한빛사논문
- 조회414
Jae Woo Jung1,2,3 Ji Eon Kim1,2 Eunmi Kim1,2, Hyejin Lee1 Haesong Lee1 Eun-Ae Shin1 Jung Weon Lee1,2,3
1Department of Pharmacy, College of Pharmacy, Seoul National University, Seoul, Republic of Korea
2Research Institute of Pharmaceutical Sciences, College of Pharmacy, Seoul National University, Seoul, Republic of Korea
3Interdisciplinary Program in Genetic Engineering, Seoul National University, Seoul, Republic of Korea
Correspondence Jung Weon Lee
Jae Woo Jung, Ji Eon Kim and Eunmi Kim contributed equally to this study.
Abstract
Transmembrane 4 L six family member 5 (TM4SF5) is involved in chronic liver disease, although its role in glucose homeostasis remains unknown. TM4SF5 deficiency caused age-dependent glucose (in)tolerance with no link to insulin sensitivity. Further, hepatic TM4SF5 binding to GLUT1 promoted glucose uptake and glycolysis. Excessive glucose repletion caused hepatocytes to secrete small extracellular vesicles (sEVs) loaded with TM4SF5 (hep-sEVTm4sf5), suggesting a role for sEVTm4sf5 in glucose metabolism and homeostasis. Hep-sEVTm4sf5 were smaller than sEVControl and recruit proteins for efficient organ tropism. Liver-derived sEVs, via a liver-closed vein circuit (LCVC) using hepatic TM4SF5-overexpressing (Alb-Tm4sf5 TG) mice (liv-sEVTm4sf5), improved glucose tolerance in Tm4sf5−/− KO mice and targeted brown adipose tissues (BATs), possibly allowing the clearance of blood glucose as heat independent of UCP1. Taken together, hep-sEVTm4sf5 might clear high extracellular glucose levels more efficiently by targeting BAT compared with hep-sEVControl, suggesting an insulin-like role for sEV™4SF5 in affecting age-related metabolic status and thus body weight (BW).
논문정보
- Research article
- 2022년 09월 (BRIC 등록일 2022-09-08)
- 국내 연구진
- 의약학 > 약학
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