D) and normal obese humans
Author(s) -
Ghansah Tomar,
Murr Michel,
Watson James E,
Yoder Sean,
Fleming David,
Nelson Nadine,
Peng Yanhua,
Apostolatos Andre,
Gower Katherine,
Patel Niketa A,
Cooper Denise R
Publication year - 2011
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.25.1_supplement.532.1
Insulin resistance is a manifestation of obesity‐induced diabetes and is characterized by chronic inflammation in the liver and adipose tissue depots. Adipose tissue is a source of pre‐adipocytes that regulate adipogenesis and induce pro‐inflammatory cytokines. Because venous blood flow from the mesenteric and omental fat depots is to the liver, signaling from them may be the link between obesity and T2D. Mesenteric and omental fat from Diabetic Obese (DO) vs. Non‐Diabetic Obese (NDO) humans was processed and stromal vascular fraction (SVF) that consists of adipocyte derived stem cells (SC) and leukocytes (LK) collected. Flow cytometry revealed a difference in percentages of CD34+CD45− (SC) and CD11b+CD45+ (LK) in DO vs. NDO. Mesenteric and omental SVF cells from DO were passaged twice prior to MID induction media. Cells harvested at 0, 2, 4, 6 and 8 days and analyzed by western blot showed differences in pAKT (S473) between mesenteric and omental SC from DO. PKCβII was expressed in both depots. Mesenteric SC expressed Caspase 9a and b but omental DO cells only expressed Caspase 9a. Exonarray confirmed splicing for PKCβII and Caspase 9a/b. There was a significant decrease in SC and LK percentages from DO vs. NDO. Other assays elucidated the differences in inflammatory states between DO and NDO. Results from this study will identify better strategies for treating T2DM and obesity‐related diseases. NIDDK 054393.