Abstract
Circulating growth hormone (GH) levels rise in response to nutrient deprivation and fall in states of nutrient excess. Because GH regulates carbohydrate, lipid, and protein metabolism, defining the mechanisms by which changes in metabolism alter GH secretion will aid in our understanding of the cause, progression, and treatment of metabolic diseases. This review will summarize what is currently known regarding the impact of systemic metabolic signals on GH-axis function. In addition, ongoing studies using the Cre/loxP system to generate mouse models with selective somatotrope resistance to metabolic signals will be discussed, where these models will serve to enhance our understanding of the specific role the somatotrope plays in sensing the metabolic environment and adjusting GH output in metabolic extremes.
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