on May 25, 2013
at 05:25 PM
The inherent definition of a statin is a drug that inhibits the enzyme HMG-CoA reductase. When this enzyme is inhibited you make less farnesyl-pyrophosphate, which itself is used to synthesize both cholesterol (explaining why statins lower cholesterol) and, among other things, an antioxidant called Coenzyme Q10 (aka ubiquinone). Here's a flow chart of the pathway:
There's a theory that reverse electron flow in the electron transport chain, which can otherwise be reversed by CoQ10, can lead to superoxide production (1), a problematic radical compound which is thought to be an underlying cause of insulin resistance (2).
Regardless of the specifics of the proposed molecular mechanism, taking statins can decrease CoQ10 levels (3) and taking a CoQ10 supplements can improve insulin sensitivity (4,5,6), and statins have been shown to increase diabetes risk (7,8), thus it seems like a logical conclusion.
So I think CoQ10 depletion is part of how statins increase diabetes risk, despite no conclusive evidence of this. Though I would bet it's only part the reason. Of the top of my head, maybe fatigue and myalgia, often side effects of statins, decrease the desire to exercise and that contributes. I don't really know for sure, though I'm not sure anyone does at this point.
on June 26, 2013
at 12:02 PM
Statins are among the most widely prescribed medications for the prevention of cardiovascular events. Although tolerated well, an association with new-onset diabetes has recently been suggested. One trial suggested a 27% increased risk of diabetes with rosuvastatin whereas another suggested patients taking pravastatin benefitted from a 30% lower risk. Use this drug forum to know more.