Phospholipase C-related catalytically inactive protein can regulate obesity, a state of peripheral inflammation.
Phospholipase C-related catalytically inactive protein can regulate obesity, a state of peripheral inflammation.
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DOI：
10.1016/j.jdsr.2016.06.001
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发表时间：
2017-02
期刊：
影响因子：
--
通讯作者：
Kanematsu T
中科院分区：
文献类型：
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作者：
Yamawaki Y;Oue K;Shirawachi S;Asano S;Harada K;Kanematsu T
肥胖症被定义为不正常或过度的脂肪积累。脂肪中的慢性炎症影响肥胖相关疾病的发展。许多报告指出，肥胖增加了许多疾病的发病风险，包括高血压、血脂异常、2型糖尿病、冠心病、中风、睡眠呼吸暂停以及乳腺癌、前列腺癌和结肠癌，导致死亡率增加。肥胖症还与慢性神经病理学病症如抑郁症和阿尔茨海默病有关。然而，有强有力的证据表明，减肥可以降低这些风险，通过限制血压和改善血清甘油三酯，总胆固醇，低密度脂蛋白（LDL）-胆固醇和高密度脂蛋白（HDL）-胆固醇的水平。预防和控制肥胖是复杂的，需要多方面的方法。阐明驱动脂肪代谢（脂肪生成和脂解）的分子机制旨在开发控制肥胖的临床治疗方法。我们最近报道了一种新的脂肪代谢调节机制：一种蛋白磷酸酶结合蛋白，磷脂酶C相关催化失活蛋白（PRIP），通过磷酸化调节调节白色脂肪细胞的脂解和棕色脂肪细胞的产热。PRIP缺乏导致小鼠脂肪积累减少和能量消耗增加，导致瘦型。在这里，我们评估PRIP作为一个新的治疗目标，控制肥胖。
Obesity is defined as abnormal or excessive fat accumulation. Chronic inflammation in fat influences the development of obesity-related diseases. Many reports state that obesity increases the risk of morbidity in many diseases, including hypertension, dyslipidemia, type 2 diabetes, coronary heart disease, stroke, sleep apnea, and breast, prostate and colon cancers, leading to increased mortality. Obesity is also associated with chronic neuropathologic conditions such as depression and Alzheimer's disease. However, there is strong evidence that weight loss reduces these risks, by limiting blood pressure and improving levels of serum triglycerides, total cholesterol, low-density lipoprotein (LDL)-cholesterol, and high-density lipoprotein (HDL)-cholesterol. Prevention and control of obesity is complex, and requires a multifaceted approach. The elucidation of molecular mechanisms driving fat metabolism (adipogenesis and lipolysis) aims at developing clinical treatments to control obesity. We recently reported a new regulatory mechanism in fat metabolism: a protein phosphatase binding protein, phospholipase C-related catalytically inactive protein (PRIP), regulates lipolysis in white adipocytes and heat production in brown adipocytes via phosphoregulation. Deficiency of PRIP in mice led to reduced fat accumulation and increased energy expenditure, resulting in a lean phenotype. Here, we evaluate PRIP as a new therapeutic target for the control of obesity.