From Fat to Chronic Inflammation
(Ivanhoe Newswire) -- Chronic inflammation within fat tissue is now recognized as a contributor to the many negative consequences that come with obesity -- from diabetes to cardiovascular disease, according to Yuichi Oike of Kumamoto University in Japan. Researchers hope a new discovery will point to a targeted therapy designed to limit the impact of the obesity epidemic.
The new culprit Oike's team identified is a fat-derived protein called angiopoietin-like protein 2 (Angptl2). In mice, Angptl2 levels are elevated in many organs, but especially in fat tissue. Those levels increase further under the oxygen-deprived conditions typically found within obese fat tissue. Researchers also found higher Angptl2 levels in the blood of humans with higher body mass index and insulin levels.
Obese mice lacking Angptl2 show less inflammation in their fat tissue and are less insulin resistant, researchers report. Likewise, otherwise healthy mice made to have higher than normal Angptl2 levels in their fat tissue develop inflammation and insulin resistance.
The researchers conclude that Angptl2 is a key adipocyte-derived inflammatory mediator linking obesity to systemic insulin resistance, and they have identified it as a new molecular target that could be used to improve the diagnosis and treatment of obesity and related metabolic diseases.
Oike is quoted as saying he thinks drugs that would act on Angptl2 not only have considerable promise, but are also likely to come with limited side effects.
"In healthy animals and people, the precise role of Angptl2 has not been clarified," he said. "However, mice in which Angptl2 was deleted genetically were born normally and showed normal growth compared to genetically normal mice. Therefore, we speculate that the possibility of the occurrence of a serious unfavorable side effect due to treatments that decrease Angptl2 expression in animals or people is low."
SOURCE: Cell Metabolism, September, 2009