Researchers from the University of California, Berkeley have discovered a gene which regulates a process in the liver that converts carbohydrates into fat.
This study offers new clues as to how the body metabolizes carbohydrates and how they contribute to obesity.
The research team, led by Professor Hei Sook Sul of UC Berkeley’s Department of Nutritional Science and Toxicology believe that the gene, DNA-PK (DNA-dependent protein kinase ), is critical to a metabolic process scientists have been trying to understand for 20 years.
Your blood glucose levels – the digested form of carbohydrates – go up after you eat a carb-rich food like pizza and wash it down with soda. That spike in blood glucose triggers the secretion of insulin, which helps different cells in your body use glucose for energy.
Glucose in the liver that isn't used up for energy is converted into fatty acids, which then circulate to other parts of the body, primarily to fat tissue.
The process of converting excess glucose into fatty acids occurs in the liver. Scientists have been unable to determine the exact molecular pathway involved prior to the discovery of DNA-PK.
What they did know was that insulin binds to receptors on the liver cells and activates protein phosphatase-1 (PP1), the first molecule of the insulin-signaling pathway inside the liver. Sul's lab had previously shown that upstream stimulatory factor (USF) is needed to activate certain genes, such as fatty acid synthase (FAS), which converts glucose to fatty acids.
The link between PP1 and USF was a mystery until a UC Berkeley graduate student in comparative biochemistry finally connected the dots in Sul’s lab and discovered that DNA-PK, which is regulated by PP1, signals the activation of USF and the process of converting glucose to fatty acids.
The research team determined that DNA-PK acts as a signaling molecule in the chain reaction that begins when insulin binds to receptors on liver cells. This helps explain why untreated Type 1 diabetics, who cannot produce insulin, may experience significant weight loss because without treatment, they have problems making enough fat.
This insulin-signaling pathway is also disrupted in Type 2 diabetes because the body still produces insulin, but the cells have become resistant to its effects.
After the researchers were able to identify DNA-PK, they tested the gene in mice fed with a diet containing 70 percent carbohydrates but with zero fat. A typical lab mouse diet is composed of both fat and carbohydrates. The researchers then disabled the DNA-PK gene in half the mice while the other half served as the control group of normal mice.
They discovered that the DNA-PK disabled mice were leaner and had 40 percent less body fat compared to the control group of normal mice because they had a problem converting carbs into fat.
The DNA-PK disabled mice were resistant to high carbohydrate-induced obesity and had lower plasma lipids, which can lower the risk of cardiovascular disease.
DNA-PK could potentially play a role in the prevention of obesity associated with the over-consumption of high-carbohydrate foods or carbohydrate addiction, such as pasta, rice, soda and sugary snacks if it is possible to create medication based on the gene.
However, this will only be another quick fix. Yes, such a pill may help you avoid getting fat from carbohydrates but the bottom line is: you’re still eating carbs and carbohydrates have been linked to almost all age-related diseases.
If you want to get fit and maintain your ideal weight, it doesn’t involve waiting for a magic pill. You have to make the necessary lifestyle changes because there are no shortcuts to good health.