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Inhibition of HO‐Adiponectin‐Dependent Pathways Contributes to Metabolic Syndrome like Phenotype in Spontaneously Hypertensive Rats on a High Fat Diet
Author(s) -
Puri Nitin,
Sodhi Komal,
Abraham Nader
Publication year - 2012
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.26.1_supplement.819.48
Subject(s) - medicine , endocrinology , copp , adiponectin , enos , ampk , metabolic syndrome , heme oxygenase , insulin resistance , chemistry , obesity , protein kinase a , heme , nitric oxide , kinase , biochemistry , nitric oxide synthase , enzyme
We examined the effects of a high fat (HF) diet on renal and cardiac function in hypertensive animals (SHR) with preexisting systemic pathologies. That upregulation of heme oxygenase (HO) abates cardiovascular abnormalities in SHR was the basis for examining the status of this system, and effects of its induction, in SHRs on HF diet. SHRs were fed lean (L, 11% fat) or HF diet (58% fat) for 8 weeks with and without weekly injections of HO inducer, cobalt protoporphyrin (CoPP, 5mg/kg). HF diet induced a metabolic syndrome‐like phenotype in SHRs with increased (p<0.05) BP, body weight, blood glucose and lipids. Renal and cardiac function deteriorated in these animals including, increased coronary resistance (p<0.05), end diastolic pressure (p<0.05) with reduced left ventricular developed pressure (p<0.05) during ischemia, in cardiac langendorff preparations. These pathophysiological alterations were accompanied by reduced tissue expression (p<0.05) of HO‐1, adiponectin, p‐eNOS and p‐AMPK; whose restoration by CoPP (p<0.05), along with recovery of cardio‐renal homeostasis (p<0.05), implicates the role of inhibition of HO‐adiponectin axis during the development of metabolic syndrome. Thus HF diet exacerbated cardiovascular‐renal dysfunction in SHR which is amenable to rescue by increases in HO‐1‐ and adiponectin‐dependent pathways, including activation of tissue p‐AKT, p‐AMPK and p‐eNOS. NIH‐ DK056601