Abstract
Anti-Diabetic Effects of Niclosamide Ethanolamine and Metformin in Mouse Models
Highlights
Type 2 diabetes has become one of the most challenging health problems in the United States and around the world [1,2]
Insulin resistance, which is closely associated with obesity and ectopic accumulation of fat in liver and muscles, precedes the development of type 2 diabetes [19,20]
It is critically important to address experimentally the potential drug-drug interaction between the mechanisms represented by NEN and by metformin, as in future clinical trials most type 2 diabetes patients would have been on metformin medication
Summary
Type 2 diabetes has become one of the most challenging health problems in the United States and around the world [1,2]. Metformin is the first-line drug for treating type 2 diabetes. The function of metformin has been attributed to its suppression of hepatic gluconeogenesis, though the underlying mechanism remains unclear. It was initially believed that metformin is a mitochondrial respiratory chain complex I inhibitor, through which metformin indirectly inhibits hepatic gluconeogenesis [3,4]. Later studies support that metformin activates AMP-Activated Protein Kinase (AMPK) and leads to reduction of gluconeogenic gene transcription [5,6,7]. Metformin is found to inhibit the mitochondrial glycerophosphate dehydrogenase directly, thereby reduces conversion of lactate and glycerol to glucose and results in decrease in hepatic gluconeogenesis [8]
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