According to a scientific paper presented by specialists from the University of Colorado Anschutz and published in the journal Nature Metabolism, it was found that the enzyme known as ketohexokinase (KHK) plays a central role in this mechanism. Experiments conducted on mice demonstrated that in cases of KHK deficiency, the test animals showed a significant weakening of cravings for alcohol. They consumed less alcohol, their response to reward-related stimuli changed, and reduced activity was recorded in the brain regions responsible for the formation of addictive behavior. Furthermore, it was discovered that inhibiting KHK activity prevents the development of alcoholic hepatopathy. These rodents did not develop typical fat infiltrates, inflammatory processes, or signs of fibrosis. Scientists believe that regulating fructose metabolism pathways may serve as a way to slow down or even completely prevent alcohol-induced liver pathologies. “Our data suggest that ethanol not only causes direct damage to hepatocytes but also interferes with sugar metabolism in such a way that, on the one hand, it potentiates the craving for alcohol, and on the other, it exacerbates liver damage. By acting on fructose metabolism processes, we open up the possibility of interrupting this destructive cycle and developing innovative therapeutic approaches for both combating alcohol addiction and treating co-occurring lesions,” emphasized Professor Miguel A. Lanaspa from the University of Colorado.
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