Stevia - can it help with Hepatic IR?

A recent study has put forward the proposal through experimental verification that indeed Stevia may help with hepatic IR by lowering the enzymes responsible for glucose production.

The main enzymes involved in hepatic glucose production are....

• Glucose 6-phosphatase ( G6Pase )
  
• Phosphoenolpyruvate carboxykinase ( PEPCK )
• Pyruvate carboxylase
• Fructose-1,6-bisphosphatase

The last one, Fructose-1,6-bisphosphatase ( FBPase ), seems to be a strong likely suspect for increased hepatic glucose production. Claims have been made that the first 2 enzymes on our list, G6Pase and PEPCK are not responsible for the increased hepatic glucose production seen in diabetes and hepatic IR.

Further incrimination comes from a 2001 study looking at Metformin's actions on the above 4 enzymes. They found that metformin decreased both endogenous glucose production and alanine gluconeogenesis, there was a strong association bewteen alanine gluconeogenesis and FBPase levels, and metformin was able to reduce hepatic FBPase levels by a whopping 50%! Importantly, they did not record any significant changes in the other gluconeogenic enzymes.

So..... it looks like all fingers are pointing firmly at --> Fructose-1,6-bisphosphatase <--

Evil bitch!

Sadly I dont have access to the full text of the stevia study so I cant really disect the meaningfulness of thier conclusions, but if stevia works by Fructose-1,6-bisphosphatase reduction that could be good news. Not only is FBPase involved in hepatic glucose production however, it may even have an affect on adiposity.

Right now I cant help but think that increased hepatic glucose production leads to increased fasting glucose oxidation and thus gets in the way of fat oxidation in the fasting state. This was somewhat alluded to in the gnolls.org post here.

This study looking and respiratory quotients brings up an interesting conclusion....

a low ratio of fat to carbohydrate oxidation is associated with subsequent weight gain independent of low energy expenditure and may contribute to the familial aggregation of obesity.

That "independent of low energy expenditure" part is interesting, something we learnt about in the last post. About how basal energy expenditure is not related to adiposity, well, that seems to agree with the independent thing mentioned above.