Adiponectin, the most abundant hormone produced by adipose tissue, circulates in 3 isoforms, including high molecular weight (HMW) adiponectin. The latter has been suggested to be a better predictor of metabolic disturbances and insulin resistance associated with obesity. This study investigated changes in total and HMW adiponectin, resistin, and homeostasis model assessment (HOMA) during a 9-month in-patient treatment program based on physical exercise and a balanced diet in 32 severely obese adolescents. Total and HMW adiponectin, resistin, and HOMA were measured at baseline (month 0) and during the program (months 3, 6, 9). In addition, a control group of 15 teenagers served as a reference for the baseline assessments. At baseline, HMW adiponectin was more markedly decreased in obese adolescents than total adiponectin, and both were lower than in controls. Conversely, resistin and HOMA were higher in obese adolescents. During the program, there was a significant change in body composition and improved insulin sensitivity among obese teenagers. In addition, HMW adiponectin and the ratio of HMW-to-total adiponectin increased throughout the study, whereas total adiponectin only increased up until the sixth month. On the contrary, resistin did not show any significant change. In obese adolescents, a long-term combination of aerobic exercise and a balanced diet, inducing change in body composition and improved insulin sensitivity, markedly increased HMW adiponectin compared with total adiponectin, without any change in resistin concentrations. Our results thus suggest that the determination of HMW adiponectin could be more useful than measurement of total adiponectin in clinical settings.
The development of personalised training programmes is crucial in the management of obesity. We evaluated the ability of 2 heart rate variability analyses to determine ventilatory thresholds (VT) in obese adolescents. 20 adolescents (mean age 14.3±1.6 years and body mass index z-score 4.2±0.1) performed an incremental test to exhaustion before and after a 9-month multidisciplinary management programme. The first (VT1) and second (VT2) ventilatory thresholds were identified by the reference method (gas exchanges). We recorded RR intervals to estimate VT1 and VT2 from heart rate variability using time-domain analysis and time-varying spectral-domain analysis. The coefficient correlations between thresholds were higher with spectral-domain analysis compared to time-domain analysis: Heart rate at VT1: r=0.91 vs. =0.66 and VT2: r=0.91 vs. =0.66; power at VT1: r=0.91 vs. =0.74 and VT2: r=0.93 vs. =0.78; spectral-domain vs. time-domain analysis respectively). No systematic bias in heart rate at VT1 and VT2 with standard deviations <6 bpm were found, confirming that spectral-domain analysis could replace the reference method for the detection of ventilatory thresholds. Furthermore, this technique is sensitive to rehabilitation and re-training, which underlines its utility in clinical practice. This inexpensive and non-invasive tool is promising for prescribing physical activity programs in obese adolescents.
Metabolic-associated fatty liver disease (MAFLD), previously called nonalcoholic fatty liver diseases (NAFLD), is one of the most important causes of chronic liver disease worldwide and will likely become the leading cause of end-stage liver disease in the decades ahead. MAFLD covers a continuum of liver diseases from fatty liver to nonalcoholic steatohepatitis (NASH), liver fibrosis/cirrhosis and hepatocellular cancer. Importantly, the growing incidence of overweight and obesity in childhood, 4% in 1975 to 18% in 2016, with persisting obesity complications into adulthood, is likely to be harmful by increasing the incidence of severe MAFLD at an earlier age. Currently, MAFLD is the leading form of chronic liver disease in children and adolescents, with a global prevalence of 3 to 10%, pointing out that early diagnosis is therefore crucial. In this review, we highlight the current knowledge concerning the epidemiology, risk factors and potential pathogenic mechanisms, as well as diagnostic and therapeutic approaches, of pediatric MAFLD.
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