内分泌
词汇介绍
拓展阅读
解析
Obesity 英 /əʊˈbiːsəti/ 美 /o'bisəti/
释 义 n.肥胖
例 句 And obesity is a huge problem in the United States, especially in the African american community and other minority communities. 在美国,肥胖症是一个严重的问题,尤其在非裔美国人和其它少数民族群体中。
概述
概述
肥胖是一种医学病症,其中过量的身体脂肪可能对健康有不利影响。当人们的体重指数(BMI)超过30kg/ m2,通常被认为是肥胖。肥胖会增加各种疾病和状况的可能性,尤其是心血管疾病,2型糖尿病,阻塞性睡眠呼吸暂停,某些类型的癌症,骨关节炎和抑郁症等。
病理原因
(1)睡眠不足;(2)内分泌干扰物(干扰脂质代谢的环境污染物);(3)周围温度变化的幅度降低;(4)吸烟减少,因为吸烟抑制食欲;(5)使用可能会导致体重增加的药物(例如,药物的增加的非典型抗精神病药物);(6)种族和年龄组的比例的增加趋向于更重;(7)怀孕年龄延后(可能导致儿童肥胖);(8)遗传的风险因素;(9)较高的BMI人群的自然选择;(10)相似体重人群的择偶都会导致肥胖风险因素增加。
病理生理学
肥胖的发展和维持涉及许多可能的病理生理机制。瘦素和生长素释放肽是在外周产生的,它们通过对中枢神经系统的作用来控制食欲。特别是,它们和其他与食欲有关的激素作用于下丘脑,下丘脑是调节食物摄入和能量消耗的核心区域。下丘脑内部有多个回路,有助于其在整合食欲中发挥作用,即黑皮质素途径是最广为人知的。回路始于下丘脑的弓形核区域,该区域分别输出至下丘脑外侧(LH)和腹侧下丘脑(VMH),大脑的进食中心和饱腹感中心。弓形核包含两组不同的神经元,第一组共表达神经肽Y(NPY)和刺骨相关肽(AgRP),并且对LH具有刺激性输入,对VMH具有抑制性输入。第二组共表达前皮素(POMC)和可卡因和苯丙胺调节的转录物(CART),并且对VMH具有刺激性输入,对LH具有抑制性输入。因此,NPY / AgRP神经元刺激进食并抑制饱腹感,而POMC / CART神经元刺激饱食并抑制进食。两组弓形核神经元均部分受瘦素调节。瘦素在刺激POMC / CART组的同时抑制NPY / AgRP组。因此,通过瘦素缺乏或瘦素抗性导致的瘦素信号传导缺乏会导致过度喂养,并可能导致肥胖的某些遗传和获得性形式。
治疗
肥胖症的主要治疗方法包括节食和体育锻炼。节食,如生活方式的改变的一部分,产生持续的体重减轻。建议结合饮食变化和运动的强化行为干预。
有五种药物可以长期使用,奥利司他,洛塞卡林,利拉鲁肽,芬特明-托吡酯和纳曲酮-安非他酮。与安慰剂相比,一年后它们导致的体重减轻范围为3.0至6.7千克(6.6-14.8磅)。
肥胖症最有效的治疗方法是减肥手术。类型包括腹腔镜可调节胃束带,Roux-en-Y胃旁路,垂直袖胃切除术和胆胰转移术。
病态肥胖成人脂肪细胞葡萄糖转运蛋白4 (GLUT4) 和aquaglyceroporin-7 (AQP7) 降低: 代谢功能障碍的可能早期标志物
发表时间:2019-10-07
影响指数:1.6
作者: Roza Mourelatou
期刊:Hormones
Obesity, whose rising trend is alarming, has reached global proportions. Morbid obesity (BMI > 40 kg/m2) is associated with a large number of metabolic comorbidities, including insulin resistance (IR), hyperlipidemia, diabetes mellitus type 2 (DM2), and cardiovascular disease. Excess energy intake results in adipocyte hypertrophy and macrophage infiltration, which can lead to chronic systemic inflammation and ectopic fat accumulation. Hypertrophy of the mature adipocytes with fat accumulation and enlargement of the lipid droplets is considered to be the result of a disrupted balance between lipolysis and lipogenesis. These abnormalities, along with reduced adipocyte differentiation and aberrant adipokine secretion, such as reduced adiponectin, cause pathological adipose tissue expansion. During lipogenesis, the insulin signaling pathway is activated, resulting in activation of the insulin receptor substrate 1 (IRS1), which phosphorylates the p85 regulatory subunit of phosphatidyl-inosytol-3 kinase (PI3-kinase), causing the activation of the p110 catalytic subunit of PI3K and the activation of serine/threonine protein kinase PKBβ/AktΙΙ, with the assistance of a small GTPase, Rab5. The final result is the translocation of glucose transporter 4 (GLUT4) to the cellular membrane for glucose uptake. Once glucose enters the adipocyte, it is converted into glycerol-3-phosphate and is incorporated, together with fatty acids (FA), into the lipid droplet to produce triglycerides (TGs). It has been reported that disruption of key components of the insulin intracellular signaling pathway and GLUT4 is associated with adipose tissue IR and decreased glucose uptake which may disrupt whole-body insulin sensitivity. It seems that decreased GLUT4 expression occurs prior to the development of hyperglycemia and that GLUT4 can be used as an early marker of DM2.
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