Ctnnb1/β-catenin inactivation in UCP1-positive adipocytes augments the browning of white adipose tissue

Chen, Na; Yuan, Mingyang; Chen, Maopei; Liu, Ruixin; Wang, Jiqiu; Lu, Peng

doi:10.1016/j.isci.2023.106552

iScience

2023

DOI: 10.1016/j.isci.2023.106552

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Ctnnb1/β-catenin inactivation in UCP1-positive adipocytes augments the browning of white adipose tissue

Na Chen¹,

Mingyang Yuan²,

Maopei Chen³

et al.

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2024

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Cited by 3 publications

References 59 publications

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Hepatic Dyrk1b impairs systemic glucose homeostasis by modulating Wbp2 expression in a kinase activity-dependent manner

Li,

Zou,

Shen

et al. 2024

Heliyon

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Hepatic Dyrk1b impairs systemic glucose homeostasis by modulating Wbp2 expression in a kinase activity-dependent manner

Li,

Zou,

Shen

et al. 2024

Heliyon

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Targeting GSK‐3β for adipose dysfunction and cardiovascular complications of metabolic disease: An entangled WNT/β‐catenin question

Alotaiq,

Khalifa,

Youssef

et al. 2024

The FASEB Journal

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Individuals with metabolic syndrome have a high risk of developing cardiovascular disorders that is closely tied to visceral adipose tissue dysfunction, as well as an altered interaction between adipose tissue and the cardiovascular system. In metabolic syndrome, adipose tissue dysfunction is associated with increased hypertrophy, reduced vascularization, and hypoxia of adipocytes, leading to a pro‐oxidative and pro‐inflammatory environment. Among the pathways regulating adipose tissue homeostasis is the wingless‐type mammary tumor virus integration site family (Wnt) signaling pathway, with both its canonical and non‐canonical arms. Various modulators of the Wnt signaling have been identified to contribute to the development of metabolic diseases and their cardiovascular complications, with a particularly significant role played by Glycogen Synthase Kinase‐3β (GSK‐3β). GSK‐3β levels and activities have various and often contrasting roles in obesity and related metabolic disorders, as well as their cardiovascular sequelae. Here, we explore the possibility that altered Wnt signaling and GSK‐3β activities could serve as a connection between adipose tissue dysfunction and the development of cardiovascular disease in individuals with metabolic syndrome. We attempt to define a context‐specific approach for intervention, which could possibly serve as a novel disease modifying therapy for the mitigation of such complications.

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Ling-gui-zhu-gan granules reduces obesity and ameliorates metabolic disorders by inducing white adipose tissue browning in obese mice

Li,

Ye,

Zhao

et al. 2024

Front. Physiol.

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BackgroundLing-gui-zhu-gan (LGZG) formula has been demonstrated to effectively ameliorate the clinical symptoms of patients with obesity or metabolic syndrome. This study aimed to explore both the effect and the underlying mechanisms of LGZG against obesity.MethodsMale C57BL/6N mice were randomized into four groups (n = 8): normal control (NC), obese (OB), metformin (Met), and LGZG. After 8 weeks of gavage administration, the pharmacological effects of LGZG on obesity and metabolism were investigated using biochemical parameters, histomorphological examination, and lipidomics techniques. Pivotal factors associated with white adipose tissue browning were evaluated using quantitative real-time polymerase chain reaction and western blotting.ResultsThe results revealed that LGZG reduced the levels of obesity markers, including body weights, body fat mass and food intake in obese mice. Further evaluations highlighted that LGZG restored glucose homeostasis and significantly improved insulin sensitivity in obese mice. Importantly, LGZG could adjust serum lipid profiles and regulate the lipidomic spectrum of intestinal contents, with noticeable shifts in the levels of certain lipids, particularly diacylglycerols and monoacylglycerols. Histopathological examinations of LGZG-treated mice also revealed more favorable adipose tissue structures than their obese counterparts. Furthermore, we found that LGZG upregulated the expression of several key thermogenesis-related factors, such as UCP1, PRDM16, PGC-1α, PPARα, PPARγ, CTBP1, and CTBP2 in white adipose tissues.ConclusionOur findings position LGZG as a novel strategy for preventing obesity and improving metabolic health.

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Ctnnb1/β-catenin inactivation in UCP1-positive adipocytes augments the browning of white adipose tissue

Cited by 3 publications

References 59 publications

Hepatic Dyrk1b impairs systemic glucose homeostasis by modulating Wbp2 expression in a kinase activity-dependent manner

Hepatic Dyrk1b impairs systemic glucose homeostasis by modulating Wbp2 expression in a kinase activity-dependent manner

Targeting GSK‐3β for adipose dysfunction and cardiovascular complications of metabolic disease: An entangled WNT/β‐catenin question

Ling-gui-zhu-gan granules reduces obesity and ameliorates metabolic disorders by inducing white adipose tissue browning in obese mice

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