In “RealAge, real stupid, real sleazy,” Dr. Michael Eades wrote:
The ‘important appetite-suppressing molecule’ under discussion is the enzyme malonyl-coenzyme A (malonyl-CoA), which is one of the major signaling molecules in the body. Malonyl CoA sits at the crossroad of fat storage and fat burning and drives the reaction one way or another.
If we’ve eaten a lot, especially a lot of carbohydrate, malonyl-CoA levels increase. Increased levels of this enzyme then shift the flow of fat away from burning and toward storing. Among its activities, Malonyl-CoA stimulates fatty-acid synthase (FAS), the enzyme that converts carbohydrate to fat. And it inhibits the enzyme (CPT-1) that carries fat into the mitochondria where it is burned for energy.
If we haven’t eaten, or if we have been eating a low-carb diet, the opposite happens. Malonyl-CoA levels are low, which removes the inhibition of CPT-1. Fat is shunted away from storage in the fat cells and instead is transported into the mitochondria where it is burned.
If you do a quick thumb through any decent medical biochemistry textbook looking for what makes malonyl-CoA go up, you’ll find that it is driven up by insulin and glucose, the surrogates for being well fed. But here is where Roizen/Oz and the team of experts go off the rails. The glucose in question isn’t dietary glucose – it’s blood glucose. As I’ve written about before, the entire amount of glucose we have circulating through us if we have a normal blood sugar level is around 4 grams, a little less than one teaspoon. If we eat a medium-sized baked potato, we ingest about 50 grams of glucose (potato starch is made of pure glucose), which is more than ten times the amount regularly circulating in our blood. Our bodies quickly deal with this excess by increasing insulin and driving the glucose into the cells. As a practical matter, dietary glucose never really impacts malonyl-CoA. What does impact it is the level of blood sugar. So if blood sugar is higher than normal, then more malonyl-CoA is made, and more fat is stored. Which is one of the reasons type II diabetics are usually obese to some extent. These people have the double whammy of two much sugar and, since they’re almost always insulin resistant, too much insulin.