Tang Hao-Neng, Tang Chen-Yi, Man Xiao-Fei, Tan Shu-Wen, Guo Yue, Tang Jun, Zhou Ci-La, Zhou Hou-De
Department of Endocrinology and Metabolism, National Clinical Research Center for Metabolic Diseases, The Second Xiangya Hospital, Central South University, 139 Ren-Min Middle Road, Changsha, Hunan 410011 China ; Department of Laboratory Medicine, The Second XiangYa Hospital, Central South University, Changsha, Hunan 410011 China.
Department of Endocrinology and Metabolism, National Clinical Research Center for Metabolic Diseases, The Second Xiangya Hospital, Central South University, 139 Ren-Min Middle Road, Changsha, Hunan 410011 China.
Nutr Metab (Lond). 2017 Jan 5;14:3. doi: 10.1186/s12986-016-0159-x. eCollection 2017.
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 WAT and interscapular 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 () 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.
禁食是治疗体重过度增加和肥胖最广泛规定且自行采用的策略，并且已显示出具有多种有益作用。本研究的目的是确定禁食及随后的再喂养对小鼠脂肪分布的确切作用。
将C57/BL6小鼠禁食24至72小时，然后进行72小时的再喂养。在禁食24、48和72小时以及再喂养12、24、48和72小时时，处死小鼠并收集血清和各种脂肪组织。检测血清生化参数、脂肪组织质量以及不同脂肪库的组织形态学分析。从各种脂肪组织中分离mRNA，并检测产热、内脏特征和脂质代谢相关基因的表达。还比较了禁食和再喂养的幼年小鼠和成年小鼠之间脂肪组织的表型。
禁食优先消耗肠系膜脂肪量并减小肠系膜脂肪库的细胞大小；然而，与内脏脂肪库相比，再喂养优先恢复腹股沟脂肪组织的质量和形态。腹股沟白色脂肪组织（WAT）和肩胛间棕色脂肪组织（BAT）中产热相关基因的表达受到抑制。线粒体生物发生以脂肪库特异性方式受到禁食的影响。此外，短期禁食导致皮下脂肪组织中内脏特征基因增加，而随着禁食时间增加这些基因的表达急剧下降。另外，与内脏脂肪组织相比，再喂养使皮下脂肪库中脂肪生成相关标志物的增强程度更大。尽管在禁食和再喂养的幼年小鼠和成年小鼠之间观察到脂肪组织有类似的表型变化，但这些改变在幼年小鼠中出现得更早且更敏感。
禁食优先消耗内脏脂肪组织中的脂质，而再喂养主要恢复皮下脂肪组织中的脂质，这表明脂肪器官可塑性在食物剥夺或再喂养时对脂肪分布的重要性。
