Suboptimal nutrition in early life, both in utero and during infancy, is linked to increased risk of adult obesity and its associated adverse metabolic health problems. Excess nutrient supply during early life can lead to metabolic programming in the offspring. Such overnutrition can occur in the offspring of obese mothers, the offspring of mothers who gain excess weight during gestation, infants of diabetic mothers and infants who undergo rapid growth, particularly weight gain, during early infancy. Postnatal overnutrition is particularly detrimental for infants who are born small for gestational age, who are overfed to attain 'catch-up growth'. Potential mechanisms underlying metabolic programming that results from excess nutrition during early life include resetting of hypothalamic energy sensing and appetite regulation, altered adipose tissue insulin sensitivity and impaired brown adipose tissue function. More detailed understanding of the mechanisms involved in metabolic programming could enable the development of therapeutic strategies for ameliorating its ill effects. Research in this field could potentially identify optimal and appropriate preventative interventions for a burgeoning population at risk of increased mortality and morbidity from obesity and its concomitant metabolic conditions.
Sex is a major factor determining adipose tissue distribution and the subsequent adverse effects of obesity-related disease including type 2 diabetes. The role of gender on juvenile obesity and the accompanying metabolic and inflammatory responses is not well established. Using an ovine model of juvenile onset obesity induced by reduced physical activity, we examined the effect of gender on metabolic, circulatory, and related inflammatory and energy-sensing profiles of the major adipose tissue depots. Despite a similar increase in fat mass with obesity between genders, males demonstrated a higher storage capacity of lipids within perirenal-abdominal adipocytes and exhibited raised insulin. In contrast, obese females became hypercortisolemic, a response that was positively correlated with central fat mass. Analysis of gene expression in perirenal-abdominal adipose tissue demonstrated the stimulation of inflammatory markers in males, but not females, with obesity. Obese females displayed increased expression of genes involved in the glucocorticoid axis and energy sensing in perirenal-abdominal, but not omental, adipose tissue, indicating a depot-specific mechanism that may be protective from the adverse effects of metabolic dysfunction and inflammation. In conclusion, young males are at a greater risk than females to the onset of comorbidities associated with juvenile-onset obesity. These sex-specific differences in cortisol and adipose tissue could explain the earlier onset of the metabolic-related diseases in males compared with females after obesity.
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