Department of Clinical and Experimental Medicine, Federico II University Medical School of Naples, Italy.
J Inflamm (Lond). 2009 Mar 16;6:6. doi: 10.1186/1476-9255-6-6.
Obesity is a leading risk factor for metabolic syndrome whose further expression is non-alcoholic fatty liver disease. Metabolic syndrome is associated with a proinflammatory state that contributes to insulin resistance. Finally, a "metabolically benign obesity" that is not accompanied by insulin resistance has recently been postulated to exist.
To find whether any inflammation markers were independently associated with the presence of insulin resistance, evaluating specific anthropometric, ultrasonographic and laboratory parameters in a population of young adult obese subjects.
Of forty two young individuals, divided into two groups (with or without insulin resistance), were studied serum C-reactive protein and fibrinogen as indexes of chronic pro-inflammatory status. Body mass index, waist circumference and metabolic syndrome presence were assessed as part of the metabolic evaluation. Ultrasonography weighted visceral and subcutaneous abdominal fat thickness, spleen size as longitudinal diameter and liver hyperechogenicity.
Serum C-reactive protein and fibrinogen as well as spleen longitudinal diameter were significantly increased in the obese young with insulin resistance compared to non-insulin resistance group. Insulin resistance was significantly associated with hepatic steatosis score at sonography (r = 0.33, P = 0.03), spleen longitudinal diameter (r = 0.35, P = 0.02) and C-reactive protein (r = 0.38, P = 0.01), but not with body mass index, visceral or subcutaneous abdominal adipose tissue, waist circumference and fibrinogen (P = 0.18, 0.46, 0.33, 0.37 and 0.4, respectively). Steatosis score at sonography was well associated with spleen volume (rho = 0.40, P = 0.01) and C-reactive protein levels (rho = 0.49, P = 0.002). Metabolic syndrome was much more frequent in obese patients with insulin resistance. These findings show that in young adults the only abdominal adiposity without insulin resistance, plays a scarce role in determining hepatic steatosis as well as metabolic syndrome.
Increases in spleen size and CRP levels represent a reliable tool in diagnosing insulin resistance.
肥胖是代谢综合征的主要危险因素，而代谢综合征的进一步表现则是非酒精性脂肪肝疾病。代谢综合征与促炎状态有关，而这种状态会导致胰岛素抵抗。最后，最近有人提出存在一种“代谢良性肥胖”，即不伴有胰岛素抵抗。
在年轻的肥胖人群中，评估特定的人体测量学、超声和实验室参数，寻找是否有任何炎症标志物与胰岛素抵抗的存在独立相关。
将 42 名年轻个体分为两组（有或无胰岛素抵抗），研究血清 C 反应蛋白和纤维蛋白原作为慢性促炎状态的指标。评估体重指数、腰围和代谢综合征的存在作为代谢评估的一部分。超声测量内脏和皮下腹部脂肪厚度、脾脏大小（作为长径）和肝脏回声增强。
与非胰岛素抵抗组相比，胰岛素抵抗的肥胖年轻人血清 C 反应蛋白和纤维蛋白原以及脾脏长径显著增加。胰岛素抵抗与超声肝脂肪变性评分显著相关（r = 0.33，P = 0.03）、脾脏长径（r = 0.35，P = 0.02）和 C 反应蛋白（r = 0.38，P = 0.01），但与体重指数、内脏或皮下腹部脂肪组织、腰围和纤维蛋白原无关（P = 0.18、0.46、0.33、0.37 和 0.4）。超声肝脂肪变性评分与脾脏体积（rho = 0.40，P = 0.01）和 C 反应蛋白水平（rho = 0.49，P = 0.002）密切相关。代谢综合征在有胰岛素抵抗的肥胖患者中更为常见。这些发现表明，在年轻成年人中，唯一没有胰岛素抵抗的腹部肥胖在确定肝脂肪变性以及代谢综合征方面作用不大。
脾脏大小和 CRP 水平的增加是诊断胰岛素抵抗的可靠工具。
