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JAZF1 heterozygous knockout mice show altered adipose development and metabolism
Authors
Seong-Kyoon Choi
Soyoen Jang
+13 more
Soyoung Jang
Jain Jeong
Myoung Ok Kim
Si-Yong Kim
Jiwon Ko
Wookbong Kwon
Sanggyu Lee
Su-geun Lim
Si Jun Park
Song Park
Zae Young Ryoo
Junkoo Yi
Duhak Yoon
Publication date
1 August 2021
Publisher
Society of Chinese Bioscientists in America
Doi
Cite
Abstract
Background: Juxtaposed with another zinc finger protein 1 (JAZF1) is associated with metabolic disorders, including type 2 diabetes mellitus (T2DM). Several studies showed that JAZF1 and body fat mass are closely related. We attempted to elucidate the JAZF1 functions on adipose development and related metabolism using in vitro and in vivo models. Results: The JAZF1 expression was precisely regulated during adipocyte differentiation of 3T3-L1 preadipocyte and mouse embryonic fibroblasts (MEFs). Homozygous JAZF1 deletion (JAZF1-KO) resulted in impaired adipocyte differentiation in MEF. The JAZF1 role in adipocyte differentiation was demonstrated by the regulation of PPARγ—a key regulator of adipocyte differentiation. Heterozygous JAZF1 deletion (JAZF1-Het) mice fed a normal diet (ND) or a high-fat diet (HFD) had less adipose tissue mass and impaired glucose homeostasis than the control (JAZF1-Cont) mice. However, other metabolic organs, such as brown adipose tissue and liver, were negligible effect on JAZF1 deficiency. Conclusion: Our findings emphasized the JAZF1 role in adipocyte differentiation and related metabolism through the heterozygous knockout mice. This study provides new insights into the JAZF1 function in adipose development and metabolism, informing strategies for treating obesity and related metabolic disorders. © 2021, The Author(s).1
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Last time updated on 22/11/2021
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