So it's protective against a 'high fat diet' in mice. Read as: high sugar, high fat. Or if it's not high in sugar, stop thinking oreos, start thinking Doritos.

Lower respiratory quotient=a decrease in glycolysis, an increase in oxidation of fat--not absolute, relative to each other as a ratio. But higher energy expenditure means of course that there is an increase in fat oxidation. Interesting that food intake also goes up.

From the graphs, it looks like actual glycogen levels go up maybe a quarter to a third. Just eyeing bar graphs here. But incorporation of labeled carbohydrate into liver glycogen looks more like ten-fold with the procedure. So there must be an increase in overall glycogen turnover--just increasing glycogen synthesis to the point where there's a ten-fold increase in labeled glucose storage in glycogen would result in much higher glycogen levels, unless there's also an increase in breakdown.

Only just occurred to me what conspiracy theorists will do with this if people with type II start walking around with personal EMF devices.

Primary effect seems to be in the liver, liver glycogen is increased.

HIgh fructose feeding doesn't primarily result in weight gain in mice. That takes a combination of fat, fructose, breed. Just replacing a high starch or glucose diet with a high fructose diet is more of a model of insulin resistance/diabetes. One thing high fructose does is put a load on the liver--compared to glucose, it's preferentially stored as liver glycogen. Perhaps by increasing liver glycogen capacity, there's a protective effect.

Increased liver glycogen might help the liver to supply glucose to the brain more reliably over the 24 hour course of a day. Some researchers have sort of a 'selfish brain' hypothesis, where the brain allows obesity to develop, needs to allow it to develop, under certain dietary etc. circumstances, to keep its own fuel supply stable.