Primary endpoint change in hepatic fat fraction. I

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Primary endpoint change in hepatic fat fraction. I don't know enough about it to know how Leron would affect hepatic fat. If Ohm or CTMedic or any of the others with wisdom felt like elucidating how that MOA would work, I'd be grateful.

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CCR5 does reduce fat but they don't elucidate it in this abstract.

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Reduced adipose inflammation was associated with reduced body weight gain and a reduction (37%, P<0.05) in white adipose fat which occurred without significant effect on food intake.
https://www.ahajournals.org/doi/10.1161/circ....18.S_503-c

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A possible explanation - Mitochondria are cells that are essential in the conversion of glucose to energy. Excessive damage to mitochondria means less efficient usage of glucose and more storage to fat. a1-antitrypsin is protective of mitochondria.

IL-13 is increased in inflammatory states. IL-13 can significantly decrease amounts of a1-antitrypsin. CCR5 blockade downregulates IL-13 leading to an increase in a1-antitrypsin and protection of mitochondria.

I originally ran into a1-antitrypsin while looking at Covid caused mitochondria damage. What's interesting is that low levels of a1-antitrypsin are also implicated in liver disease and pulmonary inflammation. No one seems to have made the connection between CCR5 blockade, IL-13, a1-antitrypsin and mediation of a variety of diseases.