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 into the quagmire of high fat and high carb human metabolism doesn't know what to do if liver glycogen stores are full and we put in lots of fat and carbohydrates we're gonna get de novo lipogenesis and we're gonna store fat
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you can get insulin resistant in the liver to the suppression of gluconeogenesis while you maintain sensitivity to the effect of insulin on the de novo wastage ennis yes that's the worst outcome yes but that's what happens
we know in the liver that insulin is responsible for de novo lipogenesis that is if you have a lot of carbohydrates glucose it will build it into glycogen and that is working fine if there's too much glucose after the glycogen is full its gonna turn it into triglycerides or fat and that is working fine so de novo lipogenesis is working fine
how can it be that you have a liver cell which can't let in the glucose so it's resistant to the insulin yet the other effect of insulin which is de novo lipogenesis is not only working fine it's actually going overtime right you can measure de novo lipogenesis and type 2 diabetes it's super super high
there's a central paradox of insulin resistance which is that insulin has actually many many different functions only one of which is letting glucose into the cell so for example we know in the liver that insulin is responsible for de novo lipogenesis that is if you have a lot of carbohydrates glucose it will build it into glycogen and that is working fine if there's too much glucose after the glycogen is full its gonna turn it into triglycerides or fat and that is working fine so de novo lipogenesis is working fine
you look at the changes in fat and this carbohydrate this is change in liver triglyceride it's up two and a half 2.3 fold you put some heavy water stable heavy water into the milkshake to track denver lipogenesis that's the conversion of glucose to fat and that's also up greater than twofold
when you have muscle insulin resistance specifically it will drive the liver fat synthesis by dnl when you have that when your liver is making more fat through dnl it makes more bldl exports so plasma triglycerides go up and hdl goes down