Plasticity of adipose tissue in response to fasting and refeeding in male mice

The effects of fasting and refeeding on fat distribution.

APR 14, 2009

Written by Hao-Neng Tang, Chen-Yi Tang, Xiao-Fei Man, Shu-Wen Tan, Yue Guo, Jun Tang, Ci-La Zhou, Hou-De Zhou

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Fasting is the most widely prescribed and self-imposed strategy for treating excessive weight gain and obesity, and has been shown to exert a number of beneficial effects. The aim of the present study was to determine the exact role of fasting and subsequent refeeding on fat distribution in mice. C57/BL6 mice fasted for 24 to 72 h and were then subjected to refeeding for 72 h. At 24, 48 and 72 h of fasting, and 12, 24, 48 and 72 h of refeeding, the mice were sacrificed, and serum and various adipose tissues were collected. Serum biochemical parameters, adipose tissue masses and histomorphological analysis of different depots

were detected. MRNA was isolated from various adipose tissues, and the expressions of thermogenesis, visceral signature and lipid metabolism-related genes were examined. The phenotypes of adipose tissues between juvenile and adult mice subjected to fasting and refeeding were also compared. Fasting preferentially consumed mesenteric fat mass and decreased the cell size of mesenteric depots; however, refeeding recovered the mass and morphology of inguinal adipose tissues preferentially compared with visceral depots. Thermogenesis-related gene expression in the inguinal white adipose tissue (WAT) and interscapular brown adipose tissue (BAT) were suppressed. Mitochondrial biogenesis was affected by fasting in a depot-specific manner. Furthermore, a short period of fasting led to an increase in visceral signature genes (Wilms tumour 1(Wt1), transcription factor 21 (Tcf21)) in subcutaneous adipose tissue, while the expression of these genes decreased sharply as the fasting time increased. Additionally, lipogenesis-related markers were enhanced to a greater extent greater in subcutaneous depots compared with those in visceral adipose tissues by refeeding. Although similar phenotypic changes in adipose tissue were observed between juvenile mice and adult mice subjected to fasting and refeeding, the alterations appeared earlier and more sensitively in juvenile mice. Fasting preferentially consumes lipids in visceral adipose tissues, whereas refeeding recovers lipids predominantly in subcutaneous adipose tissues, which indicated the significance of plasticity of adipose organs for fat distribution when subject to food deprivation or refeeding.



In summary, our results demonstrated that fasting induced preferential mobilization of lipids from the mesenteric adipose tissue depot, whereas refeeding induced preferential restoration of adipose tissue from the inguinal depot. These findings confirmed that long-term fasting and refeeding could lead to a reduction of the metabolically harmful’ visceral adipose tissue, as well as highlighting the role of plasticity of adipose organs on different anatomical sites of adipose tissue when subject to environmental changes. A definite trend is evident that modulating the plasticity of adipose organs represents a potential strategy to combat obesity. However, it should be noted that only normal mice were used in the current study and experiments on obese mice are necessary for in future research. Moreover, body fat distribution is controlled by genetic factors. Therefore, it is appropriate to explore the mechanism of the effect of fasting and refeeding on various adipose tissues via transcriptome sequencing in future research.