Thread by @nick_krontiris

This one found individuals with NAFLD to have lower peak-stimulated GH but similar IGF-1 levels, with a higher peak-stimulated GH to be associated with lower IHL and less hepatocellular damage, and a higher IGF-1 to be associated with more favorable fibrosis markers.

- Mean peak stimulated GH was lower in individuals with NAFLD, as compared to similar controls without NAFLD.

- Individuals with NAFLD had lower peak-stimulated GH versus non-NAFLD controls of similar age, BMI and sex, independent of confounders such as visceral adiposity and fasting glucose.

- Lower peak-stimulated GH was found to be independently associated with higher intrahepatic lipid content and ALT, which is consistent with the known direct lipolytic and anti-inflammatory effects of GH.

Additionally, peak-stimulated GH was independently associated with liver fat in a model that included these same endpoints, explaining 14.6% of the variability in intrahepatic lipid content and 11% of the variability in ALT.

- This suggests that higher GH secretion may be relatively protective against hepatic lipid accumulation as well as hepatocellular damage and inflammation.

- IGF-1 levels were inversely associated with predictors of fibrosis, with some potential sex differences in these relationships.

More specifically, higher IGF-1 levels were associated with more favorable FIB-4 and NAFLD fibrosis scores in men, but not women.

"This is of interest given that men generally have more IGF-1 per unit of GH than women, as estrogen induces hepatic resistance to GH."

The GH/IGF-1 axis is associated with intrahepatic lipid content and hepatocellular damage in overweight/obesity

doi.org/10.1210/clinem…

#MetabolicSyndrome #NAFLD #NASH