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The role of expression imbalance between adipose synthesis and storage mediated by PPAR-γ/FSP27 in the formation of insulin resistance in catch up growth.
Wang, Su-Xing; Wei, Jin-Gang; Chen, Lu-Lu; Hu, Xiang; Kong, Wen.
Afiliación
  • Wang SX; The Second Department of Geriatrics, Hebei General Hospital, Shijiazhuang, 050051, China.
  • Wei JG; Department of general surgery, The fifth hospital of Shijiazhuang City, Shijiazhuang, 050024, China.
  • Chen LL; Department of Endocrinology, Union Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, 430022, China. cheria_chen@126.com.
  • Hu X; Department of Endocrinology, Union Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, 430022, China.
  • Kong W; Department of Endocrinology, Union Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, 430022, China.
Lipids Health Dis ; 15(1): 173, 2016 Oct 04.
Article en En | MEDLINE | ID: mdl-27716232
BACKGROUND: 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. METHODS: 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. RESULTS: 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. CONCLUSIONS: 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.
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Texto completo: 1 Banco de datos: MEDLINE Asunto principal: Resistencia a la Insulina / Proteínas / PPAR gamma / Obesidad Límite: Animals / Humans / Male Idioma: En Revista: Lipids Health Dis Asunto de la revista: BIOQUIMICA / METABOLISMO Año: 2016 Tipo del documento: Article País de afiliación: China

Texto completo: 1 Banco de datos: MEDLINE Asunto principal: Resistencia a la Insulina / Proteínas / PPAR gamma / Obesidad Límite: Animals / Humans / Male Idioma: En Revista: Lipids Health Dis Asunto de la revista: BIOQUIMICA / METABOLISMO Año: 2016 Tipo del documento: Article País de afiliación: China