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

Abstract

BackgroundFasting 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.MethodsC57/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.ResultsFasting 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 (Wt1, 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.ConclusionsFasting 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.Electronic supplementary materialThe online version of this article (doi:10.1186/s12986-016-0159-x) contains supplementary material, which is available to authorized users.

Differential regulation of the immune system in a brain-liver-fats organ network during short term fasting

“…For instance, between Phases I and III we found decreasing expression levels of Nrg4, Lep and Ucp1 in psWAT, decreasing expression levels of Reg1 in STM, and increased expression of Egr1, Fam107a, Map3k6, and Mt1 in the LIV ( Fig. 2c; Additional file 5: Table S4), consistent with previous STF studies in rodents [11,20,[29][30][31][32]. In sum, by allowing the similarity of HVGs among the samples to drive their clustering in an organ-specific manner, we were able to detect differential temporal effects of STF on the transcriptional dynamics across multiple organs.…”

Proliferation of nutrition sensing preadipocytes upon short term HFD feeding

“…Changes in metabolism, distribution and cellularity of adipose tissue is dependent on intrinsic factors such as age, as well as extrinsic factors such as overnutrition. 2,28 We aimed to study how HFD affects adipose tissue dynamics in relation to age. To this effect, we fed mice of various ages (young (8 weeks), adult (16 weeks), middle aged (28 weeks), old (51 weeks) and very old (83 weeks)) chow or HFD for 4 days and labeled proliferating preadipocytes by administering EdU in the drinking water (Schema in Figure 1A).…”

“…2,[4][5][6][7][8][9] Conversely, removal of HFD was shown to reverse most of these changes. 2,10,11 For some time it was believed, that the total number of fat cells is set during adolescence and a change of fat mass in adults is exclusively caused by hypertrophy. 12,13 However, it was recently demonstrated that hyperplasia plays an important role in obesity and that the ability for an increase in adipocyte number persists for lifetime even after severe weight loss.…”

“…It was shown that in as short as 24h of fasting and refeeding, changes in cell size and gene expression were detectable in various adipose tissue depots. 2,3 Long-and short-term overnutrition has been shown to directly influence adipose tissue and to cause hypertrophy, inflammation, insulin resistance, and changes in plasma parameters in mice and humans. 2,[4][5][6][7][8][9] Conversely, removal of HFD was shown to reverse most of these changes.…”

“…2,3 Long-and short-term overnutrition has been shown to directly influence adipose tissue and to cause hypertrophy, inflammation, insulin resistance, and changes in plasma parameters in mice and humans. 2,[4][5][6][7][8][9] Conversely, removal of HFD was shown to reverse most of these changes. 2,10,11 For some time it was believed, that the total number of fat cells is set during adolescence and a change of fat mass in adults is exclusively caused by hypertrophy.…”