Pediatric obesity prevention:From na?ve examination of energy imbalance towards strategies that influence the competition for nutrient resources among tissues

Current pediatric obesity interventions have collectively yielded relatively unsuccessful results. In this Field of Vision, we present plausible physiologic underpinnings fostering ineffectiveness of conventional strategies grounded in requisite induction of negative energy imbalance. Moreover, such recommendations exacerbate the underlying metabolic dysfunction by further limiting metabolic fuel availability, lowering energy expenditure, and increasing hunger(recapitulating the starvation response amid apparent nutritional adequacy) which precede and promote obesity during growth and development. The qualitative aspects of musculoskeletal system(i.e., endocrine response, muscle functional capacity) are likely to improve metabolic function and increase nutrient delivery and utilization. An intricate and complex system including multiple feedback mechanisms operates to homeostatically regulate energy balance and support optimal body composition trajectories and metabolic health, during growth and development. Thus, ignoring the interdependencies of regulatory growth processes initiates a nuanced understanding of energy regulation and thus misguided attempts at preventive strategies. Importantly, these gains are not dependent upon weight-loss, rather we suggest can be achieved through resistance training. Collectively, optimizing musculoskeletal health via resistance training elicits augmentation of competitive capacity across systems. Further, substantial gains can be achieved in skeletal muscle mass, strength, and functional capacity through resistance training in a relatively short period of time.

Diabetes-related impairment in bone strength is established early in the life course

AIM: To evaluate properties of bone quantity/quality using young non-obese Type 1(T1D)-diabetic(NOD) prone and syngenic non-diabetic(NOD.scid) mice.METHODS: Quantitative bone assessment of tibia was conducted using dual-energy X-ray absorptiometry(DXA) for the evaluation of body mass,bone mineral content,body fat mass and lean mass.Qualitative assessment was accomplished by three-point breakage for assessment of force to failure and micro-computed tomography for evaluation of trabecular and cortical properties of bone.In addition,fasting blood was evaluated prior to sacrifice at week eleven and fifteen to evaluate and compare glucose homeostasis between the strains of mice.RESULTS: Our findings support a perturbation in the relationship between bone quantity,quality,and subsequently,the association between structure and strength.There were no differences in DXA-assessed body composition(body fat,% fat mass and lean mass) and bone composition(bone mineral content and bone mineral density) between strains.However,relative to NOD.scid,NOD mice had lower trabecular bone volume,relative trabecular bone volume,trabecular number and trabecular total material density(P < 0.05).Conversely,NOD mice had greater cortical total mean volume(P < 0.05).General linear models analysis adjusted for body weight revealed a significant contribution of T1D to bone health as early as 5 wk.CONCLUSION: It is well-established that diabetes is a significant risk factor for increased fractures,although the underlying mechanisms are not fully understood.Investigation of bone parameters encompassing strength and structure early in the life course will facilitate the elucidation of the pathogenesis of impaired bone integrity.