A study published in the May 31 edition of Cell Reports shows that eating high fat foods has provided new clues about howharmful molecular changes are set in motion. The findings provide a better understanding of the body's responseto consuming high fat foods and could lead to new treatment optionsfor diabetes and metabolic syndrome. High fat foods are a contributing factorfor obesity and increase the risk for developing type 2 diabetes. The researchers from the University of Michigan discovered thatfree fatty acids need a key protein called BcI10 in order todebilitate insulin action, which leads to abnormally highelevations of blood sugar. |
BcI10 are found in high fat foods andare stored in body fat. A laboratory study demonstrated that micethat had been fed a high-fat diet with a BcI10 deficiency wereprotected from developing insulin resistance. Whereas insulin helps to control blood sugar, insulin resistancecan lead to abnormally high blood sugar levels, the telltale signof diabetes. The resistance can be caused as part of metabolicsyndrome, a variety of conditions that increase the type 2 diabetesand heart disease risk.
With millions of overweight and obese Americans, type 2diabetes and metabolic syndrome are on the increase. Senior research leader, Peter C. Lucas, M.D., Ph.D., associateprofessor of pathology at the University of Michigan declares: "Thestudy also underscores how very short-term changes in diet such ashigh-fat eating for only a few days, perhaps even less, can inducea state of insulin resistance." The team decided to examine how free fatty acids cause inflammationand how they debilitate the liver's insulin action, as scientistsbelieve that the liver represents a key target for the damagingeffects of free fatty acids. Free fatty acids undergo metabolism inthe liver where they produce diacylglycerols before they cause aninflammatory response.
Diacylglycerols activates NF-kB signaling,which has been associated with metabolic and vascular diseases aswell as cancer . They concluded that in order to induce liver inflammation andinsulin resistance, fatty acids require BcI10. The study revealedthat mice with a BcL10 deficiency displayed a considerableimprovement in regulating their blood sugar levels. Lucas declares: "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.
Thisis an example of nature co-opting a mechanism fundamental to theimmune system and using it in a metabolic organ, in this case, theliver." Linda M. McAllister-Lucas, M.D., Ph.D., associate professor ofpediatric hematology/oncology at the University of Michigan, whowas the study's co-senior author concluded: "These findings reveala new and important role for Bcl10 and could lead to novel ideasfor treating patients with metabolic syndrome and type 2 diabetes." Written By Petra Rattue Copyright: Medical News Today Not to be reproduced without permission of Medical News Today Additional References Citations.
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