Niacin bound chromium treatment induces myocardial Glut-4 translocation and caveolar interaction via Akt, AMPK and eNOS phosphorylation in streptozotocin induced diabetic rats after ischemia-reperfusion injury

Suresh Varma Penumathsa, Mahesh Thirunavukkarasu, Samson Mathews Samuel, Lijun Zhan, Gautam Maulik, Manashi Bagchi, Debasis Bagchi, Nilanjana Maulik

Research output: Contribution to journalArticle

43 Citations (Scopus)

Abstract

Diabetes, one of the major risk factors of metabolic syndrome culminates in the development of Ischemic Heart Disease (IHD). Refined diets that lack micronutrients, mainly trivalent chromium (Cr3+) have been identified as the contributor in the rising incidence of diabetes. We investigated the effect of niacin-bound chromium (NBC) during ischemia/reperfusion (IR) injury in streptozotocin induced diabetic rats. Rats were randomized into: Control (Con); Diabetic (Dia) and Diabetic rats fed with NBC (Dia + NBC). After 30 days of treatment, the isolated hearts were subjected to 30 min of global ischemia followed by 2 h of reperfusion. NBC treatment demonstrated significant increase in left ventricular functions and significant reduction in infarct size and cardiomyocyte apoptosis in Dia + NBC compared with Dia. Increased Glut-4 translocation to the lipid raft fractions was also observed in Dia + NBC compared to Dia. Reduced Cav-1 and increased Cav-3 expression along with phosphorylation of Akt, eNOS and AMPK might have resulted in increased Glut-4 translocation in Dia + NBC. Our results indicate that the cardioprotective effect of NBC is mediated by increased activation of AMPK, Akt and eNOS resulting in increased translocation of Glut-4 to the caveolar raft fractions thereby alleviating the effects of IR injury in the diabetic myocardium.

Original languageEnglish
Pages (from-to)39-48
Number of pages10
JournalBiochimica et Biophysica Acta - Molecular Basis of Disease
Volume1792
Issue number1
DOIs
Publication statusPublished - 1 Jan 2009
Externally publishedYes

Fingerprint

AMP-Activated Protein Kinases
Niacin
Chromium
Streptozocin
Reperfusion Injury
Phosphorylation
Therapeutics
Micronutrients
Left Ventricular Function
Cardiac Myocytes
Reperfusion
Myocardial Ischemia
Myocardium
Ischemia
Apoptosis
Diet
Lipids
Incidence

Keywords

  • Chromium
  • Diabetes
  • eNOS
  • Glut-4
  • Heart
  • Ischemia reperfusion

ASJC Scopus subject areas

  • Molecular Biology
  • Molecular Medicine

Cite this

Niacin bound chromium treatment induces myocardial Glut-4 translocation and caveolar interaction via Akt, AMPK and eNOS phosphorylation in streptozotocin induced diabetic rats after ischemia-reperfusion injury. / Penumathsa, Suresh Varma; Thirunavukkarasu, Mahesh; Mathews Samuel, Samson; Zhan, Lijun; Maulik, Gautam; Bagchi, Manashi; Bagchi, Debasis; Maulik, Nilanjana.

In: Biochimica et Biophysica Acta - Molecular Basis of Disease, Vol. 1792, No. 1, 01.01.2009, p. 39-48.

Research output: Contribution to journalArticle

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abstract = "Diabetes, one of the major risk factors of metabolic syndrome culminates in the development of Ischemic Heart Disease (IHD). Refined diets that lack micronutrients, mainly trivalent chromium (Cr3+) have been identified as the contributor in the rising incidence of diabetes. We investigated the effect of niacin-bound chromium (NBC) during ischemia/reperfusion (IR) injury in streptozotocin induced diabetic rats. Rats were randomized into: Control (Con); Diabetic (Dia) and Diabetic rats fed with NBC (Dia + NBC). After 30 days of treatment, the isolated hearts were subjected to 30 min of global ischemia followed by 2 h of reperfusion. NBC treatment demonstrated significant increase in left ventricular functions and significant reduction in infarct size and cardiomyocyte apoptosis in Dia + NBC compared with Dia. Increased Glut-4 translocation to the lipid raft fractions was also observed in Dia + NBC compared to Dia. Reduced Cav-1 and increased Cav-3 expression along with phosphorylation of Akt, eNOS and AMPK might have resulted in increased Glut-4 translocation in Dia + NBC. Our results indicate that the cardioprotective effect of NBC is mediated by increased activation of AMPK, Akt and eNOS resulting in increased translocation of Glut-4 to the caveolar raft fractions thereby alleviating the effects of IR injury in the diabetic myocardium.",
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