Vagal hyperactivity due to ventromedial hypothalamic (VMH) lesions increases adiponectin production and release

  1. Shuji Inoue1
  1. 1 Faculty of Health Science, Kiryu University
  2. 2 Health Promotion and Exercise Program, National Institute of Health and Nutrition
  3. 3 International University of Health and Welfare Hospital
  4. 4 Department of Diabetes and Metabolic Diseases, Graduate School of Medicine, University of Tokyo
  5. 5 Department of Anatomy, Showa University School of Medicine
  6. 6 Department of Clinical Dietetics and Human Nutrition, Josai University
  7. 7 Gunma University Graduate School of Medicine
  1. Corresponding Author: Dr. Shuji Inoue, E-mail: ishuji{at}kiryu-u.ac.jp

Abstract

In obese humans and animals, adiponectin production and release in adipose tissue are downregulated by feedback inhibition, resulting in decreased serum adiponectin. We investigated adiponectin production and release in ventromedial hypothalamic (VMH)-lesioned animals. VMH-lesioned mice showed significant increases in food intake and body weight gain, with hyperinsulinemia and hyperleptinemia at 1 and 4 weeks after VMH-lesioning. Serum adiponectin was elevated in VMH-lesioned mice at 1 and 4 weeks, despite adipocyte hypertrophy in subcutaneous and visceral adipose tissues and increased body fat. Adiponectin production and mRNA also increased in both adipose tissues in VMH-lesioned mice at 1 week. These results were replicated in VMH-lesioned rats at 1 week. Daily atropine administration for 5 days or subdiaphragmatic vagotomy completely reversed the body weight gain and eliminated the increased adiponectin production and release in these rats, with reversal to a normal serum adiponectin level. Activated parasympathetic nerve by carbachol infusion for 5 days in rats increased serum adiponectin, with increased adiponectin production in visceral and subcutaneous adipose tissues without changes of body weight. These results demonstrate that activation of the parasympathetic nerve by VMH lesions stimulates production of adiponectin in visceral and subcutaneous adipose tissues and adiponectin release, resulting in elevated serum adiponectin.

  • Received April 22, 2013.
  • Accepted January 24, 2014.

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