OBJECTIVE: Leptin, an adipocyte-secreted hormone, has emerged as a potential candidate for the link between obesity and the proinflammatory state. Specifically, leptin modulates T-helper (Th) cells toward a Th1 phenotype, with the secretion of proinflammatory cytokines. The aim of this study was to evaluate the Th1/Th2 balance in obese children and its relation with hormonal and metabolic features. STUDY DESIGN: In 50 obese children and 20 control children, we measured the CD4-positive Th cells that secrete interferon (IFN)-gamma or interleukin (IL)-2 (taken as an index of Th1 cells), and IL-4 (taken as an index of Th2 cells) as well as serum glucose, insulin, insulin resistance (IR) index (as homeostasis model assessment model (HOMA)), lipid profile, aminotransferases, leptin and ghrelin. Obese children also underwent dual energy X-ray absorptiometry scan measurements, and liver ultrasound scanning. RESULTS: Geometric mean percentages of IL-2- and IL-4-CD4 secreting cells in obese children were not significantly different from those found in control children. However, the geometric mean percentage of CD4-positive T cells secreting IFN-gamma was significantly higher in the obese than in the control (P < 0.0001, t-test) group. Within the entire group of study children, the percentage of IFN-gamma-positive cells was positively associated with leptin (P = 0.002), insulin (P < 0.00 005), and HOMA-IR values (P < 0.00 005). However, when these associations were restricted to the group of obese subjects, insulin and HOMA-IR values, but not leptin, retained statistical significance. Yet, in the obese group, the percentage of IFN-gamma-positive cells was associated with nonalcoholic steatohepatitis (NASH) (P = 0.001), but not with body mass index-standard deviation score and total body fat mass. CONCLUSIONS: In obese children, a shift to Th1-cytokine profile dominated by the production of IFN-gamma is related to insulin resistance as well as to NASH independently of anthropometric features and other metabolic characteristics. The prevalent Th1 pattern of secreted cytokines may be regarded as a mechanism contributing to inflammation in obesity.
OBJECTIVE: Leptin, an adipocyte-secreted hormone, has emerged as a potential candidate for the link between obesity and the proinflammatory state. Specifically, leptin modulates T-helper (Th) cells toward a Th1 phenotype, with the secretion of proinflammatory cytokines. The aim of this study was to evaluate the Th1/Th2 balance in obesechildren and its relation with hormonal and metabolic features. STUDY DESIGN: In 50 obesechildren and 20 control children, we measured the CD4-positive Th cells that secrete interferon (IFN)-gamma or interleukin (IL)-2 (taken as an index of Th1 cells), and IL-4 (taken as an index of Th2 cells) as well as serum glucose, insulin, insulin resistance (IR) index (as homeostasis model assessment model (HOMA)), lipid profile, aminotransferases, leptin and ghrelin. Obesechildren also underwent dual energy X-ray absorptiometry scan measurements, and liver ultrasound scanning. RESULTS: Geometric mean percentages of IL-2- and IL-4-CD4 secreting cells in obesechildren were not significantly different from those found in control children. However, the geometric mean percentage of CD4-positive T cells secreting IFN-gamma was significantly higher in the obese than in the control (P < 0.0001, t-test) group. Within the entire group of study children, the percentage of IFN-gamma-positive cells was positively associated with leptin (P = 0.002), insulin (P < 0.00 005), and HOMA-IR values (P < 0.00 005). However, when these associations were restricted to the group of obese subjects, insulin and HOMA-IR values, but not leptin, retained statistical significance. Yet, in the obese group, the percentage of IFN-gamma-positive cells was associated with nonalcoholic steatohepatitis (NASH) (P = 0.001), but not with body mass index-standard deviation score and total body fat mass. CONCLUSIONS: In obesechildren, a shift to Th1-cytokine profile dominated by the production of IFN-gamma is related to insulin resistance as well as to NASH independently of anthropometric features and other metabolic characteristics. The prevalent Th1 pattern of secreted cytokines may be regarded as a mechanism contributing to inflammation in obesity.
Authors: Anne E Dixon; Scott E Johnson; Laurianne V Griffes; Danielle M Raymond; Ramona Ramdeo; Avigail Soloveichik; Benjamin T Suratt; Rubin I Cohen Journal: J Asthma Date: 2011-10 Impact factor: 2.515
Authors: Robert W O'Rourke; Ashley E White; Monja D Metcalf; Brian R Winters; Brian S Diggs; Xinxia Zhu; Daniel L Marks Journal: Metabolism Date: 2012-03-03 Impact factor: 8.694
Authors: Magar Ghazarian; Xavier S Revelo; Mark K Nøhr; Helen Luck; Kejing Zeng; Helena Lei; Sue Tsai; Stephanie A Schroer; Yoo Jin Park; Melissa Hui Yen Chng; Lei Shen; June Ann D'Angelo; Peter Horton; William C Chapman; Diane Brockmeier; Minna Woo; Edgar G Engleman; Oyedele Adeyi; Naoto Hirano; Tianru Jin; Adam J Gehring; Shawn Winer; Daniel A Winer Journal: Sci Immunol Date: 2017-04-21
Authors: Charmaine S Tam; Alexander Viardot; Karine Clément; Joan Tordjman; Katherine Tonks; Jerry R Greenfield; Lesley V Campbell; Dorit Samocha-Bonet; Leonie K Heilbronn Journal: Diabetes Date: 2010-06-14 Impact factor: 9.461
Authors: Tuo Deng; Christopher J Lyon; Laurie J Minze; Jianxin Lin; Jia Zou; Joey Z Liu; Yuelan Ren; Zheng Yin; Dale J Hamilton; Patrick R Reardon; Vadim Sherman; Helen Y Wang; Kevin J Phillips; Paul Webb; Stephen T C Wong; Rong-Fu Wang; Willa A Hsueh Journal: Cell Metab Date: 2013-03-05 Impact factor: 27.287