Much of the time we hear lots of negativity about T3 (liothyronine, triiodothyronine). We are told it will have horrendous effects on us - even in small doses.
While this study is on mice, it claims very significant benefits of T3 in relation to alcohol and liver disease.
Mechanism of triiodothyronine alleviating acute alcoholic liver injury and delaying alcoholic liver fibrosis progression
Renli Luo 1 2 , Sanqiang Li 1 2 , Mengli Yang 1 2 , Junfei Wu 1 2 , Jiayang Feng 1 2 , Yue Sun 1 2 , Yadi Zhao 1 2 , Longfei Mao 1
PMID: 40170552 DOI: 10.1177/09603271251332505
Abstract
Introduction
Alcoholic liver disease poses a severe threat to human health. The thyroid hormone Triiodothyronine (T3) is closely related to liver metabolism. This study investigated the effect and mechanism of T3 in alcoholic liver injury.
Methods
Acute alcoholic liver injury model was established in mice by alcohol administration. Alcoholic liver fibrosis models were established in vivo and in vitro using hepatic stellate cells (HSC)-T6 cells and mice. The role and regulatory mechanism of T3 in the occurrence and progression of alcoholic acute liver injury and fibrosis were analyzed by evaluating key factors involved in cell proliferation and apoptosis, inflammatory response, oxidative stress, and autophagy using histopathological staining.
Results
The results showed that T3 at low and medium concentrations reduced inflammation and oxidative damage in acute alcoholic liver injury and inhibited HSC activation and delayed the onset and progression of alcoholic liver fibrosis in mice. T3 inhibited the PI3K/AKT and NF-κB signal pathway, increased Nrf2 expression levels, and restored liver autophagy. However, high T3 concentrations had the opposite effect.
Discussion
Optimal T3 concentrations protects the liver from alcoholic liver injury by inhibiting inflammatory response and oxidative stress injury and by restoring hepatocyte proliferation, apoptosis, and autophagy.
Keywords: alcoholic liver disease; autophagy; hepatic stellate cells; liver fibrosis; oxidative stress; thyroid hormone.
Open access:
https://pubmed.ncbi.nlm.nih.gov/40170552/
https://doi.org/10.1177/09603271251332505
https://journals.sagepub.com/doi/10.1177/09603271251332505
