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Institute
Objective
Insulin regulates mitochondrial function, thereby propagating an efficient metabolism. Conversely, diabetes and insulin resistance are linked to mitochondrial dysfunction with a decreased expression of the mitochondrial chaperone HSP60. The aim of this investigation was to determine the effect of a reduced HSP60 expression on the development of obesity and insulin resistance.
Methods
Control and heterozygous whole-body HSP60 knockout (Hsp60+/−) mice were fed a high-fat diet (HFD, 60% calories from fat) for 16 weeks and subjected to extensive metabolic phenotyping. To understand the effect of HSP60 on white adipose tissue, microarray analysis of gonadal WAT was performed, ex vivo experiments were performed, and a lentiviral knockdown of HSP60 in 3T3-L1 cells was conducted to gain detailed insights into the effect of reduced HSP60 levels on adipocyte homeostasis.
Results
Male Hsp60+/− mice exhibited lower body weight with lower fat mass. These mice exhibited improved insulin sensitivity compared to control, as assessed by Matsuda Index and HOMA-IR. Accordingly, insulin levels were significantly reduced in Hsp60+/− mice in a glucose tolerance test. However, Hsp60+/− mice exhibited an altered adipose tissue metabolism with elevated insulin-independent glucose uptake, adipocyte hyperplasia in the presence of mitochondrial dysfunction, altered autophagy, and local insulin resistance.
Conclusions
We discovered that the reduction of HSP60 in mice predominantly affects adipose tissue homeostasis, leading to beneficial alterations in body weight, body composition, and adipocyte morphology, albeit exhibiting local insulin resistance.
Loss to follow-up in a randomized controlled trial study for pediatric weight management (EPOC)
(2016)
Background
Attrition is a serious problem in intervention studies. The current study analyzed the attrition rate during follow-up in a randomized controlled pediatric weight management program (EPOC study) within a tertiary care setting.
Methods
Five hundred twenty-three parents and their 7–13-year-old children with obesity participated in the randomized controlled intervention trial. Follow-up data were assessed 6 and 12 months after the end of treatment. Attrition was defined as providing no objective weight data. Demographic and psychological baseline characteristics were used to predict attrition at 6- and 12-month follow-up using multivariate logistic regression analyses.
Results
Objective weight data were available for 49.6 (67.0) % of the children 6 (12) months after the end of treatment. Completers and non-completers at the 6- and 12-month follow-up differed in the amount of weight loss during their inpatient stay, their initial BMI-SDS, educational level of the parents, and child’s quality of life and well-being. Additionally, completers supported their child more than non-completers, and at the 12-month follow-up, families with a more structured eating environment were less likely to drop out. On a multivariate level, only educational background and structure of the eating environment remained significant.
Conclusions
The minor differences between the completers and the non-completers suggest that our retention strategies were successful. Further research should focus on prevention of attrition in families with a lower educational background.