Sarcopenia, sarcopenic obesity and inflammation: Results from the 1999-2004 National Health and Nutrition Examination Survey.

Sarcopenia, sarcopenic obesity and inflammation: Results from the 1999-2004 National Health and Nutrition Examination Survey.
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DOI:
10.1016/j.clnu.2016.03.028
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发表时间:
2016-12
期刊:
Clinical nutrition (Edinburgh, Scotland)
影响因子:
--
通讯作者:
Bartels SJ
Bartels SJ
中科院分区:
其他
文献类型:
--
作者:
Batsis JA;Mackenzie TA;Jones JD;Lopez-Jimenez F;Bartels SJ

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美国国立卫生研究院骨骼肌减少症项目基金会验证了阑尾瘦肉块(ALM)的切入点,以识别有功能损害风险的个体。认识到脂肪组织和肌肉之间可能存在的潜在机制,我们试图应用最近的定义,并确定肌肉减少症和肌肉减少性肥胖患者与葡萄糖稳态和炎症标志物的关系。1999-2004年全国健康和营养调查采用DEXA方法确定了4984名年龄≥60岁的成年人。使用ALM(男性<19.75 kg,女性<15.02 kg)定义肌肉减少症,并根据体重指数(BMI,男性<0.789 kg/m2,女性<0.512 kg/m2)调整ALM。肌少性肥胖被定义为通过体脂(男性≥25%,女性≥35%)满足肌少症和肥胖标准的受试者。我们评估了ALM和ALM:BMI与炎症和葡萄糖稳态标志物之间的关系,两者都是连续变量,但在调整了包括促炎慢性疾病(如糖尿病和癌症)在内的混杂变量后,也将其归类为肌肉减少型肥胖或非肌肉减少型肥胖。平均年龄71.1岁,女性占56.5%。肌少症和肌少性肥胖患病率分别为(ALM定义:29.9和24.4%;ALM:BMI定义:23.0和22.7%)。与ALM和ln c反应蛋白(β=0.0287, p=0.001)、纤维蛋白原(β=0.519, p<0.001)和HOMA-IR (β=0.359, p<0.001)有显著相关性。使用ALM:BMI,观察到ln CRP (β= - 2.58, p=0.001)、纤维蛋白原(β= - 124.2, p<0.001)和HOMA-IR (β= - 6.63, p<0.001)有显著相关性。使用ALM:BMI定义的肌少性肥胖与CRP (β=0.422, p<0.001),纤维蛋白原(β=22.5, p<0.001),但与HOMA-IR (β=1.19, p=0.13)无关。纤维蛋白原和CRP水平升高与肌少性肥胖(ALM:BMI定义)密切相关,在调整糖尿病和癌症后仍持续存在。ALM:BMI与炎症和HOMA-IR之间存在生物学上合理的关联,而单独使用ALM时未观察到这种关联。未来的研究应该验证这些定义,以防止不同的结果被确定。
The Foundation for the National Institutes of Health Sarcopenia Project validated cutpoints for appendicular lean mass (ALM) to identify individuals at risk for functional impairment. Recognizing possible underlying mechanisms between adipose tissue and muscle, we sought to apply the recent definitions and determine the relationship with markers of glucose homeostasis and inflammation in individuals with sarcopenia and sarcopenic obesity. The National Health and Nutrition Examination Surveys 1999–2004 were used to identify 4,984 adults aged ≥60 years with DEXA measures. Sarcopenia was defined using ALM (men<19.75 kg, women<15.02 kg) and ALM adjusted for body mass index (BMI; men<0.789 kg/m2, women<0.512 kg/m2). Sarcopenic obesity was defined as subjects fulfilling the criteria for sarcopenia and obesity by body fat (men ≥25%, women ≥35%). We assessed the association between ALM and ALM:BMI with inflammatory and markers of glucose homestasis, both as continuous variables but also classifying as having sarcopenic obesity or not after adjusting for confounding variables including pro-inflammatory chronic diseases such as diabetes and cancer. Mean age was 71.1 years (56.5%) females. Prevalence of sarcopenia and sarcopenic obesity were (ALM definition: 29.9 and 24.4%; ALM:BMI definition: 23.0 and 22.7%). There were significant associations with ALM and ln C-reactive protein (β=0.0287;p=0.001), fibrinogen (β=0.519;p<0.001), and HOMA-IR (β=0.359;p<0.001). Using ALM:BMI, significant associations were observed with ln CRP (β=−2.58;p=0.001), fibrinogen (β=−124.2;p<0.001), and HOMA-IR (β=−6.63;p<0.001). Sarcopenic obesity using the ALM:BMI definition demonstrated significant associations with CRP (β=0.422;p<0.001), fibrinogen (β=22.5;p<0.001), but not HOMA-IR (β=1.19;p=0.13). Strong associations with seen with increased levels of fibrinogen and CRP with sarcopenic obesity (ALM:BMI definition) that persisted after adjusting for diabetes and cancer. Biologically plausible associations exist between ALM:BMI and inflammation and HOMA-IR that were not observed when using ALM alone. Future study should validate each of these definitions to prevent disparate results from being determined.
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