Attenuation Of Insulin Resistance, Metabolic Syndrome And Hepatic Oxidative Stress By Resveratrol In Fructose Fed Rats

592 words - 3 pages

Diabetes mellitus comprises a group of metabolic disorders and most challenging health problems in the 21st century. Apart from the mortality associated with myocardial infarction, diabetic patients have almost twice the rate of mortality because of congestive heart failure than nondiabetic humans (Stone et al., 1989). Both hyperglycemia and insulin resistance can increase the risk of cardiovascular complications and defects specific to diabetic myocardium accounts for more than 80% deaths among diabetics (Amos et al., 1997). The alteration of cardiac muscle in diabetes has led to the recognition of a new cardiac disease termed 'diabetic cardiomyopathy' (DCM) (Kannel et al., 1974). Several etiological factors like hyperglycemia, metabolic abnormalities and redox imbalance (oxidative stress) may affect the diabetic myocardium. Overwhelming effect of all of them leads to cardiac abnormalities including myocardial hypertrophy, impairment of contractile proteins, accumulation ...view middle of the document...

NFkB, one of the transcription factors, is activated during oxidative stress (Kratsovnik et al., 2005). Nuclear factor-kappa B (NFkB) is a pleiotropic transcription factor associated to the regulation of many heart diseases (Gordon, et al., 2011). Oxidative stress causes translocation of NFkB to the nucleus and transcript several deleterious genes (Won et al., 2006). However, to achieve NFkB activation it has to undergo multiple post translational modifications including acetylation, phosphorylation, ubiquitinylation and oxidation (Huang et al., 2010). Acetylation is a small post translational modification that adds up an acetyl group to the lysine residues of proteins. Acetylation plays a prominent role in regulating the nuclear action of NFkB (Chen et al., 2005). Acetylation of discrete lysine residues in Rel A, a subunit of NFkB modulates distinct functions of NFkB, including transcriptional activation, DNA binding and assembly with its inhibitor IkBα (Chen et al., 2005). Acetylation of lysine at 310 and some lesser extent to lysine at 221 residue play key role to show overall transcriptional activity of NFkB (Chen et al., 2002). Similarly acetylation of histone (H3) is also responsible for NFkB activation.
Increased NFkB activity through acetylation is controlled by a feedback mechanism, i.e. deacetylation of NFkB. Histone deacetylases (HDAC’s) are the group of enzymes that cause deacetylation of histone proteins. Unlike the other class I and II HDACs, sirtuins, a class III HDACs require nicotinamide adenosine dinucleotide (NAD) as a cofactor, to show its deacetylation action on both histone and non-histone proteins (Buck et al, 2004). Deacetylation of p65 subunit of NFkB by sirtuins i.e. SIRT-1 and SIRT-2 was reported by different investigators (Yeung et al., 2004 and Rothgiesser et al., 2010). Deacetylation of p65 might be an important mechanism by which NFkB activity can be reversed. Different activators of SIRT-1 and SIRT-2 could be useful to attenuate diabetic cardiomyopathy by inhibiting NFkB activity. In the present study, we have administered resveratrol a well-known activator of SIRT-1 to fructose fed diabetic rats for 8 weeks to demonstrate if resveratrol can reduce NFkB activation and ameliorate cardiac oxidative stress through deacetylation of NFkB.

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