tag:blogger.com,1999:blog-827769867360256958.post1079195421343130592..comments2024-01-14T03:16:09.597-08:00Comments on Kindke's Scrap Notes: Fucked up glucose digestion in obesityKindkehttp://www.blogger.com/profile/15841418412425329998noreply@blogger.comBlogger1125tag:blogger.com,1999:blog-827769867360256958.post-5881327326937240762014-12-01T02:25:56.898-08:002014-12-01T02:25:56.898-08:00The speculation about possibly enhanced duodenal g...The speculation about possibly enhanced duodenal glucose transporters is very interesting.<br /><br />Your talk of carb refinement/digestibility reminds me of this paper "Comparison with ancestral diets suggests dense acellular carbohydrates promote an inflammatory microbiota, and may be the primary dietary cause of leptin resistance and obesity”. You might find it worth your time.<br /><br />I think the causality pathway you outlined here is correct but I see it as an extension/refinement of the causal chain, not as an overturning of "...hyperglycemia and hyperinsulinemia in obese people is due to insulin resistance…”. The latter simply points to the tipping-point variable (insulin) as being primarily responsible for the actual accumulation of FAs in adipose cells. Your/the papers' causal chain simply place refined CHO as the prime external candidate capable of triggering that deciding variable (insulin). That makes all the sense in the world. However, it seems like insulin is still ‘central’ because (for e.g.) circadian timing could replace refined CHO & your causal chain would still make total sense.<br /><br />I don’t think it's semantics - actually, the morphological changes to the intestine might be a proxy marker for CHO-induced IR &/or adipocyte enlargement/proliferation. It’d be helpful to distinguish between other sources of IR or manners in which adipocytes make become dysregulated.<br /><br />We know from Bill’s last post how important circadian timing is acetylating/deacetylating histonesraphihttps://www.blogger.com/profile/08992252569979714724noreply@blogger.com