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.
everyone assumes well you get fat therefore your fat cells make cytokines like tnf-alpha and il-6 those then go via the portal system to the liver and cause the liver to be dysfunctional and therefore you increase hepatic glucose output that then causes your beta cells to have to over produce insulin and then that drives the 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.
but the transition from just insulin resistance in liver and muscle to fasting hyperglycemia depends on inflammation and it's through this mechanism where now you have localized inflammation in the fat cell tnf alpha il-6 i'm sure there's other things will promote increased lipolysis in the fat cell more lipolysis more fatty acid delivery to liver dags go up epsilon gets activated you block insulin action so less glucose being taken up into glycogen