Abstract
Extensive epidemiological and experimental evidence have shown that exposure to an adverse intrauterine environment as observed in offspring of pregnancies complicated by obesity or diabetes, can program susceptibility to metabolic, endocrine and cardiovascular disorders later in life. Although most studies have concentrated on the maternal environment, it is also becoming evident that paternal exposure to obesity or diabetes can result in the later development of metabolic disorders in the offspring. Such programmed effects might not be limited to the first directly exposed generation, but could be transmitted to subsequent generations. This suggests the existence of mechanisms by which metabolic changes in parental phenotype are transmissible to offspring. The mechanisms which underpin the transmission of the programmed effects across generations are still unclear. However, epigenetic regulation of transcription has emerged as a strong candidate for mediating the heritability of metabolic diseases. Here, we review the most relevant evidence from human and animal studies showing transmission of programming effects of obesity or diabetes across generations, and the current mechanisms underlying either maternal or paternal influences on the metabolic status of offspring.
Highlights
Extensive epidemiological and experimental evidence have shown that exposure to an adverse intrauterine environment as observed in offspring of pregnancies complicated by obesity or diabetes, can program susceptibility to metabolic, endocrine and cardiovascular disorders later in life
Evidence for this has been seen in the offspring of Pima Indian women with pre-existent type 2 diabetes (T2D) or gestational diabetes. These offspring were larger for gestational age at birth and were heavier and had impaired glucose tolerance (IGT) in childhood compared to offspring of pre-diabetic or non-diabetic women [23]. These findings indicate that intrauterine exposure to a diabetic environment increases the risk of obesity and T2D beyond that attributable to genetic factors, at least in Pima Indians
Gestational exposure to maternal obesity resulted in obesity and impaired glucose tolerance only in the adult offspring, suggesting that their obese phenotype is not related to placental dysfunction [57]
Summary
Parental contribution programming adult obesity/diabetes in offspring. the offspring. The preconception period (sperm cell maturation) is a critical period for paternal obesity/diabetes (brown rodent) to shape the risk for the offspring to develop obesity or diabetes (right obesity/diabetes (brown rodent) to shape the risk for the offspring to develop obesity or diabetes panel). Both fetal and suckling periods have been shown to be critical time-windows in determining. It is admitted that exposure to an adverse metabolic milieu prior to pregnancy accounts for some of the adverse outcomes observed in associated with diabetes, to develop in the offspring. Gestational exposure to maternal obesity resulted in obesity and impaired glucose tolerance only in the adult offspring, suggesting that their obese phenotype is not related to placental dysfunction [57]
Sign-in/Register to view highlights & summary Sign-in/Register to access full text options 
Free) 
Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Schedule a call
