Weight Loss - Carbohydrate protein causes excess Carbs to be Stored as Body Fat

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A substance called ChREBP (carbohydrate response element binding protein) is a unique trigger that causes excess carbohydrates to be stored as fatty acids as body fat. The study was first published in the current issue of the American Journal of Physiology-Endocrinology and Metabolism.

The study is a continuation of a five year old discovery of the ChREBP which is a separate acting trigger for fat storage. It was originally thought that Insulin was the only fat storage system in the body previous to this discovery.

The current study looked at how the absence of ChREBP in mice would prevent them from becoming obese. When the ChREBP was missing, the mice had lower blood triglyceride levels and it also reduced the insulin resistance which is the cause of type 2 diabetes.

"Carbohydrates are broken down into glucose and other simple sugars by digestion," explained Kosaku Uyeda of the UT Southwestern Medical Center, in Dallas. Uyeda is also associated with the Veterans Affairs Medical Center in Dallas and is also the principal investigator. "These sugars enter the bloodstream and are mostly taken up by the liver."

The function of the liver will determine what to do with the sugars. If the body has no need for more energy at the time the liver along with ChREBP will convert the glucose into fatty acids and store it as body fat.

"Many people believe that evolutionary pressure favored those who could convert excess carbohydrate to fat and store it because they were better able to survive food shortages," said Uyeda. "Unfortunately for the waistlines and health of many people today, the conversion of glucose into fatty acids by the liver occurs all too readily."

The mice in this study were divided into four groups; one without working ChREBP gene, another did not produce leptin, the third group had both a disabled ChREBP gene with no leptin function, and the fourth group were a control group with out any modifications.

The results of the first group with the non-functional ChREBP gene were not able to make this protein. They did not convert much of the carbohydrates into fat and stayed relatively skinny even though they were eating a extremely high carbohydrate diet.

The second group without the ability to produce leptin, which is a hormone for appetite control ate large amounts of food and became obese with developments of insulin resistance. The leptin hormone will signal the brain that you are full and to stop eating. The more insulin resistance occurs the more likely you can develop Type 2 Diabetes.

The third group had the combination of the first and second group. They did not have the leptin hormone so that they would eat more and would be susceptible to becoming obese. They also at the same time, had a non-functioning ChREBP gene. This group showed that even though they would be at risk for over eating they did not become obese.

"We found that the third group (that did not have ChREBP and did not produce leptin) did not become obese, had lower blood glucose levels than the obese group and were less insulin resistant," Uyeda said. "We also were very surprised to find that these mice ate much less than the obese mice of the second group."

"These results show the important role ChREBP plays in metabolism and appetite control in mice and, presumably, humans," Uyeda said. "Ultimately we hope to develop drugs to inactivate and control ChREBP to overcome these two major health problems of obesity and diabetes."

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