Protein Targeting to Glycogen (PTG): A Promising Player in Glucose and Lipid Metabolism

Abstract

Protein phosphorylation and dephosphorylation are widely considered to be the key regulatory factors of cell function, and are often referred to as “molecular switches” in the regulation of cell metabolic processes. A large number of studies have shown that the phosphorylation/dephosphorylation of related signal molecules plays a key role in the regulation of liver glucose and lipid metabolism. As a new therapeutic strategy for metabolic diseases, the potential of using inhibitor-based therapies to fight diabetes has gained scientific momentum. PTG, a protein phosphatase, also known as glycogen targeting protein, is a member of the protein phosphatase 1 (PP1) family. It can play a role by catalyzing the dephosphorylation of phosphorylated protein molecules, especially regulating many aspects of glucose and lipid metabolism. In this review, we briefly summarize the role of PTG in glucose and lipid metabolism, and update its role in metabolic regulation, with special attention to glucose homeostasis and lipid metabolism.

TEAD1, MYO7A and NDUFC2 are novel functional genes associated with glucose metabolism in BXD recombinant inbred population

“…During short‐term fasting periods, glycogenolysis is mainly motivated in the liver; hepatocyte‐stored glycogen breaks down into glucose and is released into the blood 8,9 . As the starvation time is prolonged and glycogen stores have been exhausted, gluconeogenesis, that is, de novo glucose synthesis from available precursors, becomes the alternative way to maintain blood glucose levels 10,11 . Over the past two decades, various research approaches, including linkage analyses, candidate gene investigations, and large‐scale genome‐wide association studies (GWAS), have successfully identified numerous genetic variants, genomic regions, and susceptibility genes associated with disorders in glucose metabolism 12,13 .…”

“…8,9 As the starvation time is prolonged and glycogen stores have been exhausted, gluconeogenesis, that is, de novo glucose synthesis from available precursors, becomes the alternative way to maintain blood glucose levels. 10,11 Over the past two decades, various research approaches, including linkage analyses, candidate gene investigations, and large-scale genome-wide association studies (GWAS), have successfully identified numerous genetic variants, genomic regions, and susceptibility genes associated with disorders in glucose metabolism. 12,13 For example, 568 genetic loci, including 318 novel loci, for diabetes were identified in 1 178 873 samples from Biobank Japan and other studies.…”

TEAD1, MYO7A and NDUFC2 are novel functional genes associated with glucose metabolism in BXD recombinant inbred population

“…During short-term fasting periods, glycogenolysis is mainly motivated in the liver; hepatocyte stored glycogen breaks down into glucose and released into the blood [8,9]. As the starvation time is prolonged and glycogen stores have been exhausted, gluconeogenesis, that is de novo glucose synthesis from available precursors becomes the alternative way to maintain blood glucose levels [10,11]. Over the past two decades, linkage analyses, candidate gene approaches, and large-scale genome-wide association studies (GWAS) have successfully linked hundreds of genetic variants, genomic regions and disease susceptible genes to glucose metabolism disorders [12,13].…”