Early Life Nutrition and Energy Balance Disorders in Offspring in Later Life

Abstract

The global pandemic of obesity and type 2 diabetes is often causally linked to changes in diet and lifestyle; namely increased intake of calorically dense foods and concomitant reductions in physical activity. Epidemiological studies in humans and controlled animal intervention studies have now shown that nutritional programming in early periods of life is a phenomenon that affects metabolic and physiological functions throughout life. This link is conceptualised as the developmental programming hypothesis whereby environmental influences during critical periods of developmental plasticity can elicit lifelong effects on the health and well-being of the offspring. The mechanisms by which early environmental insults can have long-term effects on offspring remain poorly defined. However there is evidence from intervention studies which indicate altered wiring of the hypothalamic circuits that regulate energy balance and epigenetic effects including altered DNA methylation of key adipokines including leptin. Studies that elucidate the mechanisms behind these associations will have a positive impact on the health of future populations and adopting a life course perspective will allow identification of phenotype and markers of risk earlier, with the possibility of nutritional and other lifestyle interventions that have obvious implications for prevention of non-communicable diseases.

Milk’s Role as an Epigenetic Regulator in Health and Disease

“…Accelerated growth during infancy and increased BMI in early life are known to enhance the risk for obesity [289,290,291], T2DM [292,293], allergy [294,295,296] and cancer later in life [297,298,299]. …”

Preventing childhood obesity: Early‐life messages from epidemiology

“…However, there is now a wealth of experimental and other evidence suggesting that exposure to maternal obesity in fetal life has lifelong effects on the offspring's risk of obesity, which occur before such shared environmental influences act in postnatal life (Reynolds et al . ; Catalano & Shankar ). There are two lines of epidemiological evidence that are important.…”

“…Apart from a genetic predisposition, part of the observed familial concordance is likely to be explained by a shared environment and patterns of behaviour, including common dietary habits (Fisk et al 2011;Schrempft et al 2016). However, there is now a wealth of experimental and other evidence suggesting that exposure to maternal obesity in fetal life has lifelong effects on the offspring's risk of obesity, which occur before such shared environmental influences act in postnatal life (Reynolds et al 2015;Catalano & Shankar 2017). There are two lines of epidemiological evidence that are important.…”

Liraglutide pharmacotherapy reduces body weight and improves glycaemic control in juvenile obese/hyperglycaemic male and female rats

“…[12][13][14] While genetic and environmental factors both affect the development of obesity, [15][16][17] several studies have shown that in utero and early-life exposure to a high-fat, highsucrose diet (HFSD) produces long-term metabolic effects on offspring with regard to energy balance and glycaemic control. [18][19][20] We used a rodent model that mimics a classic human phenomenon of HFSD exposure during pregnancy that drives hyperphagia and weight gain in offspring to determine whether subsequent juvenile intervention with liraglutide could treat and prevent the onset of obesity and chronic hyperglycaemia during adolescence and early adulthood.…”

“…Different letters within each figure indicate significant difference from each other. Data are given as mean AE SEM life [18][19][20]. As our obesogenic environment continues to drive increasing frequency of maternal obesity, the risk of adolescent obesity and associated metabolic diseases is of severe medical and economic concern.…”