Amazing stuff!
"The research team found that when the PPP1R3B gene is more active, the liver tends to store more energy as glycogen. The liver stores more energy as fat when the gene is less active. This shift between glycogen and fat storage is crucial because it affects how the body manages blood sugar and fat levels. ..."
From the abstract:
"The PPP1R3B gene, encoding PPP1R3B protein, is critical for liver glycogen synthesis and maintaining blood glucose levels. Genetic variants affecting PPP1R3B expression are associated with several metabolic traits and liver disease, but the precise mechanisms are not fully understood.
We studied the effects of both Ppp1r3b overexpression and deletion in mice and cell models and found that both changes in Ppp1r3b expression result in dysregulated metabolism and liver damage, with overexpression increasing liver glycogen stores, while deletion resulted in higher liver lipid accumulation.
These patterns were confirmed in humans where variants increasing PPP1R3B expression had lower liver fat and decreased plasma lipids, whereas putative loss-of-function variants were associated with increased liver fat and elevated plasma lipids. These findings support that PPP1R3B is a crucial regulator of hepatic metabolism beyond glycogen synthesis and that genetic variants affecting PPP1R3B expression levels influence if hepatic energy is stored as glycogen or triglycerides."
Scientists Discover Key Gene Impacts Liver Energy Storage, Affecting Metabolic Disease Risk (original news release) "A new study ... reveals that a single gene plays a big role in how the liver stores energy, a process that’s critical for overall health and for managing diseases like type 2 diabetes. ... the research focuses on the PPP1R3B gene. This gene tells the liver how to handle energy: store it as glycogen (a form of sugar) or triglycerides (a type of fat)."
Ppp1r3b is a metabolic switch that shifts hepatic energy storage from lipid to glycogen (open access)
Fig. 1. Mice with hepatocyte Ppp1r3b deletion develop metabolic dysfunction contributing to hepatic steatosis with age, while Ppp1r3b-overexpressing mice rapidly increase glycogen synthesis and storage contributing to liver damage with aging.
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