Surged Leptin/Ghrelin Secretion Associated With Anorexia Nervosa

Surged Leptin/Ghrelin Secretion Associated With Anorexia Nervosa

Takaya, Junji; Hattori, Yuko; Ishizaki, Yuko; Kaneko, Kazunari

Journal of Pediatric Gastroenterology and Nutrition . 47(5):670-671, November 2008.

Anorexia nervosa is the most common life-threatening condition of all psychiatric disorders. Although physical signs of extracellular volume depletion and plasma volume concentration are often studied in anorexia nervosa, few studies have focused on adipocytokines and glucose balance.

Anorexia nervosa is associated with altered carbohydrate and lipid metabolism, multiple endocrine perturbations, and other dysfunctions. Although studies regarding insulin sensitivity in anorexia nervosa have had rather contradictory results, some have found increased insulin sensitivity , and others have postulated decreased or unchanged insulin sensitivity .

Many experimental and clinical studies have shown that the adipose tissue-derived hormone leptin is a key player in the regulation of food intake and energy balance. In addition to leptin, several other adipose tissue-derived hormones with suggested roles in the regulation of energy metabolism and insulin sensitivity have been discovered recently. Although most studies have focused on changes in endocrine function of adipocytes in obesity, adipose tissue also plays an important role in patients with malnutrition and decreased body fat content: serum leptin levels are severely suppressed in patients with both protein-energy malnutrition and anorexia nervosa.

We hypothesized that impaired ghrelin/leptin secretion in anorexia nervosa may be involved in the pathogenesis of this eating disorder. To examine this hypothesis and to further investigate the role of ghrelin in regulating energy homeostasis, we analyzed serial changes in circulating ghrelin and leptin in a patient with anorexia nervosa and examined a possible correlation of these hormones with nutritional status before and after weight gain

source : Department of Pediatrics, Kansai Medical University, Osaka, Japan and the Mami Mizutani Foundation.

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