Beyond its primary usage in the treatment of type 2 diabetes, empagliflozin, an inhibitor of sodium-glucose co-transporter 2 (SGLT2), has demonstrated potential advantages in other areas. Recent data suggests that empagliflozin may have a wider function in treating metabolic health conditions such non-alcoholic fatty liver disease (NAFLD) by lowering liver fat content in people with and without diabetes.
Excess fat builds up in the liver (NAFLD) and can lead to more serious consequences such as liver fibrosis and non-alcoholic steatohepatitis (NASH). It is of great clinical interest to discover therapeutic approaches to address NAFLD, given its increasing prevalence. The mechanism by which empagliflozin reduces liver fat has been explained in a number of ways. Its diuretic action causes weight loss, which significantly reduces the buildup of hepatic fat.
Empagliflozin has been shown in clinical investigations to significantly reduce liver fat content, as measured by proton density fat fraction (PDFF) based on magnetic resonance imaging (MRI). These results are seen in populations with and without diabetes, indicating the medication’s wider application in the treatment of metabolic diseases. These discoveries have broad ramifications. They emphasize how crucial it is to think about SGLT2 inhibitors for disorders other than diabetes management while managing illnesses like non-alcoholic fatty liver disease (NAFLD). Future studies should concentrate on comprehending empagliflozin’s long-term effects on liver health and its possible contribution to stopping NAFLD from developing into more serious liver illnesses.
In conclusion, the capacity of empagliflozin to lower liver fat in a variety of patient populations offers a potential approach to treating the growing challenge of fatty liver disease, supporting the use of SGLT2 inhibitors in broader metabolic health management.
Main article link: https://diabetesjournals.org/care/article-abstract/47/4/668/154175/Empagliflozin-Reduces-Liver-Fat-in-Individuals?redirectedFrom=fulltext
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