Salas-Salvadó J, Bulló M, García-Lorda P, Figueredo R, Del Castillo D, Bonada A, Balanzà R
Unitat de Nutrició Humana, Facultat de Medicina i Ciències de la Salut, Departament de Bioquímica i Biotecnologia, Universitat Rovira i Virgili, C/Sant Llorenç, Reus, Spain.
Int J Obes (Lond). 2006 Dec;30(12):1714-20. doi: 10.1038/sj.ijo.0803348. Epub 2006 Apr 25.
It has been suggested that weight loss can improve systemic inflammation associated with obesity by decreasing the adipose production of pro-inflammatory cytokines. This suggestion, however, remains controversial.
To analyse the effect of weight loss on peripheral inflammatory markers and subcutaneous adipocytokine production.
Patients were studied at baseline, at the end of the weight loss period, and after 2 weeks of weight stabilisation.
Nineteen morbid obese non-diabetic patients and 20 lean control subjects.
During the weight loss period patients followed a 6-week low-calorie diet.
Plasma levels of inflammatory markers, maximal in vitro whole-blood cytokine production, subcutaneous adipose tissue expression and content of several cytokines.
Obese subjects had higher circulating levels of C reactive protein (CRP), serum amyloid A (SAA), interleukin IL-6, IL-1 and soluble tumor necrosis factor receptors (sTNFR). Weight loss was associated with a significant decrease in CRP, SAA, leucocytes and plasma IL-6. Maximal in vitro cytokine production of IL-1 and sTNFR1 increased during this period. Weight loss did not induce significant changes in the adipose concentrations of IL-6, IL-1 or sTNF-receptors. However, adipose expression of IL-6, IL-1, TNFalpha, membrane cofactor protein-1 and adiponectin increased at the end of the weight loss period. During weight maintenance, circulating inflammatory parameters increased and in some cases returned to baseline.
A low-calorie diet is associated with an improvement in the systemic inflammatory status. This seems to be due to energy restriction rather than to adipose mass loss, since inflammatory levels return to baseline soon after weight stabilisation. Furthermore, a negative energy balance and fat mobilisation are associated with increased subcutaneous cytokine adipose expression.
有人提出，体重减轻可通过减少促炎细胞因子的脂肪生成来改善与肥胖相关的全身炎症。然而，这一观点仍存在争议。
分析体重减轻对外周炎症标志物和皮下脂肪细胞因子产生的影响。
在基线、体重减轻期结束时以及体重稳定2周后对患者进行研究。
19名病态肥胖的非糖尿病患者和20名瘦对照组受试者。
在体重减轻期间，患者遵循为期6周的低热量饮食。
炎症标志物的血浆水平、体外全血细胞因子的最大产生量、皮下脂肪组织中几种细胞因子的表达和含量。
肥胖受试者的C反应蛋白（CRP）、血清淀粉样蛋白A（SAA）、白细胞介素IL-6、IL-1和可溶性肿瘤坏死因子受体（sTNFR）的循环水平较高。体重减轻与CRP、SAA、白细胞和血浆IL-6的显著降低相关。在此期间，IL-1和sTNFR1的体外细胞因子最大产生量增加。体重减轻并未引起IL-6、IL-1或sTNF受体的脂肪浓度发生显著变化。然而，在体重减轻期结束时，IL-6、IL-1、TNFα、膜辅因子蛋白-1和脂联素的脂肪表达增加。在体重维持期间，循环炎症参数增加，在某些情况下恢复到基线水平。
低热量饮食与全身炎症状态的改善有关。这似乎是由于能量限制而非脂肪量减少，因为体重稳定后不久炎症水平就会恢复到基线。此外，负能量平衡和脂肪动员与皮下细胞因子脂肪表达增加有关。
