The evidence is convergent. Multiple independent sources reach the same conclusion, the underlying mechanism is well-characterized, and even the field's most cautious voices treat it as worth doing.
When you get glucose to the muscle the glucose goes into the muscle if you're not moving the muscle it's not going to turn more glucose to energy it will switch from free fatty acid to glucose but that but there's no more glucose burning so it goes to glycogen right and it goes to glycogen but you keep on putting glucose in the muscle and there's just so much glycogen that the muscle can store so the muscle has to become insulin resistance
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.
as this big fatty liver goes down the insulin resistance starts to melt away
I've shown you that block is a transport and then i've given you a molecular understanding of how that insulin resistance in muscle happens my view is slip and dice of glycerol is blocked leading to activation of a novel protein kinase c epsilon theta blocking insulin signaling okay so let's now and then i've shown you how muscle insulin resistance can lead to fat accumulation in liver atherogenic disobedima and fatty liver
you now make it harder for your carbohydrate storage unit to accept carbohydrates and of course that leads to hyperglycemia and ultimately diabetes