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Glycogen storage diseases (GSDs) belong to the group of inborn errors of carbohydrate metabolism. Hepatic GSDs predominantly involve the liver and most present with hepatomegaly. Biochemically they show known disturbances in glucose and fatty acids metabolism, namely fasting hypoglycaemia and increased triglycerides. Additionally, increased biotinidase (BTD) enzyme activity has been shown to be associated with many GSD types, whereas the mechanism by which BTD enzyme activity is altered remains unknown so far. We aimed to delineate chan
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