What is the Origin of Hepatic GH Resistance?

This endocrinological term stems from the understanding of the hypothalamic-pituitary-somatotropic axis, where the liver is the main effector organ for GH's anabolic actions. The concept of resistance arose from clinical observations of patients with growth failure who had high GH but low IGF-1, indicating a post-receptor defect.

What is the Mechanism of Hepatic GH Resistance?

The resistance mechanism typically involves a defect at the level of the Growth Hormone Receptor (GHR) or downstream signaling pathways within the hepatocyte, such as impaired activation of the Janus kinase/signal transducer and activator of transcription (JAK-STAT) cascade. This molecular blockade prevents the GH signal from triggering the necessary gene transcription for IGF-1 synthesis. Consequently, the body is deprived of IGF-1's anabolic and metabolic signaling, perpetuating the state of resistance.

Hepatic GH Resistance

Meaning

Hepatic GH Resistance is a clinical state characterized by a reduced biological response of the liver (hepatic) tissue to circulating Growth Hormone (GH), despite the presence of normal or elevated levels of the hormone itself. This unresponsiveness leads directly to a failure in the liver’s primary endocrine function of synthesizing and secreting Insulin-like Growth Factor 1 (IGF-1). The resulting low IGF-1 levels are a hallmark of this condition, often presenting with growth failure in children or metabolic dysfunction in adults.

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