| First Author | Chen Y | Year | 2022 |
| Journal | iScience | Volume | 25 |
| Issue | 9 | Pages | 104894 |
| PubMed ID | 36060061 | Mgi Jnum | J:328844 |
| Mgi Id | MGI:7335658 | Doi | 10.1016/j.isci.2022.104894 |
| Citation | Chen Y, et al. (2022) L2Delta13, a splicing isoform of lysyl oxidase-like 2, causes adipose tissue loss via the gut microbiota and lipid metabolism. iScience 25(9):104894 |
| abstractText | Obesity is primarily characterized by the dysregulation of lipid metabolism and gut microbiota. Here, we found that the body weight of transgenic mice overexpressing L2Delta13, a selectively spliced isoform of lysyl oxidase-like 2 (LOXL2), was lower than that of wild-type (WT) mice. Numerous microbiotas were significantly changed and most microbial metabolites were abnormal in L2Delta13 mice. Lipid metabolites in feces were negatively correlated with those in plasma, suggesting that L2Delta13 may affect lipid uptake, and potentially, adipose tissue homeostasis. This was supported by the weight loss and decreased area of adipose tissue in L2Delta13 mice. Adipogenic differentiation of primary stromal vascular fraction cells showed that the lipid droplets of L2Delta13 cells were significantly smaller than those of WT cells. Adipocyte differentiation-associated genes were also downregulated in adipose tissue from L2Delta13 mice. Thus, L2Delta13 can induce adipose tissue loss in mice by affecting gut microbiota homeostasis and multi-tissue lipid metabolism. |
