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Pathogenesis And Pathophysiology Of Ventromedial Hypothalamic (VMH) Lesion-induced Obese Rats-comparison With Other Hypothalamic Induced Obese Rats | 14872
ISSN: 2165-7904

Journal of Obesity & Weight Loss Therapy
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Pathogenesis and pathophysiology of ventromedial hypothalamic (VMH) lesion-induced obese rats-comparison with other hypothalamic induced obese rats

2nd International Conference and Exhibition on Obesity & Weight Management

Shuji Inoue

Accepted Abstracts: J Obes Weight Loss Ther

DOI: 10.4172/2165-7904.S1.012

Abstract
We have been investigating the pathogenesis and pathophysiology of ventromedial hypothalamic (VMH) lesion-induced obese animals, a representative model of hypothalamic obesity, for 40 years and recently, we discovered a new type of hypothalamic obesity induced by bilateral destructions of the area between bilateral VMHs which is corresponding to the area between arcuate nuclei (ARN) and paraventricular nuclei (PVN) in the hypothalamus (referred to as Between-VMHs; B-VMHs) in rats. The talk deals with comparison of pathogenesis and pathophysiology between VMH lesions-induced hypothalamic obesity and other hypothalamic lesion-induced obesity including B-VMHs lesions-induced obesity. VMH lesioned rats show more hyperphagia and more obesity, and higher levels of serum insulin and leptin than B-VMHs lesioned rats. Disconnection of α-MSH pathway by determined histochemical neural fiber staining in ARC-PVH axis for food intake regulatory system contributes to hyperphagia and obesity in B-VMHs lesioned rats, but the origin of hyperphagia in VMH lesioned rats is more complex. Basal and postabsorptive hyperinsulinemia induced by autonomic derangement (vagal hyperactivity with sympathetic hypoactivity) is the primary cause of VMH lesions-induced obesity. On the other hand, in other hypothalamic obesity (destruction of PVM, ARC, Between VMH, and LH) including B-VMHs lesion-induced obesity, hyperphagia with postabsorptive hyperinsulinemia is the primary cause of obesity. Cell proliferation in visceral organs (stomach, small intestine, liver and pancreas) by histochemical stainings and electron microscopic examinations are observed in VMH lesioned rats, which is due to vagal hyperactivity in autonomic derangements by VMH lesions, in contrast, no cell proliferation in the visceral organs are observed in B-VMHs lesioned rats due to a lack of autonomic derangements, similar no cell proliferation may appear in other hypothalamic lesioned rats in a similar mechanism. More recently, we have discovered that adiponectin production and release are increased, which lead to elevated serum adiponectin in VMH lesions-induced obese animals inspite of enlarged adipocytes and increased body fat also due to vegal hyperactivity.
Biography
Shuji Inoue has completed his M.D. at the age of 26 years old and got Ph.D. from University of Tokyo, School of Medicine. He has been working for investigating the pathogenesis and pathophysiology of hypothalamic obesity for 40years. He is the vice-president and dean of Faculty of Health Care, Kiryu University, Japan. He has published more than 200 English papers in reputed journals and is now serving as Editor-in-Chief of Obesity Research & Clinical Practice.
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