Eddy Edson
Well-Known Member
- Relationship to Diabetes
- In remission from Type 2
In mice, anyway.
http://news.vumc.org/2018/09/06/teams-findings-could-spur-new-treatments-for-type-2-diabetes/
Fructose 1,6-bisphosphatase (FBP1) is a rate-controlling enzyme in the production of glucose by the liver.
In a series of elegant experiments, the researchers demonstrated that the enzyme also functions as a major contributor to the therapeutic action of metformin.
In particular, they found that metformin induces mild energy stress in the liver, leading to an increase of adenosine monophosphate (AMP).
This chemical compound, in turn, inhibits FBP1 and turns down glucose production by the liver.
Wasserman, director of the National Institutes of Health-funded Mouse Metabolic Phenotyping Center (MMPC) at Vanderbilt University Medical Center, is a pioneer in the development and optimization of miniaturized experimental techniques for conducting metabolic studies in a mouse model.
Using a variation of techniques developed here, the Vanderbilt researchers showed that in mice with a mutated and abnormally functioning FBP1 enzyme, the glucose-lowering effect of metformin was significantly reduced.
These findings validate FBP1’s role in lowering blood glucose, and suggest that it may be possible to mimic the energy-stressing effect of metformin on the liver through the use of natural substances that avoid the drug’s side effects, notably diarrhea and abdominal discomfort.
http://news.vumc.org/2018/09/06/teams-findings-could-spur-new-treatments-for-type-2-diabetes/
Fructose 1,6-bisphosphatase (FBP1) is a rate-controlling enzyme in the production of glucose by the liver.
In a series of elegant experiments, the researchers demonstrated that the enzyme also functions as a major contributor to the therapeutic action of metformin.
In particular, they found that metformin induces mild energy stress in the liver, leading to an increase of adenosine monophosphate (AMP).
This chemical compound, in turn, inhibits FBP1 and turns down glucose production by the liver.
Wasserman, director of the National Institutes of Health-funded Mouse Metabolic Phenotyping Center (MMPC) at Vanderbilt University Medical Center, is a pioneer in the development and optimization of miniaturized experimental techniques for conducting metabolic studies in a mouse model.
Using a variation of techniques developed here, the Vanderbilt researchers showed that in mice with a mutated and abnormally functioning FBP1 enzyme, the glucose-lowering effect of metformin was significantly reduced.
These findings validate FBP1’s role in lowering blood glucose, and suggest that it may be possible to mimic the energy-stressing effect of metformin on the liver through the use of natural substances that avoid the drug’s side effects, notably diarrhea and abdominal discomfort.
