Wang Su-Xing, Wei Jin-Gang, Chen Lu-Lu, Hu Xiang, Kong Wen
The Second Department of Geriatrics, Hebei General Hospital, Shijiazhuang, 050051, China.
Department of general surgery, The fifth hospital of Shijiazhuang City, Shijiazhuang, 050024, China.
Lipids Health Dis. 2016 Oct 4;15(1):173. doi: 10.1186/s12944-016-0319-z.
Catch up growth (CUG) motivated by under-nutrition can lead to insulin resistance (IR) and visceral fat over-accumulation. However, the precise mechanisms on IR induced by adipose tissue changes during CUG remain unresolved.
Experimental rats were divided into three groups: normal chow group, catch up growth group and resveratrol administrated group. The whole experiment was carried out in four stages: 4, 6, 8 and 12 weeks. Peroxisome-proliferator activated receptor gamma (PPAR-γ) and fat-specific protein 27 (FSP27) expression level in epididymal adipose tissues (EAT) and subcutaneous adipose tissues (SAT) were detected along with other IR indicators.
Calorie restriction (CR) significantly increased PPAR-γ expression in EAT while decreased FSP27 expression. During re-feeding, both of the expression of PPAR-γ and FSP27 increased, even FSP27 returned to normal level when CUG for 4 weeks. Although PPAR-γ expression declined slightly at 8 weeks, it was still much stronger than normal chow groups. However, no changes were seen in SAT. Relative insufficiency of FSP27 expression in EAT results in a decrease in lipid storage capacity, causing a series of path physiological changes that led to the formation of IR. Resveratrol inhibited the expression of PPAR-γ and promoted FSP27 expression, thus fundamentally improving IR.
The imbalance between adipose synthesis and storage mediated by PPAR-γ / FSP27 in the EAT plays a pivotal role in the formation of IR during CUG. Resveratrol can correct fat formation and storage imbalance status by up-regulating FSP27 and down-regulating PPAR-γ expression level, ameliorating insulin sensitivity.
营养不良引发的追赶生长（CUG）可导致胰岛素抵抗（IR）和内脏脂肪过度蓄积。然而，追赶生长期间脂肪组织变化诱导胰岛素抵抗的精确机制仍未明确。
将实验大鼠分为三组：正常饮食组、追赶生长组和白藜芦醇给药组。整个实验分四个阶段进行：4周、6周、8周和12周。检测附睾脂肪组织（EAT）和皮下脂肪组织（SAT）中过氧化物酶体增殖物激活受体γ（PPAR-γ）和脂肪特异性蛋白27（FSP27）的表达水平以及其他胰岛素抵抗指标。
热量限制（CR）显著增加附睾脂肪组织中PPAR-γ的表达，同时降低FSP27的表达。在重新喂食期间，PPAR-γ和FSP27的表达均增加，甚至在追赶生长4周时FSP27恢复到正常水平。尽管PPAR-γ表达在8周时略有下降，但仍远高于正常饮食组。然而，皮下脂肪组织未见变化。附睾脂肪组织中FSP27表达相对不足导致脂质储存能力下降，引发一系列病理生理变化，导致胰岛素抵抗的形成。白藜芦醇抑制PPAR-γ的表达并促进FSP27的表达，从而从根本上改善胰岛素抵抗。
附睾脂肪组织中由PPAR-γ/FSP27介导的脂肪合成与储存失衡在追赶生长期间胰岛素抵抗的形成中起关键作用。白藜芦醇可通过上调FSP27和下调PPAR-γ表达水平纠正脂肪形成与储存失衡状态，改善胰岛素敏感性。
