Regulatory roles and mechanisms of alternative RNA splicing in adipogenesis and human metabolic health

Cell & Bioscience

Table 1 Major splicing regulators involved in adipogenesis processes of white, brown, and beige adipose tissues

Splicing regulators	Phenotypes in transgenic animals	Splicing targets	Splicing effects	References
Sam68	The Sam68-KO(knockout) mice: a lean phenotype with reduced body weight and adiposity; WAT browner; increased thermogenesis; reduced lipid stores in BAT; improved insulin sensitivity; abnormal neuronal processes; defective spermatogenesis and osteogenesis	mTOR; Rps6kb1	Enhance WAT adipogenesis; impair browning trans-differentiation	[66,67,68,69,70,71,72,73,74]
FTO	1. The FTO-KO mice: increased postnatal lethality; a lean phenotype; postnatal growth retardation; decreased adiposity; increased energy expenditure 2. The FTO-overexpression mice: obesity with an increase in fat mass; hyperphagia; marked glucose intolerance	RUNX1T1	Enhance WAT adipogenesis	[75,76,77,78,79]
SRSF10	The SRSF10-KO mice: multiple cardiac defects; severely impaired WAT development in embryos	LPIN1; PGC-1α	Enhance WAT adipogenesis	[80,81,82]
RBM4	The RBM4a-KO mice: impaired development of BAT, muscles, and pancreatic β-islets; hyperlipidemia	PRDM16; MBNL1 BAT splicing cascades: RBM4a-SRSF3-MAP4K4; RBM4-MEF2C; RBM4-Nova1-SR-SF6; RBM4-SRPK1; RBM4-Acin1-SRSF3	Enhance BAT adipogenesis	[62, 63, 83,84,85,86,87,88]

ISSN: 2045-3701