AMPK tagged posts

Scientists Block RNA Silencing Protein in Liver to Prevent Obesity and Diabetes in Mice

Effects of hepatic Ago2-deficiency on MD-miRNA expression in the liver

Effects of hepatic Ago2-deficiency on MD-miRNA expression in the liver

New treatment for a major health problem? Obesity and its related ailments like type 2 diabetes and fatty liver disease pose a major global health burden, but researchers report in Nature Communications that blocking an RNA-silencing protein in the livers of mice keeps the animals from getting fat and diabetic conditions.

Takahisa Nakamura, PhD, and colleagues at Cincinnati Children’s Hospital Medical Center genetically deleted a protein called Argonaute 2 (Ago2) from the livers of mice. Ago2 controls the silencing of RNA in cells, affecting energy metabolism in the body, according to the study...

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Discovery may be key to Obesity, Diabetes Rx

Nischarin Inhibition Alters Energy Metabolism by Activating AMP-Activated Protein Kinase. Journal of Biological Chemistry, 2017; jbc.M117.784256 DOI: 10.1074/jbc.M117.784256

Nischarin Inhibition Alters Energy Metabolism by Activating AMP-Activated Protein Kinase. Journal of Biological Chemistry, 2017; jbc.M117.784256 DOI: 10.1074/jbc.M117.784256

Research has demonstrate protein Nischarin may treat or prevent metabolic diseases including obesity and diabetes. Nischarin is a novel protein discovered by the Alahari lab. The research team demonstrated that it functions as a molecular scaffold that holds and interacts with several protein partners in a number of biological processes. The lab’s earlier research found that Nischarin acts as a tumor suppressor that may inhibit the spread, or metastasis, of breast and other cancers.

The current research project, conducted in a knockout mouse model, found that Nischarin interacts with and controls the activity of a gen...

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Scientists discover Molecular Handle behind some Cancers’ preference for Fat

Highlights •Prolyl hydroxylase 3 (PHD3) hydroxylates and activates the metabolic enzyme ACC2 •During nutrient abundance, the PHD3/ACC2 axis represses fatty acid oxidation (FAO) •PHD3 is low in AML, fueling a reliance on fats that can be targeted with FAO inhibitors •Re-expressing PHD3 limits FAO via ACC2 and suppresses AML in culture and in vivo

Highlights •Prolyl hydroxylase 3 (PHD3) hydroxylates and activates the metabolic enzyme ACC2 •During nutrient abundance, the PHD3/ACC2 axis represses fatty acid oxidation (FAO) •PHD3 is low in AML, fueling a reliance on fats that can be targeted with FAO inhibitors •Re-expressing PHD3 limits FAO via ACC2 and suppresses AML in culture and in vivo

A handful of cancers favor fat over sugar, a propensity that has long mystified scientists. Now, a study from Harvard Medical School reveals how certain tumors develop a taste for fat as their life-sustaining fuel. The findings show how a signaling pathway that normally keeps fat-burning in check goes awry in some cancers, revving up fat consumption and fueling tumor growth.

Specifically, the study found a protein called prolyl hydroxylase ...

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