ISSN 1470-3947 (print) | ISSN 1479-6848 (online)

Endocrine Abstracts (2008) 16 P568

Relationship between obesity, IL-17 and IL-23 and insulin resistance

Mirjana Sumarac-Dumanovic1, Dragan Micic1, Maja Simic1, Danica Stamenkovic-Pejkovic1, Darko Stevanovic2, Jagoda Jorga4, Goran Cvijovic1, Svetlana Zoric1 & Vladimir Trajkovic3


1Institute Of Endocrinology, Belgrade, Serbia; 2Institute of Physiology, Belgrade, Serbia; 3Insitute of Microbiology and Immunology, Belgrade, Serbia; 4Insitute of Nutrition, Belgrade, Serbia.


In most obese patients, obesity is associated with a low-grade inflammation of white adipose tissue resulting from chronic activation of the innate immune system and which can subsequently lead to insulin resistance, impaired glucose tolerance and even diabetes. It is still not clear role of acquired immune response in obesity and related comorbidites such as asthma, cancer or autoimmune diseases. The aim of our study was to compare level s of IL-17 and IL23 in sever obese women with nonobese healthy women as well as to investigate relationship between these interleukins with insulin sensitivity in same persons. In that order, thirty obese women (BMI=35.59±0.83 kg/m2, age=35.53±1.59 yrs) with normal fasting glucose and 15 healthy control women (BMI=20.43±0.66 kg/m2, age=27.87±0.77 years) were included in the study. In each of the investigated subjects, following parameters were measured: IL-17, IL-23, fasting glucose and fasting insulin, HOMA-IR as marker of insulin sensitivity. There was significant difference in circulating levels of IL-17 between obese and nonobese women (16.16±1.13 vs 9.42±1.16, P<0.05) as well as in IL-23 (9.35±1.87 vs 2.10±1.33, P<0.05). HOMA-IR was lower in control women but difference was not statistically significant (4.05±0.44 vs 2.95±0.48, P>0.05).There was significant correlation between BMI and IL-17 (r=0.483, P<0.05) as well as BMI and HOMA-IR (r=0.415, P<0.05). In conclusion, it can be considered that obesity corresponds to a sub-clinical inflammatory condition that promotes the production of pro-inflammatory factors primary involved in acquired immune response but further investigations are necessary to elucidate these interrelationship.

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