| First Author | Xu WD | Year | 2024 |
| Journal | Pharmacol Res Perspect | Volume | 12 |
| Issue | 1 | Pages | e1160 |
| PubMed ID | 38174807 | Mgi Jnum | J:361154 |
| Mgi Id | MGI:7856006 | Doi | 10.1002/prp2.1160 |
| Citation | Xu WD, et al. (2024) The blockade of the TGF-beta pathway alleviates abnormal glucose and lipid metabolism of lipodystrophy not obesity. Pharmacol Res Perspect 12(1):e1160 |
| abstractText | TGF-beta is thought to be involved in the physiological functions of early organ development and pathological changes in substantial organ fibrosis, while studies around adipose tissue function and systemic disorders of glucolipid metabolism are still scarce. In this investigation, two animal models, aP2-SREBP-1c mice and ob/ob mice, were used. TGF-beta pathway showed up-regulated in the inguinal white adipose tissue (iWAT) of the two models. SB431542, a TGF-beta inhibitor, successfully increased inguinal white adipocyte size by more than 1.5 times and decreased the weight of Peripheral organs including liver, Spleen and Kidney to 73.05%/62.18%/73.23% of pre-administration weights. The iWAT showed elevated expression of GLUTs and lipases, followed by a recovery of circulation GLU, TG, NEFA, and GLYCEROL to the wild-type levels in aP2-SREBP-1c mice. In contrast, TGF-beta inhibition did not have similar effects on that of ob/ob mice. In vitro, TGF-beta blocker treated mature adipocytes had considerably higher levels of glycerol and triglycerides than the control group, whereas GLUTs and lipases expression levels were unchanged. These findings show that inhibiting the abnormally upregulated TGF-beta pathway will only restore iWAT expansion and ameliorate the global metabolic malfunction of glucose and lipids in lipodystrophy, not obesity. |
