= 17), aerobic (50%–85% of V˙O2peak) and resistance (6–10 maximum repetition [RM]) training)] three times per week, 60 min per session, or a control group (N = 13). Anthropometric measures, maximal strength for leg press and bench press, peak oxygen uptake (V˙O2peak) and serum concentrations of C-reactive protein (CRP), tumor necrosis factor α (TNF-α), interleukin-6 (IL-6), IL-10, IL-15, resistin, leptin, and adiponectin were determined before (M1) and after 8 (M2), 16 (M3), and 24 (M4) wk of the experimental design. Results Significant increases were observed in the maximal strength for bench press and leg press, V˙O2peak, and serum concentrations of adiponectin and IL-15 for CT. Concomitantly, significant decreases were observed in percentage body fat and serum concentrations of CRP, resistin, and leptin for CT after the experimental period. Conclusion Twenty-four weeks of moderate- to high-intensity CT reduced markers of subclinical inflammation associated with obesity and improved insulin resistance and functional capabilities of obese middle-age men, regardless of dietary intervention and weight loss....

The effects of training on FNDC5/irisin and its association with fitness and metabolic marker improvements induced by training have been poorly investigated in humans. Thus, the present study assessed the effects of combined training (CT) on FNDC5/irisin levels, metabolic markers and fitness adaptations in obese men. Middle‐age obese men (age 49.13 ± 5.75, body mass index (BMI) 30.86 ± 1.63) were randomly distributed in the CT group (n = 12) and control group (CG n = 10). The CT consisted of strength followed by aerobic training, 3 times/week, for 24 weeks. Body composition, physical fitness, plasma FNDC5/irisin, biochemical markers and metabolic scores/index were evaluated. CT maintained FNDC5/irisin levels (µg/mL) (pre: 4.15 ± 0.32, post: 4.21 ± 0.32; p = .96) and improved body composition, metabolic and physical fitness markers. In the CG, decreased FNDC5/irisin (µg/mL) (pre: 4.36 ± 0.23, post: 3.57 ± 0.94; p = .01) and reduced strength (supine exercise/kg) (pre: 71 ± 14.7, post: 60.1 ± 14.05; p < .01) were observed, along with a trend to increase HOMA‐IR (pre: 2.63 ± 1.11, post: 3.14 ± 1.27; p = .07) and other indicators of metabolic deterioration. An inverse correlation was found between the change (Δ%) in levels of FNDC5/irisin and Δ% glucose, Δ% total cholesterol, Δ% triglycerides and Δ% waist circumference, in addition to a positive relation with Δ% muscle strength. In conclusion, CT maintained FNDC5/irisin levels and provided metabolic and fitness benefits. The correlation between FNDC5/irisin changes and metabolic parameters, as well as the FNDC5/irisin reduction associated with fitness and metabolic worsening in the CG, suggests a relationship between FNDC5/irisin and a healthy metabolic status in humans.

Inflammation is the most relevant mechanism linking obesity with insulin-resistance and metabolic disease. It impacts the structure and function of tissues and organs involved in metabolism, such as the liver, pancreatic islets and the hypothalamus. Brown adipose tissue has emerged as an important component of whole body energy homeostasis, controlling caloric expenditure through the regulation of non-shivering thermogenesis. However, little is known about the impact of systemic inflammation on the structure and function of brown adipose tissue. The relations between IL10 and mitochondria structure/function and also with thermogenesis were evaluated by bioinformatics using human and rodent data. Real-time PCR, immunoblot, fluorescence and transmission electron microscopy were employed to determine the effect of IL10 in the brown adipose tissue of wild type and IL10 knockout mice. IL10 knockout mice, a model of systemic inflammation, present severe structural abnormalities of brown adipose tissue mitochondria, which are round-shaped with loss of cristae structure and increased fragmentation. IL10 deficiency leads to newborn cold intolerance and impaired UCP1-dependent brown adipose tissue mitochondrial respiration. The reduction of systemic inflammation with an anti-TNFα monoclonal antibody partially rescued the structural but not the functional abnormalities of brown adipose tissue mitochondria. Using bioinformatics analyses we show that in both humans and mice, IL10 transcripts correlate with mitochondrial lipid metabolism and caspase gene expression. IL10 and systemic inflammation play a central role in the regulation of brown adipose tissue by controlling mitochondrial structure and function. FUND: Sao Paulo Research Foundation grant 2013/07607-8.

Keywords Irisin; metabolism; obese; type 2 diabetes; lipopolysaccharide