产热
内科学
内分泌学
动力学(音乐)
产热素
脂肪组织
生物
化学
细胞生物学
医学
心理学
教育学
作者
Carolline Santos Miranda,Flávia Maria Silva-Veiga,Daiana Araujo Santana-Oliveira,Isabela Macedo Lopes Vasques-Monteiro,Julio Beltrame Daleprane,Vanessa Souza‐Mello
出处
期刊:Nutrition
[Elsevier]
日期:2024-01-01
卷期号:117: 112253-112253
被引量:1
标识
DOI:10.1016/j.nut.2023.112253
摘要
To investigate the role of PPAR activation (single PPARα or PPARγ, and dual PPARαγ) on UCP1-dependent and independent thermogenic pathways and mitochondrial metabolism in the subcutaneous white adipose tissue of high-fat-fed mice. Male C57BL/6 mice received either a control diet (C, 10% lipids) or a high-fat diet (HF, 50% lipids) for 12 weeks. Then, the HF group was divided to receive the treatments for four weeks: HFγ (pioglitazone, 10 mg/kg), HFα (WY-14643, 3.5 mg/kg), and HFαγ (tesaglitazar, 4 mg/kg). The HF group was overweight, insulin resistant, and had subcutaneous white adipocyte dysfunction. Treatment with PPARα and PPARαγ reduced body mass, mitigated insulin resistance, and induced browning with increased UCP1-dependent and independent thermogenesis activation and improved mitochondrial metabolism to support the beige adipocyte phenotype. PPARα and dual PPARαγ activation recruited UCP1+ beige adipocytes and favored UCP-1 independent thermogenesis, yielding body mass and insulin sensitivity normalization. Preserved mitochondrial metabolism emerges as a potential target for obesity treatment using PPAR agonists, with possible clinical applications.
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