Adenovirus-mediated leptin expression normalises hypertension associated with diet-induced obesity

W. Zhang, S. Telemaque, R. A. Augustyniak, P. Anderson, G. D. Thomas, J. An, Z. Wang, C. B. Newgard, R. G. Victor

Research output: Contribution to journalArticlepeer-review

6 Scopus citations

Abstract

In our previous study, moderate increases in plasma leptin levels achieved via administration of recombinant adenovirus containing the rat leptin cDNA were shown to correct the abnormal metabolic profile in rats with diet-induced obesity, suggesting that these animals had developed resistance to the metabolic effects of leptin, which could be reversed by leptin gene over-expression. However, the effect of this therapeutic strategy on blood pressure was not investigated. The present study aimed to determine whether a moderate increase of endogenous plasma leptin levels affected arterial blood pressure in rats with diet-induced obesity and hypertension. The major finding from the present study was that the natural rise in plasma leptin with weight-gain is insufficient to counterbalance high blood pressure associated with obesity, additional increases of circulating leptin levels with adenoviral leptin gene therapy led to normalisation of blood pressure in high-fat diet-induced obese and hypertensive rats. Mechanistically, the reduction of blood pressure by leptin in obese rats was likely independent of α-adrenergic and acetylcholinergic receptor mediation. This is the first study to demonstrate that further increases in circulating leptin levels by leptin gene transfer during obesity could reduce blood pressure.

Original languageEnglish (US)
Pages (from-to)175-180
Number of pages6
JournalJournal of Neuroendocrinology
Volume22
Issue number3
DOIs
StatePublished - Mar 2010

Keywords

  • Arterial blood pressure
  • Gene therapy
  • High-fat diet
  • Hypertension
  • Leptin
  • Metabolic syndrome
  • Obesity
  • Recombinant adenovirus

ASJC Scopus subject areas

  • Endocrinology, Diabetes and Metabolism
  • Endocrinology
  • Endocrine and Autonomic Systems
  • Cellular and Molecular Neuroscience

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