Contribution of Adipokine Gene Expression in Mesenteric Adipose Tissue to the Pathogenesis of Insulin Resistance in Obese Patients


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Abstract

Mesenteric adipose tissue, being a component of visceral adipose tissue, has a high lipolytic activity. Excessive accumulation of visceral adipose tissue increases the risk of metabolic disorders leading to severe consequences. Therefore, the aim of the presented study was to estimate the production of adipokine and proinflammatory molecules by the adipose tissue of small intestine mesentery evaluating its contribution to the formation of insulin resistance in obesity. The role of the activity of LEP, SERPINA12, RARRES2, and TNFα genes encoding leptin, vaspin, chemerin, and TNFα in adipose tissue of small intestinal mesentery in patients with abdominal obesity with a different state of carbohydrate metabolism was studied. The changes in serum/plasma content of the examined mediators that we detected are closely associated with their production in the adipose tissue of small intestinal mesentery. The revealed interrelations between the production of mediators (adipokines, proinflammatory molecules) studied with the parameters of carbohydrate metabolism indicate an important role of mesenteric adipose tissue in the formation of insulin resistance in obesity.

About the authors

M. A. Vulf (Vasilenko)

Baltic Federal University

Author for correspondence.
Email: mary-jean@yandex.ru
Russian Federation, Kaliningrad

D. A. Skuratovskaia

Baltic Federal University

Email: mary-jean@yandex.ru
Russian Federation, Kaliningrad

E. V. Kirienkova

Baltic Federal University

Email: mary-jean@yandex.ru
Russian Federation, Kaliningrad

P. A. Zatolokin

Baltic Federal University; Regional Clinical Hospital of the Kaliningrad region

Email: mary-jean@yandex.ru
Russian Federation, Kaliningrad; Kaliningrad

N. I. Mironyuk

Regional Clinical Hospital of the Kaliningrad region

Email: mary-jean@yandex.ru
Russian Federation, Kaliningrad

L. S. Litvinova

Baltic Federal University

Email: mary-jean@yandex.ru
Russian Federation, Kaliningrad

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