Adipokines and cytokines have modified values in the metabolic syndrome (MetSyn), without knowing if they are the cause or the effect of insulin resistance. Multiple studies evaluating adipokines and cytokines in MetSyn presented controversial results.
The aim of this study was to evaluate adiponectin, leptin, resistin, CRP and TNFα in obese subjects with endocrine diseases that associate insulin resistance before and after a low calorie diet.
Subjects and methods: This study enrolled 59 subjects that were clinically evaluated. Blood samples were taken in fasting conditions in order to determine the biochemical profile, adipokine and cytokine levels, before and after a 3 months diet. Insulin resistance was appreciated using HOMA index. The MetSyn was diagnosed according to Diabetes International Federation definition.
Results were statistically analyzed using SPSS 15 program.
Results: Subjects were divided into 2 groups-37 subjects with MetSyn and 22 subjects- control group.
Compared mean values from both groups during the first visit, revealed statistically significant differences for both groups regarding triglycerides (P<0.001), HDL-cholesterol (P<0.001), diastolic blood pressure (P=0.012), leptin (P=0.005), insulin (P=0.049), glycaemia (P=0.013), HOMA (P=0.033) and TNF-α (P=0.026), differences kept for triglycerides (P=0.03) and glycaemia (P=0.033) after 3 month diet.
Adiponectin values were low, leptin, CRP and TNFα levels were high and resistin concentration was normal in both groups. Adipokines and cytokines values were lower after 3 months diet, but with higher adiponectin and resistin values in the MetSyn group. Weight loss determined a slightly improvement in insulin sensibility.
Conclusions: Obese subjects with different endocrine diseases that associate MetSyn have low levels of adiponectin, high leptin, CRP and TNF-α values and normal resistin concentrations without being influenced by the associated endocrinopathy. Weight loss determines an improvement of insulin sensibility. Adipokinesvariations cannot be the cause of insulin sensibility reestablishing, being more the result of visceral adiposity reduction.
25 - 29 Apr 2009
European Society of Endocrinology