Excess nutrient supply in early life and its later metabolic consequences

Abstract

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.

Childhood Cardiometabolic Outcomes of Maternal Obesity During Pregnancy

“…The observed effects were also not mediated by pregnancy complications, birth characteristics, or infant growth, which are all identified risk factors related to both maternal prepregnancy BMI and health of offspring. [38][39][40][41] Thus, our findings suggest that associations of maternal prepregnancy BMI with offspring cardiometabolic health outcomes may, at least partly, be explained by direct intrauterine mechanisms. This may include higher maternal plasma concentrations and placental transfer of glucose, amino acids, and free fatty acids during pregnancy, which may influence programming of offspring adiposity and an adverse cardiometabolic profile in later life.…”

Maternal High Folic Acid Supplement Promotes Glucose Intolerance and Insulin Resistance in Male Mouse Offspring Fed a High-Fat Diet

“…Habitual HFD generally induces dyslipidaemia, glucose disturbance, abnormal secretion of inflammatory factors, and further promotes insulin resistance and diabetes [2]. In addition to HFD, as suggested by accumulating evidence, unbalanced maternal nutrition also contributes to the incidence and development of glucose disturbance and insulin resistance in offspring [3]. Intrauterine exposure to improper nutrition affects the expression of foetal genes, and programs the future risk of metabolic diseases in their later life [4], involving epigenetic changes such as aberrant DNA methylation as probable mechanisms.…”

A critical review: early life nutrition and prenatal programming for adult disease

“…, Frias & Grove , Ojha et al . ) which has an impact of placental development and function. Maternal obesity results in foetal hyperlipidaemia, systemic inflammation, hyperinsulinemia and lipotoxicity (Frias & Grove , Segovia et al .…”