NAFLD: From Pathogenesis to Clinical Impact This article was published in January 2021 on MDP1 (Multidisciplinary Digital Publishing Institute), they are discussing the role IR (Insulin resistance), mitochondria (cell membrane) dysfunctions, and adipose tissue (fat) and causation of NAFLD/NASH.
Tesamorelin decreases insulin resistance, improves mitochondrial function and reduces visceral fat, the totality of data is real, promising and innovative when other approaches have failed miserably.
“IR plays a key role in the development of NAFLD, as it causes an increase in hepatic lipogenesis(fatty liver) and an inhibition of adipose tissue lipolysis(breakdown of fat), with a subsequent elevated flow of fatty acids in the liver.
All structural and functional alterations in the mitochondria contribute to the pathogenesis of NAFLD.
Reduced levels of adiponectin (protein braking down fat) during obesity may result in mitochondrial dysfunction and insulin resistance. As a whole, the reduced levels of adiponectin and the increased levels of leptin (hormone made by fat cells) in patients can induce steatosis and liver inflammation, thus activating fibrogenesis.
As discussed, visceral adipose tissue can cause NAFLD and NASH, also inducing a chronic inflammatory state.”
https://res.mdpi.com/d_attachment/processes/processes-09-00135/article_deploy/processes-09-00135.pdf