Abstract

It has now well established that alterations in the environment during early life development can have effects on the health of the offspring across the lifecourse and evidence for transmission of these adverse disease traits to future generations. A key component underpinning this early life developmental programming is that of dysregulation of the growth hormone-insulin-like growth factor (GH-IGF) axis. Phenotypic outcomes in programmed offspring closely resemble those associated with GH deficiency (GHD), including increased fat mass, altered insulin sensitivity and cardiovascular disorders. The GH-IGF axis plays a key developmental role in essentially all tissues and organs and work across a wide range of animal models has suggested that manipulation of this axis in the early life period can ameliorate the effects of adverse developmental programming, albeit in a sex-specific manner. Further understanding of how different exposures in the early life period, including altered nutrition, impact upon this axis is essential to define translatable strategies to reverse the consequences of early life adversity and improve health outcomes across the lifecourse.

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