It's called the obesity paradox. Although obese people are more apt to suffer from inflammatory diseases, such as diabetes, heart disease, and stroke, they are also more likely to survive a major attack caused by one of those conditions.
University of Illinois scientists Gregory Freund and Christina Sherry shed light on the reasons for this phenomenon in a study in this month's issue of Endocrinology.
"Fat is a very complex and active tissueit has important functions beyond providing energy and insulating us from the cold," said Freund, a professor in the U of I College of Medicine's Department of Pathology and a faculty member in the U of I Division of Nutritional Sciences.
"We now know that leptin, a hormone secreted by fat tissue, plays a key role in regulating the immune system. When we exposed mice to hypoxia (simulating an event, such as a heart attack, in which a part of the body is deprived of oxygen), leptin triggered the immune system to increase production of an anti-inflammatory molecule, interleukin-1 receptor antagonist (IL-1RA)," he said.
"And, when we gave non-obese mice leptin injections, they recovered three times faster. Leptin did not hasten recovery though in IL-1RA knockout mice," Sherry said. That earlier work was published in a recent issue of Brain, Behavior, and Immunity.
In the Endocrinology study, one group of mice was fed a high-fat diet for 12 weeks (Sherry described this group as being in a mildly obese, pre-diabetic state), while another group was fed a normal diet. The obese mice recovered from acute hypoxia five times faster than the mice fed normal diets.
In a second experiment, Freund and Sherry examined macrophages (or immune cells) that were resident in peritoneal fat tissue from both groups of mice. In mice fed the high-fat diet, there was a very significant increase in IL-1RA as compared to mice fed the normal diet (330 pg vs.15 pg).
|Contact: Phyllis Picklesimer|
University of Illinois at Urbana-Champaign