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.
one is you can knock out akt or foxo and give insulin to the mouse and you can still turn off gluconeogenesis in a fasted mouse which is totally dependent on gluconeogenesis that speaks to the fact you don't need these key insulin signaling pathways to regulate gluconeogenesis
Every Sunday: the week’s new conflicts and verdict changes — and nothing else.
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.
traditionally pretty much the major textbooks physiology biochemistry insulin is thought to be turn off gluconeogenesis through transcriptional mechanisms and again this is the spoxo phosphorylation by akt exclusion from the nucleus then you get down regulation of pepsi cake excuse me and six phosphatase foxo is the transcription regulator for these down regulation