Literature DB >> 18442634

The association between insulin resistance and cytokines in adolescents: the role of weight status and exercise.

Daniela A Rubin1, Robert G McMurray, Joanne S Harrell, Anthony C Hackney, Deborah E Thorpe, Andrea M Haqq.   

Abstract

Increased adiposity is associated with insulin resistance (IR) and an inflammatory response in adults. We tested the hypotheses that cytokines associated with adiposity are also correlated with IR in early adolescents and that these relationships are moderated by weight status, levels of vigorous physical activity (VPA), or maximal aerobic power (pVO2max). Body mass, stature, and a fasting blood sample were obtained from 120 midpubertal adolescents (60 girls and 60 boys). Habitual VPA was obtained by a survey. Predicted VO2max was determined using a cycle ergometer test. Weight status was based on body mass index (BMI) percentiles (normal weight=BMI<75th percentile, overweight=BMI>95th percentile). Glucose, insulin, adiponectin, resistin, tumor necrosis factor-alpha (TNF-alpha), and interleukin-6 were measured; and IR index was based on the Homeostatic Model Assessment. Adiponectin, resistin, and TNF-alpha were associated with IR in all adolescents (R2=0.329, P<.001; R2=0.152, P=.001; and R2=0.141, P=.002; respectively); but interleukin-6 was not (R2=0.148, P=.114). The degree of association between adiponectin and IR was stronger in overweight than in normal-weight adolescents (P<.050). When regression models included weight status, neither TNF-alpha nor resistin was significantly related to IR (P>.050). Exercise did not moderate the association between these cytokines and IR. However, higher levels of VPA and/or pVO2max were associated with higher adiponectin, lower resistin, and lower TNF-alpha in at least one of the sexes. Our results indicate that the pathophysiology of obesity is already established in early adolescents. Increased adiposity, resulting in reduced adiponectin and increased resistin and TNF-alpha, may link these cytokines with IR in adolescents.

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Year:  2008        PMID: 18442634      PMCID: PMC2678573          DOI: 10.1016/j.metabol.2008.01.005

Source DB:  PubMed          Journal:  Metabolism        ISSN: 0026-0495            Impact factor:   8.694


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