The headline is broadly defensible, but the qualifications matter. Effect sizes vary by population, the strongest claims rest on shorter trials, and credible voices push back on how it's typically framed.
when you simply mutate that three nutrient alone now you have perfectly normal hepatic insulin sensitivity as reflected by insulin's ability to suppress hepatic glucose production and this is despite the same amount of liver fat same amount of liver dags in the liver
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Native comments, Twitter mentions, and Reddit threads about this claim — surfaced together so the conversation isn't fragmented across platforms.
Bookmarking — the dossier-vs-overview split is the right call. Most of the time I want overview; sometimes I want receipts.
Would love a "what would change this verdict" RSS feed. Sign me up if it exists.
here in this paper we made mice where we replaced the threonine in that key position the 11 this is the mouse homolog the 1150 is the homolog for the 11 16 humans so all the threonines are instead alanines and i won't get into the data and say the mice are perfectly normal normal chow normal insulin sensitivity nothing near normal size normal growth but when max fed these mice a high fat diet the wild type mice get profound hepatic insulin resistance