O besity is a complex chronic disease in which abnormal or excess body fat (adiposity) impairs health, increases the risk of long-term medical complications and reduces lifespan. 1 Epidemiologic studies define obesity using the body mass index (BMI; weight/height 2), which can stratify obesity-related health risks at the population level. Obesity is operationally defined as a BMI exceeding 30 kg/m 2 and is subclassified into class 1 (30-34.9), class 2 (35-39.9) and class 3 (≥ 40). At the population level, health complications from excess body fat increase as BMI increases. 2 At the individual level, complications occur because of excess adiposity, location and distribution of adiposity and many other factors, including environmental, genetic, biologic and socioeconomic factors (Box 1). 11 Over the past 3 decades, the prevalence of obesity has steadily increased throughout the world, 12 and in Canada, it has increased threefold since 1985. 13 Importantly, severe obesity has increased more than fourfold and, in 2016, affected an estimated 1.9 million Canadian adults. 13 Obesity has become a major public health issue that increases health care costs 14,15 and negatively affects physical and psychological health. 16 People with obesity experience pervasive weight bias and stigma, which contributes (independent of weight or BMI) to increased morbidity and mortality. 17 Obesity is caused by the complex interplay of multiple genetic, metabolic, behavioural and environmental factors, with the latter thought to be the proximate cause of the substantial

Our study demonstrated that hypoxia-induced IUGR is associated with the development of chronic cardiopulmonary dysfunction during ageing. The implication of these findings is the potential usefulness of neonatal diagnosis as a predictor of cardiopulmonary outcomes during adulthood.

Our results suggest that hypoxia-induced IUGR has long-term effects on cardiac susceptibility to IR injury that are independent of sex and age. Moreover, we identified a mismatch in glucose metabolism, leading to proton accumulation in the post-ischaemic myocardium of offspring born IUGR as a potential mechanism involved.

OBJECTIVE-It is recognized that there is a remarkable variability in the systemic response to high-fat (HF) diets that cannot be completely explained by genetic factors. In addition, pregnancy complications leading to intrauterine growth restriction (IUGR) have been associated with an increased risk of developing metabolic syndrome (MetS) later in life. Thus, we hypothesized that offspring born with IUGR exhibit permanent metabolic changes that make them more susceptible to HF diet-induced MetS.RESEARCH DESIGN AND METHODS-SD rats born normal (control) or with hypoxia-induced IUGR were randomized to lowfat (10% fat) or HF (45% fat) diets. After 9 weeks of feeding, physiological and molecular pathways involved in the MetS were evaluated.RESULTS-IUGR offspring exhibited decreased energy intake and physical activity relative to controls. In offspring fed a HF diet, IUGR was associated with decreased total body fat content, a relative increase in intra-abdominal fat deposition and adipocyte size, an increase in fasting plasma concentrations of leptin, triglyceride and free fatty acids, and an increased concentration of triglycerides and ceramides in both liver and skeletal muscle. These changes in lipid homeostasis were accompanied by in vivo insulin resistance and impaired glucose tolerance and associated with increased phosphorylation of protein kinase C u, inhibition of insulin receptor substrate 1, and a decreased activation of protein kinase B (PKB; also known as Akt) in liver and skeletal muscle in response to insulin.CONCLUSIONS-IUGR enhances specific deleterious metabolic responses to a HF diet. Our results suggest that offspring born with IUGR may require special attention and follow-up to prevent the early onset of MetS. Diabetes 60: [507][508][509][510][511][512][513][514][515][516] 2011