Children with overweight, obesity, and morbid obesity benefit equally from an ongoing, outpatient, tailored lifestyle intervention, and demonstrate significant weight loss and improvement of cardiovascular risk parameters.

Insulin resistance (IR) occurs in a transient manner during puberty. Obese adolescents may be at risk for persistent IR during puberty. The objective of the study is to review the literature on the association of the anthropometry and lifestyle characteristics with insulin sensitivity in overweight and obese adolescents, and include data from a new study. Relevant papers were selected and reviewed. In addition, 137 overweight and obese adolescents (42 male/95 female, age 14.4 ± 2.3 years, BMI z-score +3.3 ± 0.7, HOMA-IR 3.4 ± 1.8) from the Centre for Overweight Adolescent and Children's Healthcare (MUMC+) were included in this study. Anthropometrics, Tanner stages, sleep characteristics, food intake behaviour and physical activity were determined, and possible associations with homeostasis model assessment of insulin resistance (HOMA-IR) were tested. Results: Overweight and obese adolescents with unfavourable fat partitioning and family history of NIDDM are at risk for persistent IR. Overweight and obese adolescents from the new cohort showed a higher HOMA-IR postpubertally. BMI z-score, age, pubertal stage and prepubertally total sleeping time (TST) and sleep efficiency (SE) were identified as significant contributors. Overweight and obese adolescents showed a persistently higher instead of transiently higher HOMA-IR during puberty, associated with BMI z-score, age, pubertal stage and prepubertally less TST and SE. Keywords: food intake behaviour, physical activity, pubertal persistent insulin resistance, pubertal transient insulin resistance, sleep Date submitted 9 April 2015; date of final acceptance 2 June 2015 IntroductionDuring puberty, adolescents undergo a series of biological, cognitive and psychosocial changes. One of the hallmarks of puberty is a change in endocrine conditions and changes in anthropometric factors, such as height, body weight and body composition. In parallel, behavioural changes, such as sleeping time, food intake behaviour and physical activity, driven both by biological processes or social and academic pressures, occur [1][2][3][4][5][6][7][8][9]. Together, these factors pose an increased risk for the development of excess weight and obesity, as well as comorbidities such as insulin resistance (IR), type 2 diabetes and cardiovascular disease, but also non-alcoholic fatty liver disease and obstructive sleep apnea syndrome [9].This review discusses insulin insensitivity during puberty, reviewing the existing evidence for possibly related changes in body weight, especially overweight and obesity, sleep characteristics, physical activity and food intake behaviour.In addition, data from a new, recent study on possible relationships between sleep efficiency (SE) and insulin sensitivity in overweight and obese adolescents are reported. Transient IR at PubertyPuberty is associated with transient IR and hyperglycaemia [10,11], due to an impaired ability of insulin to stimulateCorresponding to: Prof. Dr M. S. Westerterp-Plantenga, Department of Human Biology, Maastricht University, P.O. Box ...

The objective was to assess the effects of a weight loss and subsequent weight maintenance period comprising two diets differing in protein intake, on brain reward reactivity to visual food cues. Brain reward reactivity was assessed with functional magnetic resonance imaging in 27 overweight/obese individuals with impaired fasting glucose and/or impaired glucose tolerance (HOMA-IR: 3.7 ± 1.7; BMI: 31.8 ± 3.2 kg/m2; fasting glucose: 6.4 ± 0.6 mmol/L) before and after an 8-week low energy diet followed by a 2-year weight maintenance period, with either high protein (HP) or medium protein (MP) dietary guidelines. Brain reactivity and possible relationships with protein intake, anthropometrics, insulin resistance and eating behaviour were assessed. Brain reactivity, BMI, HOMA-IR and protein intake did not change differently between the groups during the intervention. In the whole group, protein intake during weight maintenance was negatively related to changes in high calorie images>low calorie images (H > L) brain activation in the superior/middle frontal gyrus and the inferior temporal gyrus (p < 0.005, corrected for multiple comparisons). H > L brain activation was positively associated with changes in body weight and body-fat percentage and inversely associated with changes in dietary restraint in multiple reward, gustatory and processing regions (p < 0.005, corrected for multiple comparisons). In conclusion, changes in food reward-related brain activation were inversely associated with protein intake and dietary restraint during weight maintenance after weight loss and positively associated with changes in body weight and body-fat percentage.

To aim of this study was to evaluate characteristics of the retinal microvasculature, but particularly potential associations with classic and novel (endothelial function and low-grade inflammation)markers for cardiovascular risk, in a cohort of children with overweight and (morbid) obesity. Central retinal arteriolar equivalent(CRAE) and central retinal venular equivalent(CRVE) were assessed. CRAE was significantly lower and AVR significantly higher in children with morbid obesity than in children with overweight and normal weight(p < 0.01). CRVE did not differ significantly between the four weight categories. A multiple linear regression model with CRAE as dependent variable showed that only DBP z-score(β = −2.848,p = 0.029) and plasma glucose concentrations(β = 6.029,p = 0.019) contributed significantly to the variation in CRAE. Remarkably, despite a correlation between CRAE and circulating concentrations of the adhesion molecules VCAM-1 or ICAM-1, markers for inflammation and endothelial function did not contribute to the variation in CRAE. This is the first study showing in population of children with overweight and obesity that the retinal arteriolar microvasculature, but not venular diameter is aberrant, with increasing BMI z-score. CRAE was significantly associated with several cardiovascular risk markers, and multiple linear regression showed that a higher diastolic blood pressure z-score and lower fasting plasma glucose concentrations significantly contributed to the variance in CRAE.