Several years ago, Daniel and Shawn Winer began to speculate that different types of immune cells, including T cells and B cells, can cause inflammation in the fatty tissue that surrounds and cushions organs in the body. This inflammation occurs in mice fed a high-fat, high-calorie diet when the rapidly growing fat cells outstrip their blood supply and begin to die. (It’s also seen in humans with type-2 diabetes.) The dying cells spew their contents, and immune system cells called macrophages are summoned to clean up the mess.
“This immune reaction causes havoc in the fatty tissue,” said Engleman, “and we’ve found that it involves two other immune system cells — T cells and B cells — in addition to macrophages.” The resulting onslaught by the immune system inhibits the ability of the remaining fat cells to respond to insulin and causes fatty acids to be shed into the blood. This sets in motion a physiological cascade that leads to fatty liver disease, high cholesterol, high blood pressure and further insulin resistance throughout the body.
The researchers found that mice genetically engineered to lack B cells were protected from developing insulin resistance even when they grew obese on the high-fat diet. However, injecting these mice with B cells or purified antibodies from obese, insulin-resistant mice significantly impaired their ability to metabolize glucose and caused their fasting insulin levels to increase.
The researchers then studied 32 age- and weight-matched overweight people who differed only in their sensitivity to insulin. “We were able to show that people with insulin resistance make antibodies to a select group of their own proteins,” said Engleman. “In contrast, equally overweight people who are not insulin-resistant do not express these antibodies. http://med.stanford.edu/ism/2011/april/engleman.html
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