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

• Published in: Human physiology Vol. 44; no. 4; pp. 474 - 480
• Main Authors: Vulf (Vasilenko), M. A., Skuratovskaia, D. A., Kirienkova, E. V., Zatolokin, P. A., Mironyuk, N. I., Litvinova, L. S.
• Format: Journal Article
• Language: English
• Published: Moscow Pleiades Publishing 01-07-2018; Springer Nature B.V
• Subjects: Adipose tissue; Biomedical and Life Sciences; Biomedicine; Carbohydrate metabolism; Gene expression; Human Physiology; Inflammation; Insulin; Insulin resistance; Leptin; Life Sciences; Mesentery; Metabolic disorders; Metabolism; Obesity; Small intestine; Tumor necrosis factor-α; mesenteric adipose tissue; enzyme immunoassay; type 2 diabetes mellitus (DM); adipokines; PCR; obesity
• ISSN: 0362-1197; 1608-3164
• DOI: 10.1134/S036211971804014X

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
,
SERPINA
12,
RARRES
2, and
TNF
α genes encoding leptin, vaspin, chemerin, and
TNF
α 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.