High-Fat Diet Promotes Glycogen Storage, Counter-Intuitively.

The title of this study is a bit misleading.  It's actually a fascination look into what a High-Fat, Low-Carb diet does in the body.  This is an important paper because many scientists seem to think that because a high-fat diet makes peripheral tissues insulin resistant, and diabetes does the same, the two are therefore equivalent.

"Dietary fat content alters insulin-mediated glucose metabolism in healthy men." 

"...Six healthy men were studied on 3 occasions after consuming for 11 d diets with identical energy and protein contents but different percentages of energy as fat and carbohydrate as follows: 0% and 85% [low-fat, high-carbohydrate (LFHC) diet], 41% and 44% [intermediate-fat, intermediate-carbohydrate (IFIC) diet], and 83% and 2% [high-fat, low-carbohydrate (HFLC) diet].... 

"Conclusion: A high-fat, low-carbohydrate intake reduces the ability of insulin to suppress endogenous glucose production and alters the relation between oxidative and nonoxidative glucose disposal in a way that favors storage of glucose."

But the meat isn't in the abstract.  If we read on:

"...Remarkably, in the context of diabetes risk, 2 aspects of glucose homeostasis actually improved after consumption of the HFLC diet: decreased basal endogenous glucose production and improved insulin-stimulated nonoxidative glucose disposal. This observation might prove critical in the design of future studies."

Over-production of glucose by the liver is one of the signature features of type II diabetes, in fact, and is the main reason that those diabetics have hyperglycemia (high blood sugar).

This also helps to explain one of the more counter-intuitive findings of the FASTER study.  This study explains:

"Even though the dietary fat content did not conclusively alter total glucose disposal, there were marked effects of dietary fat content on both oxidative and nonoxidative glucose disposal. Higher dietary fat contents resulted in increased insulin-stimulated nonoxidative glucose disposal and reduced carbohydrate oxidation, suggesting that insulin stimulates glycogen synthesis more effectively when dietary fat intakes increase and carbohydrate intakes decrease. This agrees with the increase in glycogen synthase activity by insulin observed after the consumption of high-fat diets (3). In contrast, the HFLC diet inhibited the stimulatory effects of insulin on glucose oxidation. Therefore, a high-fat, low-carbohydrate diet appears to result in a dissociation with respect to the effects of insulin on oxidative and nonoxidative glucose pathways."

The FASTER study (which I've not really blogged about, much to my surprise, just this) found that HFLC athletes used as much glycogen as high-carb athletes, and recovered glycogen stores just as quickly.  If an HFLC diet promotes glycogen replenishment, that would explain how the glycogen stores recovered so quickly, as the liver's clearly capable of producing far more glucose than the body really needs, as demonstrated in type II diabetes.

I'll also note my post on thyroid hormones, which observes that much of the effect of glucose disposal is controlled by thyroid hormones, not just insulin.  This study doesn't discuss that effect at all.  The reduction in T3, which stimulates oxidative glucose disposal, could well explain this effect,