Coconut oil has found its way into German kitchens more and more frequently in recent years, although its supposed health-promoting effect is controversial. Scientists at the University of Bonn have now been able to show how it is metabolized in the liver. Your results could also have consequences for the treatment of certain diarrheal diseases. The results were published in the journal Molecular Metabolism.
Coconut oil differs from rapeseed or olive oil in the fatty acids it contains. Fatty acids are made up of carbon atoms bonded together, usually 18. In coconut oil, however, most of these chains are significantly shorter and contain only 8 to 12 carbon atoms. In the liver, these medium-chain fatty acids are partially converted into storage fats (triglycerides). How exactly this happens was previously largely unknown.
The new study now sheds light on this: “There are two enzymes in the liver for storage fat synthesis, DGAT1 and DGAT2,” explains Dr. Klaus Wunderling from the LIMES Institute (the acronym stands for “Life & Medical Sciences”) at the University of Bonn. “We have now seen in the liver cells of mice that DGAT1 mainly processes medium-chain fatty acids and DGAT2 processes long-chain fatty acids.”
In their experiments, the scientists blocked DGAT1 with a special inhibitor. The synthesis of storage fats from medium-chain fatty acids decreased by 70 percent. However, the blockade of DGAT2 led to a decreased processing of long-chain fatty acids. “The enzymes seem to prefer different chain lengths,” concludes Prof. Dr. Christoph Thiele from the LIMES Institute, who led the study and is also a member of the Immunosensation Cluster of Excellence.
Surprising side effect
Whether fatty acids are actually used in the liver to build up storage fat depends on the current energy requirement. When the body needs a lot of energy, the so-called beta-oxidation is started – the fatty acids are in a sense “burned” directly. This metabolic pathway is of great medical interest. In the case of diabetes, for example, it can be useful to reduce beta-oxidation. Because then the body has to meet its energy needs from glucose instead – the blood sugar level drops, which has a positive effect on the disease.
Therefore, around 40 years ago, pharmaceutical researchers developed a corresponding inhibitor, Etomoxir. It binds to enzymes for beta oxidation and brings them to a standstill. However, it quickly became apparent that Etomoxir had massive side effects.
The Bonn researchers have now discovered a possible reason for this: with Etomoxir, they inhibited the combustion of medium-chain fatty acids in mice in the expectation that this would stimulate the production of storage fat. “Instead, fat synthesis also decreased significantly, but only from storage fats with medium-chain fatty acids,” explains Wunderling. “We therefore suspect that Etomoxir also switches off the DGAT1 enzyme.” Such effects must be taken into account in the future when developing new inhibitors for beta oxidation.
Another interesting result is that Austrian and Dutch scientists published a few years ago: They examined patients suffering from chronic diarrheal diseases. They found changes in the DGAT1 gene in 20 of them, which rendered them functionless. “We now want to find out whether the impaired processing of medium-chain fatty acids is responsible for the digestive problems,” says Wunderling. The DGAT1 enzyme is not only active in the liver, but also in the intestine. Perhaps his disorder therefore causes diarrhea when those affected ingest medium-chain fatty acids. Wunderling: “In that case, you could possibly simply help them – through adequate nutrition.”
Wunderling K., Leopold C., Jamitzky I. et al. The hepatic synthesis of triacylglycerols, which contain medium-chain fatty acids, is dominated by diacylglycerol acyltransferase 1 and effectively inhibited by Etomoxir. Molecular metabolism. 2021; 45: 101150. doi: 10.1016 / j.molmet.2020.101150
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