MCT for Health

Provocative headline, right? Gluconeogenesis is the enzymatic production of glucose from other substrates, usually from lactate or glycerol. It occurs mostly in the liver, but it’s active in other organs too—I think even in the kidneys. That’s not important. It’s part of the so-called Cori cycle, where lactate produced by muscle exertion is recycled into glucose in the liver. Feel that? We know that exercise is healthy, including the production of lactate by muscle activity. We even have studies showing that adding lactate improves the metabolism of obese mice . When I wrote about this, I couldn’t imagine there could be another mechanism than the one where lactate facilitates the entry of acetate into cells via MCT1 membrane transporters. Maybe there is another mechanism paradoxically related to the activation of gluconeogenesis itself.  The headline could also have been something like: Endogenous Production of Nonessential Amino Acids Treats Obesity. But that wouldn’t sound as pa...

Although all nutrition experts keep convincing us that we eat too little protein—because we supposedly need all essential amino acids to build muscle—things may be far more complicated. I’d say this view of metabolism comes from findings based on studying athletes. But I’m definitely not an athlete. I understand that top athletes need to regenerate muscle with enough branched-chain amino acids (BCAAs), for example. However, the general population doesn’t wear down their muscles very much and probably recycles amino acids to a greater extent without needing to supply new ones. Mice in studies are active, but they don’t undergo any special performance training. So they may be a good model for the general population. I’ve already written here about how protein affects mouse longevity . Now let’s discuss one study that examined the short-term effects of lower protein intake on the organism using a mouse model . The study lasted only one week. Yet the changes are very striking. I increasing...

In several previous posts I showed how fructose production in the liver affects metabolism through a vicious cycle of obesity . Fructose created from glucose through the polyol pathway in the liver—acts specifically via the enzyme fructokinase (KHK), which activates fructose—affects the acetylation of dozens of other enzymes through sirtuins. This makes fructose the main regulator of hepatic calorie partitioning, determining where excess energy from food is directed: either into liver glycogen or into fat, which is then sent out as VLDL to be processed by the body. In addition to regulating the allocation of calories between immediate use and transformation into fat (for storage or burning in the body), fructose also helps regulate hunger. Blocking hepatic fructokinase makes it impossible to convert calories into fat and increases the storage of excess calories in liver glycogen. A regulatory mechanism via the brain then ensures a lower need to eat and suppresses hunger. Excesses there...

I didn’t even realize that The Vicious Cycle of Obesity could be quite a good explanation for commenting on the results of an interesting longevity study. On X, an innocent question appeared: Quote Someone needs to explain this. "In total, 1224 participants lived to their 100th birthday" Higher levels of total cholesterol and iron and lower levels of glucose, creatinine, uric acid, aspartate aminotransferase, gamma-glutamyl transferase, alkaline phosphatase, lactate dehydrogenase, and total iron-binding capacity were associated with reaching 100 years. End of quote What is the author of the question getting at? At the results of an interesting Swedish study , in which the authors sought to describe and compare the biomarker profiles of people between the ages of 64 and 99 who eventually became centenarians, with their peers who did not reach 100 years of age. They examined how homogeneous the biomarker profiles of centenarians were earlier in life. For this, they used data f...

I’ll loosely follow up on an earlier post, where I examined the properties of fructose and acetate and how they act against each other . That post mainly dealt with enzyme acetylation — that is, the change of their “decoration” by an acetyl group. Fructose suppresses the deacetylase SIRT2 and probably also SIRT1. Acetate, on the other hand, activates SIRT1 and possibly SIRT2. Both substances thus act as regulators of the same processes, but in opposite directions. They therefore ensure balance. That’s important, because if there is an excess of one substance, its effect can be compensated by the other; we’re not left without a means of compensation — and that’s crucial. Today I’d like to connect this model with the vicious cycle of obesity , as I described in previous posts. Few people realize that the effect of polyunsaturated oils on metabolism is, in fact, the effect of fructose produced via the polyol pathway in the liver through the presence of aldehydes such as 4-HNE. This is how...