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CD38 deficiency suppresses adipogenesis and lipogenesis in adipose tissues through activating Sirt1/PPARγ signaling
Ling-Fang Wang1,2, Lian-Jie Miao1,2, Xiao-Nv Wang1
1Institute of Translational Medicine, Nanchang University, Nanchang, China.
Abstract:
It has been recently reported that CD38 was highly expressed in adipose tissues from obese people and CD38-deficient mice were resistant to high-fat diet (HFD)-induced obesity. However, the role of CD38 in the regulation of adipogenesis and lipogenesis is unknown. In this study, to explore the roles of CD38 in adipogenesis and lipogenesis in vivo and in vitro, obesity models were generated with male CD38-/- and WT mice fed with HFD. The adipocyte differentiations were induced with MEFs from WT and CD38-/- mice, 3T3-L1 and C3H10T1/2 cells in vitro. The lipid accumulations and the alternations of CD38 and the genes involved in adipogenesis and lipogenesis were determined with the adipose tissues from the HFD-fed mice or the MEFs, 3T3-L1 and C3H10T1/2 cells during induction of adipocyte differentiation. The results showed that CD38-/- male mice were significantly resistant to HFD-induced obesity. CD38 expressions in adipocytes were significantly increased in WT mice fed with HFD, and the similar results were obtained from WT MEFs, 3T3-L1 and C3H10T1/2 during induction of adipocyte differentiation. The expressions of PPARγ, AP2 and C/EBPα were markedly attenuated in adipocytes from HFD-fed CD38-/- mice and CD38-/- MEFs at late stage of adipocyte differentiation. Moreover, the expressions of SREBP1 and FASN were also significantly decreased in CD38-/- MEFs. Finally, the CD38 deficiency-mediated activations of Sirt1 signalling were up-regulated or down-regulated by resveratrol and nicotinamide, respectively. These results suggest that CD38 deficiency impairs adipogenesis and lipogenesis through activating Sirt1/PPARγ-FASN signalling pathway during the development of obesity.
Insights
CD38 deficiency protects against obesity by inhibiting adipogenesis and lipogenesis. This occurs through the Sirt1/PPARγ-FASN signaling pathway, impacting fat accumulation during obesity development.
Area of Science:
- Metabolic research
- Obesity research
- Molecular biology
Background:
- CD38 is highly expressed in adipose tissue of obese individuals.
- CD38-deficient mice exhibit resistance to high-fat diet (HFD)-induced obesity.
- The precise role of CD38 in adipogenesis and lipogenesis remains unclear.
Purpose of the Study:
- To investigate the role of CD38 in regulating adipogenesis and lipogenesis.
- To explore the underlying molecular mechanisms in vivo and in vitro.
Main Methods:
- Generation of obesity models using CD38-deficient (CD38-/-) and wild-type (WT) mice fed HFD.
- Induction of adipocyte differentiation in mouse embryonic fibroblasts (MEFs), 3T3-L1, and C3H10T1/2 cells.
- Assessment of lipid accumulation and gene expression related to adipogenesis and lipogenesis.
Main Results:
- CD38-/- mice showed significant resistance to HFD-induced obesity.
- CD38 expression increased in adipocytes of HFD-fed WT mice and in differentiating cells.
- Expressions of PPARγ, AP2, C/EBPα, SREBP1, and FASN were attenuated in CD38-/- cells.
- CD38 deficiency activated Sirt1 signaling, modulated by resveratrol and nicotinamide.
Conclusions:
- CD38 deficiency impairs adipogenesis and lipogenesis.
- This impairment is mediated by the activation of the Sirt1/PPARγ-FASN signaling pathway.
- Targeting CD38 may offer a therapeutic strategy for obesity.
