Impact of fetal programming on mitochondrial function and susceptibility to obesity and type 2 diabetes

The worldwide incidence of metabolic disorders such as type 2 diabetes and obesity continues to increase. The WHO predicts that these metabolic disorders will be a major cause of death by 2030, placing a substantial economic burden on the healthcare system globally. It now is accepted widely that metabolic diseases of adulthood, including type 2 diabetes and obesity, might have their origins in the womb. Almost three decades ago, the concept of fetal origins of adult diseases was first proposed by Barker and colleagues, who reported that adults born at low birth weight had greater likelihood of developing cardiovascular diseases and diabetes. Based on these pioneering observations, a field of research now popularly known as developmental origins of health and disease (DOHaD) emerged. It now is clear that perturbations during early life have long-lasting effects on metabolic health. Improved understanding about the role of the early life environment on the progression of metabolic diseases has triggered efforts to design preventive strategies for these diseases at the time of their origin.