Portly beer belly portends metabolic misfortune more than BMI.

BioMed Central - Even in apparently healthy Japanese men, visceral fat accumulation in the abdomen has now been correlated with much higher inflammatory markers hs-CRP and IL-6, and significantly lower adiponectin levels. These new findings now put abdominal fat in center stage in the search for understanding the clinical development of metabolic syndrome in patients.

Visceral fat tissue is known to release various inflammatory and anti-inflammatory cytokines, but few studies have determined precisely the relationship between abdominal obesity and inflammatory markers in metabolic syndrome. To clarify the importance of abdominal obesity in sub-clinical inflammation, Japanese researchers examined the changes of inflammatory markers in clustering of metabolic syndrome components with or without abdominal obesity.

326 apparently healthy Japanese men (age: 30 to 59 years) underwent health examination in the Osaka University Health Care Center. Components of the metabolic syndrome were assessed: serum levels of high sensitivity C-reactive protein (hs-CRP), interleukin (IL)-6 and adiponectin. Subjects with abdominal obesity (waist circumference ≥ 85 cm) showed higher serum hs-CRP and IL-6 levels and a lower adiponectin level than those without abdominal obesity. Serum levels of hs-CRP and IL-6 significantly increased in association with clustering of metabolic syndrome components in the subjects with abdominal obesity, but not in those without abdominal obesity. Significant negative correlation between adiponectin and hs-CRP was observed in the subjects with abdominal obesity, however this correlation was not detected in obese subjects defined by body mass index ≥ 25. Adiponectin, an anti-inflammatory protein, has been demonstrated to be
insulin-sensitizing and anti-atherogenic factor, and is considered a key component of metabolic syndrome. Serum adiponectin level was significantly lower in the subjects with abdominal obesity than those without it.

The authors conclude that inflammatory status is not exaggerated by clustering of metabolic syndrome components in the subjects without abdominal obesity. Abdominal obesity may exhibit distinct effects on inflammatory and anti-inflammatory proteins and modulate inflammatory networks in patients with metabolic syndrome.

The National Cholesterol Education Program (NCEP)-Adult Treatment Panel (ATP) III, and the American Heart Association (AHA)/National Heart Lung and Blood Institute (NHLBI) proposed definitions of the metabolic syndrome as a cluster of at least 3 of 5 following risk factors: abdominal obesity, high blood pressure, high serum triglycerides, low HDL cholesterol, and elevated fasting blood glucose. The primary mechanism for clustering of metabolic abnormalities has yet to be elucidated, but insulin resistance or accumulation of visceral fat is highly suspect as a central factor. As for visceral fat, the International Diabetes Federation (IDF) newly recommended a definition in which abdominal obesity is the essential component of metabolic syndrome. It is likely that clustering of metabolic abnormalities has synergistic effects on cardiovascular complications beyond the sum of effects of individual abnormalities. In this study, the inflammatory networks associated with abdominal obesity were distinct from those associated with mere “obesity”. Després and Lemienx proposed visceral fat as a dysfunctional adipose tissue, and this study supports this idea.

Reference: “Abdominal obesity exhibits distinct effect on inflammatory network in apparently healthy Japanese men.” Cardiovascular Diabetology 2007, 6:27 Makoto Nishida, et al.