Franco-Czech Laboratory for Clinical Research on Obesity, Third Faculty of Medicine, Prague, CZ-100 00, Czech Republic.
J Clin Endocrinol Metab. 2012 Jul;97(7):E1176-81. doi: 10.1210/jc.2011-2380. Epub 2012 Apr 24.
Obesity is associated with altered plasma levels of adipokines involved in the development of insulin resistance and obesity-related metabolic disturbances.
The aim was to investigate diet-induced changes in adipokine production in sc abdominal adipose tissue (SAT) during a 6-month, multiphase, weight-reducing dietary intervention.
DESIGN, SETTING, PARTICIPANTS, AND INTERVENTIONS: Forty-eight obese women followed a dietary intervention consisting of a very low-calorie diet (VLCD) (1 month), followed by a weight-stabilization (WS) period, which consisted of a low-calorie diet (2 months), and a weight-maintenance diet (3 months).
Before and at the end of the VLCD and WS, samples of plasma and SAT were obtained. In a subgroup of 26 women, secretion of adipokines was determined in SAT explants, and in a subgroup of 22 women, SAT mRNA expression was measured.
Body weight decreased and insulin sensitivity increased during the intervention. Plasma levels, SAT mRNA expression, and secretion rates of adipocyte-produced adipokines (leptin, serum amyloid A, and haptoglobin) decreased during the VLCD and increased during the WS period. Adipokines produced mainly from stroma-vascular cells (IL-6, IL-8, IL-10, IL-1Ra, TNFα, plasminogen activator inhibitor-1, and monocyte chemoattractant protein-1) increased or remained unchanged during VLCD and decreased to levels equal to or lower than prediet levels during the WS period. The diet-induced changes in homeostasis model assessment of insulin resistance correlated with changes in leptin plasma levels during VLCD, WS, and the entire dietary intervention period.
Diet-induced regulation of adipokine production in SAT differs according to their cellular origin (adipocytes vs. stroma-vascular cells) and diet phase (VLCD vs. WS). Insulin-sensitivity changes were associated only with those of plasma leptin.
肥胖与参与胰岛素抵抗和肥胖相关代谢紊乱发展的脂肪因子的血浆水平改变有关。
本研究旨在探讨在为期 6 个月的多阶段减肥饮食干预过程中，腹部皮下脂肪组织（SAT）中脂肪因子产生的饮食诱导变化。
设计、环境、参与者和干预措施：48 名肥胖女性遵循饮食干预措施，包括极低热量饮食（VLCD）（1 个月），随后是体重稳定（WS）期，包括低热量饮食（2 个月）和维持体重的饮食（3 个月）。
在 VLCD 和 WS 之前和结束时，获取血浆和 SAT 样本。在 26 名女性的亚组中，测定 SAT 外植体中脂肪因子的分泌情况，在 22 名女性的亚组中，测量 SAT mRNA 表达。
干预过程中体重减轻，胰岛素敏感性增加。血浆水平、SAT mRNA 表达和脂肪细胞产生的脂肪因子（瘦素、血清淀粉样 A 和触珠蛋白）的分泌率在 VLCD 期间下降，在 WS 期间增加。主要由基质血管细胞产生的脂肪因子（IL-6、IL-8、IL-10、IL-1Ra、TNFα、纤溶酶原激活物抑制剂-1 和单核细胞趋化蛋白-1）在 VLCD 和 WS 期间增加或保持不变，并且在 WS 期间下降到与饮食前水平相等或更低的水平。稳态模型评估胰岛素抵抗的饮食诱导变化与 VLCD、WS 和整个饮食干预期间的瘦素血浆水平变化相关。
SAT 中脂肪因子产生的饮食诱导调节根据其细胞起源（脂肪细胞与基质血管细胞）和饮食阶段（VLCD 与 WS）而不同。胰岛素敏感性的变化仅与血浆瘦素的变化相关。
