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首页> 外文期刊>Endocrinology >Reduced adiposity and high-fat diet-induced adipose inflammation in mice deficient for phosphodiesterase 4B.
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Reduced adiposity and high-fat diet-induced adipose inflammation in mice deficient for phosphodiesterase 4B.

机译：缺乏磷酸二酯酶4B的小鼠的肥胖症和高脂饮食诱导的脂肪炎症减少。

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摘要

The concept that obesity is an inflammatory state has changed our understanding of this condition and suggested that pharmacological interventions targeting inflammation may be useful strategies to improve metabolic complications of obesity. Phosphodiesterase 4 (PDE4) inhibitors exhibit profound antiinflammatory effects, but whether PDE4 inhibition suppresses obesity-induced inflammation is unknown. Among PDE4 isoforms, PDE4B is the major species mediating inflammatory responses. We therefore examined obesity-related phenotypes in mice deficient for PDE4B. Compared with wild-type littermates, PDE4B-null mice were leaner, with lower fat pad weights, smaller adipocytes, and decreased serum leptin levels on both chow and high-fat diets (HFDs). PDE4B deficiency suppressed TNF-alpha mRNA levels and macrophage infiltration in white adipose tissue in mice on HFD, but insulin sensitivity was unaltered. PDE4B-null mice on HFDs had increased locomotor activity. These results suggest a previously unappreciated role for PDE4B in the regulation of energy balance and that PDE4B inhibitors could have utility in treatment of obesity and for suppression of obesity-induced inflammation in white adipose tissue.
机译：肥胖是一种炎症状态的概念已经改变了我们对这种疾病的理解，并表明针对炎症的药理干预措施可能是改善肥胖代谢并发症的有用策略。磷酸二酯酶4（PDE4）抑制剂具有深厚的抗炎作用，但是PDE4抑制作用是否能抑制肥胖引起的炎症尚不清楚。在PDE4同工型中，PDE4B是介导炎症反应的主要物种。因此，我们在缺乏PDE4B的小鼠中检查了肥胖相关的表型。与野生型同窝仔相比，无PDE4B的小鼠更瘦，脂肪垫重量更轻，脂肪细胞更小，高脂饮食和高脂饮食（HFD）的血清瘦素水平降低。 PDE4B缺乏抑制了HFD小鼠的白色脂肪组织中的TNF-αmRNA水平和巨噬细胞浸润，但胰岛素敏感性未改变。 HFDs上的PDE4B-null小鼠运动能力增强。这些结果表明，PDE4B在调节能量平衡方面的作用是前所未有的，PDE4B抑制剂可用于治疗肥胖症和抑制肥胖引起的白色脂肪组织炎症。

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