A new study published in Scientific advances It reveals that a single gene plays an important role in how the liver stores energy, a process that is critical for general health and to handle diseases such as type 2 diabetes. Directed by Kate Towsend Creasy, PHD, Assistant Professor of Nutrition Sciences in the Department of Bio -Outral Health Sciences, the research focuses on the PPP1R3B gene. This gene tells the liver how to handle energy: guide it as glycogen (a sugar form) or triglycerides (a type of fat).
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 change between glycogen and fat storage is crucial because it affects the way the body manages blood sugar and fat levels.
Large -scale genomic studies on humans have reported that mutations in the PPP1R3B gene are associated with several metabolic conditions, including type 2 diabetes and fatty liver disease. However, it was not clear how the gene was involved in these conditions.
“Our research shows that PPP1R3B is like a control switch in the liver,” Creasy said. “He directs if the liver stores energy for rapid use in glycogen or for longer -term storage such as fat. We also saw changes in the way in which mice and cells efficiently with genetic manipulations of PPP1R3B could use glucose or fat for energy. This discovery could help us find new ways to help people with metabolic diseases with precision nutrition approaches with precision nutrition precision nutrition approaches, based on their genetics. ” “
Co-authors from the Perelman School of Medicine Include: MINAL B. MEHTA, Joseph Park, David Zhang, and Swapnil V. Shewale (All Based In The Department of Genetics), Carolin V. Schneider (Division of Translational Medicine and Human Genetics), John S. Millar (Institute for Diabetes, Obesity, Obesity Metabolism), Marijana Vujkovic (Division of Translational Medicine and Human Genetic and the Institute of Diabetes, Obesity and Metabolism), Nicholas J. Hand (Department of Physiology), Paul M. Titchenell (Institute of Diabetes, Obesity and Metabolism and the Department of Physiology), Joseph A. Baur (Institute of Diabetes, Obesity and Metabolism Department of Physiology), and Daniel J. Rader (Division of the Division of the Division and Division of Genetics and the Department of Generations of Humans and the Department of General of the Department of Calvulas and Humans. Genetics, and the Institute of Diabetes, Obesity and Metabolism). The National Health Institutes supported this research.