Interleukin-15 treatment improves glucose homeostasis and insulin sensitivity in obese mice

被引:58
作者
Barra, N. G. [1 ,2 ]
Chew, M. V. [1 ,2 ]
Holloway, A. C. [3 ]
Ashkar, A. A. [1 ,2 ]
机构
[1] McMaster Univ, Ctr Gene Therapeut, Dept Pathol & Mol Med, Hamilton, ON L8S 4K1, Canada
[2] McMaster Univ, Inst Infect Dis Res, Hamilton, ON L8S 4K1, Canada
[3] McMaster Univ, Dept Obstet & Gynecol, Hamilton, ON L8S 4K1, Canada
基金
加拿大健康研究院;
关键词
antiobesity drug; diabetes complications; experimental pharmacology; glucose metabolism; insulin resistance; ADIPOSE-TISSUE; RESISTANCE; ISLETS; IL-15; CELLS;
D O I
10.1111/j.1463-1326.2011.01495.x
中图分类号
R5 [内科学];
学科分类号
1002 ; 100201 ;
摘要
The prevalence of metabolic diseases associated with obesity, such as type 2 diabetes, continues to rise along with obesity rates. Recently, obesity has been described as an inflammatory condition, suggesting a link between the dysregulation in proinflammatory cytokine production and the aetiology of these metabolic diseases. While known as an immunomodulatory cytokine, Interleukin-15 (IL-15) has been shown to have effects on adipose tissue and induce weight loss in diet-induced obese mice. As weight loss improves glucose homeostasis, the goal of this study was to determine whether IL-15 impacts glucose regulation in a mouse model of diet-induced obesity. Our data demonstrate that IL-15 treatment significantly improves insulin sensitivity and glucose and insulin responses to an oral glucose challenge compared to obese counterparts and/or lean controls. These results show that IL-15 may be a novel therapeutic target for the treatment of obesity and its associated abnormal glucose regulation.
引用
收藏
页码:190 / 193
页数:4
相关论文
共 12 条
[11]   Greater Weight Loss and Hormonal Changes After 6 Months Diet With Carbohydrates Eaten Mostly at Dinner [J].
Sofer, Sigal ;
Eliraz, Abraham ;
Kaplan, Sara ;
Voet, Hillary ;
Fink, Gershon ;
Kima, Tzadok ;
Madar, Zecharia .
OBESITY, 2011, 19 (10) :2006-2014
[12]   Effects of interleukin-15 on suppression of rat pancreatic islets in vitro induced by proinflammatory cytokines [J].
Wallström, J ;
Andersson, AK ;
Sandler, S .
IMMUNOLOGY LETTERS, 2003, 88 (02) :141-145