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Chen, W.S., Peng, X.D., Wang, Y., Xu, P.Z., Chen, M.L., Luo, Y., Jeon, S.M., Coleman, K., Haschek, W.M., Bass, J., et al. (2009) Leptin Deficiency and Beta-Cell Dysfunction Underlie Type 2 Diabetes in Compound AKT Knockout Mice. Molecular and Cellular Biology, 29, 3151-3162. http://dx.doi.org/10.1128/MCB.01792-08

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• TITLE: Hyperglycemia Induced Changes in Vascular AKT3 May Inhibit Pressure-Induced Apoptosis in the Rat Inferior Venae Cavae

  AUTHORS: Kevin M. Rice, Ravi Kumar Arvapalli, Eric R. Blough

  KEYWORDS: Diabetes, Zucker Rat, Inferior Venae Cavae, AKT3

  JOURNAL NAME: Open Journal of Endocrine and Metabolic Diseases, Vol.5 No.4, April 23, 2015

  ABSTRACT: Background: Vein graft failure after bypass surgery is greatly increase in patients with diabetes mellitus. The cellular mechanisms underlying the cause of this failure are largely unexplored. Protein kinase B/AKT is a mechanically sensitive regulator of cellular growth and apoptosis. Herein we examine whether diabetes affects the regulation of AKT in response to increased venous loading. Methods: Inferior venae cavae (IVC) from the non-diabetic lean (LNZ) and the diabetic obesesyndrome X Zucker(OSXZ) rats were isolated and incubated ex vivo under basal or pressurized conditions (120 mmHg). Protein expression, basal activation and the ability of increased pressure to activate AKT3 and apoptosis-related signaling were evaluated by immunoblot analysis. Results: Compared to that seen in the non-diabetic lean animals, increased venous pressure in the OSXZ rats was not characterized by increases in APAF-1 concentration, XIAP proteolysis, AIF cleavage, or Bad phosphorylation. This evidence of decreased apoptotic signaling was associated with increased basal p-AKT3 levels (+136% ± 13% P