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Regulation Of Diabetic Cardiomyopathy By Caloric Restriction Is Mediated By Intracellular Signaling Pathways Involving 'Sirt1 And Pgc-1alpha', Maayan Waldman, Keren Cohen, Dor Yadin, Vadim Nudelman, Michal Laniado-Schwartzman, Nader G. Abraham, Edith Hochhauser
Regulation Of Diabetic Cardiomyopathy By Caloric Restriction Is Mediated By Intracellular Signaling Pathways Involving 'Sirt1 And Pgc-1alpha', Maayan Waldman, Keren Cohen, Dor Yadin, Vadim Nudelman, Michal Laniado-Schwartzman, Nader G. Abraham, Edith Hochhauser
Nader G. Abraham
BACKGROUND: Metabolic disorders such as obesity, insulin resistance and type 2 diabetes mellitus (DM2) are all linked to diabetic cardiomyopathy that lead to heart failure. Cardiomyopathy is initially characterized by cardiomyocyte hypertrophy, followed by mitochondrial dysfunction and fibrosis, both of which are aggravated by angiotensin. Caloric restriction (CR) is cardioprotective in animal models of heart disease through its catabolic activity and activation of the expression of adaptive genes. We hypothesized that in the diabetic heart; this effect involves antioxidant defenses and is mediated by SIRT1 and the transcriptional coactivator PGC-1alpha (Peroxisome proliferator-activated receptor-gamma coactivator). METHODS: Obese Leptin resistant (db/db) mice …
Development Of Nash In Obese Mice Is Confounded By Adipose Tissue Increase In Inflammatory Nov And Oxidative Stress, David Sacerdoti, Shailendra P. Singh, Joseph Schragenheim, Lars Bellner, Aliza Meissner, Ilana Grant, Nader G. Abraham
Development Of Nash In Obese Mice Is Confounded By Adipose Tissue Increase In Inflammatory Nov And Oxidative Stress, David Sacerdoti, Shailendra P. Singh, Joseph Schragenheim, Lars Bellner, Aliza Meissner, Ilana Grant, Nader G. Abraham
Nader G. Abraham
Aim: Nonalcoholic steatohepatitis (NASH) is the consequence of insulin resistance, fatty acid accumulation, oxidative stress, and lipotoxicity. We hypothesize that an increase in the inflammatory adipokine NOV decreases antioxidant Heme Oxygenase 1 (HO-1) levels in adipose and hepatic tissue, resulting in the development of NASH in obese mice. Methods: Mice were fed a high fat diet (HFD) and obese animals were administered an HO-1 inducer with or without an inhibitor of HO activity to examine levels of adipose-derived NOV and possible links between increased synthesis of inflammatory adipokines and hepatic pathology. Results: NASH mice displayed decreased HO-1 levels and HO …