This article published few days ago is describing the role of IGFBP-6 in various conditions including fibrosis among many hepatic fibrosis. Tesamorelin reduces circulating IGFBP-6 resulting in reduction of the liver fat/prevention of fibrosis.
Abstract:
“The Insulin-like growth factors binding protein-6 (IGFBP-6) is involved in a relevant number of cellular activities and represents an important factor in the immune response, particularly in human dendritic cells (DCs). Over the past several years, significant insights into the IGF-independent effects of IGFBP-6 were discovered, such as the induction of chemotaxis, capacity to increase oxidative burst and neutrophils degranulation, ability to induce metabolic changes in DCs, and, more recently, the regulation of the Sonic Hedgehog (SHH) signaling pathway during fibrosis.”
From the article:
“There is significant evidence demonstrating the role of IGFBP-6 in fibrotic and connective tissue, also starting with the point that both TGF-β and oxidative stress conditions increase IGFBP-6 expression levels in fibroblasts.
Likewise, IGF-1 and IGFBPs are involved in the pathophysiology of Non-Alcoholic Fatty Liver Disease (NAFLD) and in the regulation of glucose homeostasis. In the liver, the decrease of IGF-1 levels contributes to the development of NAFLD and non-alcoholic steatohepatitis, also related to the hepatic expression of several IGFBPs. Specifically, IGFBP6 levels are higher in relation to increasing steatosis, while the hepatic expression of IGFBP-6 is strongly positively associated with fibrosis, steatosis grade, and NAFLD activity score [54]. Remarkably, circulating IGFBP-6 resulted significantly reduced after the treatment with the GHRH-analogue Tesamorelin, which reduces liver fat and prevents fibrosis in patients with NAFLD.”
ijms-23-04358-v2 (3).pdf