Mounting criticism of NIH's relationship with the alcohol industry

Re:Mounting criticism of NIH's relationship with the alcohol... by subcosmos on Tuesday April 03, 2018 @04:16PM (#16748665)

Insulin is a driver for obesity, but its really secondary. The primary condition that precedes most metabolic syndrome complications is liver fat accumulation. When this happens, liver cells become insulin resistant and consequently start synthesizing glucose unnecessarily, which floods the bloodstream with excess glucose and subsequently drives insulin higher to sink it into peripheral tissues. Its been demonstrated over decades that the hyperglycemia of diabetes is caused by this liver synthesis of glucose, and not dietary factors.

Alcohol (ethanol) gets processed by the liver and enters the denovo lipogenesis pathway, becoming fat, which can accumulate in the liver if the lipid transporting machinery (LDL particles) are overwhelmed. This leads to Alcoholic Fatty Liver Disease (AFLD) and the "beer belly". Excess fructose consumption has been tied to Nonalcoholic Fatty Liver Disease (NAFLD) for many of the same reasons.

Some day we'll figure out why lipid droplet accumulation leads to insulin resistance. Some people think its tied to fuel selection and the evolved starvation response.

https://www.ncbi.nlm.nih.gov/pubmed/87483

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Re:Mounting criticism of NIH's relationship with the alcohol... by DenisM on Tuesday April 03, 2018 @08:16PM (#16750721)

First you say it's not primarily about insulin, then you say that excess of glucose drives up insulin, leading to fat deposits. It's the insulin that directly controls fat deposits at th cellular level, is it not? And you do not have to have insulin resistance in order to drive your insulin up - just eating a pile of pastries will do it. You probably know more than me, could you please clarify?

[ Parent | on HN ]