A University of Michigan Health System study provides new cluesabout the health-damaging molecular changes set in motion by eatinghigh-fat foods. A better understanding of the body’s response to indulgent eatingcould lead to new approaches for treating diabetes and metabolic syndrome. High fat foods can contribute to obesity , which increases the risk for developing type 2 diabetes. The researchers learned a key protein called Bcl10 is needed forthe free fatty acids, which are found in high-fat food and storedin body fat, to impair insulin action and lead to abnormally highblood sugar. In the laboratory study, mice deficient in Bcl10 were protectedfrom developing insulin resistance when fed a high-fat diet. GSM Multimedia Phone Watch
Thefindings will be published May 31 in Cell Reports . Insulin helps control blood sugar, but insulin resistance can leadto the abnormally high blood sugar levels that are the hallmark ofdiabetes. Insulin resistance can occur as part of metabolicsyndrome, a cluster of conditions that increase the risk for type 2diabetes and heart disease . As millions of Americans become overweight and obese, type 2diabetes and metabolic syndrome are on the rise. “The study also underscores how very short-term changes in dietsuch as high-fat eating for only a few days, perhaps even less, caninduce a state of insulin resistance,” says senior study authorPeter C. GSM Listening Bug
Lucas, M.D., Ph.D., associate professor of pathology atthe University of Michigan. Researchers began by investigating how free fatty acids induceinflammation and impair insulin action in the liver. It’s thoughtthe liver is a major target for the harmful effects of free fattyacids. In the liver, free fatty acids undergo metabolism to producediacylglycerols prior to inducing the inflammatory response. Infrared Hunting Cameras Manufacturer
Diacylglycerols also activate NF-kB signaling which has been linkedwith cancer , metabolic and vascular diseases. The team of researchers concluded that Bcl10 is required for fattyacids to induce inflammation in the liver and insulin resistance.In the study, Bcl10 deficient mice showed significant improvementin regulation of blood sugar. “We were surprised to learn that Bcl10, a protein previously knownfor its critical role in immune cell response to infection, alsoplays a critical role in the liver’s response to fatty acid,” saysLucas. “This is an example of nature co-opting a mechanismfundamental to the immune system and using it in a metabolic organ,in this case, the liver.” “These findings reveal a new and important role for Bcl10 and couldlead to novel ideas for treating patients with metabolic syndromeand type 2 diabetes,” say co-senior author Linda M.McAllister-Lucas, M.D., Ph.D., associate professor of pediatrichematology/oncology at the University of Michigan.
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