Cell Metab:戒酒药物能减肥之“双硫仑”

2020-08-17 森普 免疫细胞研究bioworld

研究中,研究人员使用双硫氟仑(DSF)来对抗饮食引起的肥胖,使体重正常化并改善与身体成分和胰岛素反应相关的各种生理结果。其发现双硫氟仑(DSF)对饮食引起的肥胖的预防和治疗作用。

在Cell Metabolism期刊上发表文章Disulfifiram Treatment Normalizes Body Weight in Obese Mice。在本研究中,研究人员使用双硫氟仑(DSF)来对抗饮食引起的肥胖,使体重正常化并改善与身体成分和胰岛素反应相关的各种生理结果。其发现双硫氟仑(DSF)对饮食引起的肥胖的预防和治疗作用,以及DSF降低喂养效率并恢复胰岛素应答。除此之外DSF可以减轻肥胖小鼠的肝骨化和胰岛增生。

对于许多肥胖者来说,改变行为和生活方式对于长期保持减肥效果是有效的,因此,需要通过外科手术和/或药物干预来改变食欲或卡路里的吸收。目前美国FDA批准的用于控制肥胖的减肥药包括奥利司他、氯卡司林、芬特明/托吡喃胺、布基恩、二甲双胍、纳曲酮和利拉格鲁肽。然而,与肥胖作斗争需要长期使用安全有效的药物,最好是能够减轻其并发疾病的药物,如改善全身血糖和脂质稳态。

在过去的五十年里,二硫氟(DSF,化学上称为四乙基硫脲二硫醚,商业上称为抗滥用药)已被广泛用于酒精中毒的厌恶治疗。这是一种FDA批准的药物,耐受性好,副作用少。

DSF和二硫代氨基甲酸家族的相关成员,如吡rrolidinedithiocarbamate (PDTC),最初被发现是完整细胞中转录因子NFkB的抑制剂并且可降低急性胰腺炎中游离谷胱甘肽和白介素-18的水平。

虽然DSF在体内对抗炎症是有效的,但尚不清楚该药物是否也能有效防止体内平衡机制的失调,由高脂肪饮食引起的消费。在这项研究中,研究人员评估了长期使用DSF作为预防和治疗节食引起的小鼠肥胖的药物。此外,研究人员通过评估一些生理和组织学参数,分析了治疗小鼠在体重、形态测量、代谢性能以及胰腺和肝脏结构方面的变化。

其中一些结果也在大鼠身上进行了研究。总的来说,研究人员的结果表明,DSF在预防和治疗两方面使体重正常化,同时逆转通常与饮食引起的肥胖相关的代谢异常。

研究人员评估了DSF对14周雄性C57BL/6J小鼠表型和代谢参数的影响。在食物中加入DSF的小鼠的体重始终低于各自的HFD和SD对照组。为了确定对DSF治疗的生理反应和适应,研究人员采用了在研究人员实验室常规使用的完善的时间表。非重大的差异在日常食物摄取DSF和对照组之间观察到整个研究的持续时间,加上饲养效率的大幅削减,定义为变化在BW数量的卡路里摄入,DSF-treated动物喂一个HFD或者SD饮食。排除食品适口性混杂因素,禁食动物在家里笼子里有一个预先确定的数量的食物在黑暗周期和食物消耗的数量在一个小时内被记录,发现在老鼠DSF大于对照组。在饮食中补充DSF会显着增加瘦脂肪比,而与饮食无关,与下体脂肪质量一致。接下来,研究人员将小鼠放置在代谢室中60小时,评估了DSF对体内能量代谢测量的影响。通过测量呼吸交换率(RER)来检测底物利用率。RER接近0.7表示脂类利用率,而RER为1.0表示碳水化合物被用作能源。在实验过程中,无论DSF是否存在,HFD小鼠的RER均为0.78,其消耗O2、产生CO2和产热的日变化规律都不同。将3个暗周期和2个光周期测得的参数取平均值。HFDL和HFDH小鼠的O2利用率和CO2产量显着低于对照组,转化为更少的能量消耗(EE)。在DSF存在或不存在的情况下,sd喂养的小鼠的RER水平为0.9 -0.95。与SD对照组相比,在SDL和SDH小鼠中也观察到DSF对O2消耗、CO2产生和热量产生的日变化模式的显着但较弱的影响。

由于脂质积累和局部炎症,食用HFD与肝损伤有关。对小鼠冷冻固定肝组织进行组织化学分析,以确定DSF对饮食引起的肝脂肪变性和纤维化增加的影响。使用HFD 41周的小鼠表现出相当水平的脂肪和胶原浸润,以及较低的糖原沉积。在喂食sd的小鼠的肝脏中也观察到类似的信号,尽管程度较轻。在两个饮食组中,DSF完全阻止了这种炎症前表现和糖原的损失,扫描电子显微镜证实了在DSF治疗后肝脏脂肪含量的急剧减少。HFD喂养导致肝星状细胞数量显着增加,被认为具有储存膳食脂肪和促进纤维化的作用。补充DSF降低了两个饮食组的星状细胞数量,肝窦内皮的孔隙率几乎没有变化。DSF减弱了HFD引起的肝甘油三酯水平的大幅升高。总之,这些发现表明,长期使用DSF可以通过防止饮食引起的肝功能障碍和损伤来维持肝脏稳态。有证据表明胰岛细胞增生先于胰岛素抵抗的发展。因此,研究人员通过形态测量和免疫组化方法来评估DSF对胰腺b细胞功能的影响。与HFD对照相比,采用DSF饲喂的HFDH小鼠胰岛总大小和增生性胰岛数量显着减少,同时大量a细胞(胰高血糖素阳性)积累,而b细胞(胰岛素阳性)减少。尽管如此,HFDH小鼠每个胰岛的a细胞数量与HFD对照组相似它们更小的总胰岛大小。在sd饲喂的小鼠中,补充DSF也会减少胰岛的大小,但不会改变a细胞和b细胞的百分比。各组动物每个胰岛a细胞总数与胰岛总大小一致。看来DSF引起的胰岛素敏感性的改善是由于b细胞增生的减少和饮食引起的胰岛素分泌失调的纠正。

尽管HFDL和HFDH小鼠的摄食量与HFD对照组相同(雄鼠和雌鼠分别为3.0 0.1和2.4 0.1 g/小鼠/日),但与体重一致的HFD对照组相比,HFDL和hdh小鼠的摄食效率显着降低。正如所料,老鼠对慢性HFD最初12周获得了大量的重量和肥胖和胰岛素抵抗的表现出特征如6小时后血糖快速升高和延迟血糖间隙在ITT。继续使用HFD 12周的小鼠在这些表型中表现出恶化,而SD替代导致体重、肥胖和空腹血糖水平正常化。更重要的是,在喂食DSF的小鼠中,HFD引起的体重增加和各种形态变化得到了逆转。同样,通过核磁共振或MRI测量,两种剂量的DSF均可减少肥胖和增加瘦/脂肪比例,以及降低循环血糖水平。HFDL和HFDH小鼠体重的迅速下降,加上代谢益处的增加,反映了返回SD喂养的小鼠的情况。

持续的食物摄入量减少至少可以部分解释DSF对体重减轻的影响。当单独使用HFD+DSF小鼠时,喂养效率(定义为BW变化与消耗热量的比值)随着时间的推移而降低。研究人员推测,这种代谢的增加是由于在12周的HFD喂养期间白色脂肪组织(WATs)中可用脂肪酸的活跃酯化所致。

接下来,研究人员在另一个肥胖的临床前模型中进行了研究,以确定DSF的这些效应的可译性。为了达到这个目标,3个月大的雄性斯普拉格道利大鼠,被认为容易发展成肥胖,被维持12周,要么只吃标准周,要么吃低剂量和高剂量DSF(100和200毫克/公斤体重)的周。三组动物食用相同数量的食物,体重增加速率相同,除了DSF干预开始后延迟2周。使用EchoMRI评估治疗2、4、8周时的身体成分,并使用BW对数据进行标准化。在DSF处理的大鼠中,脂肪量的显着减少和瘦肉组织量的增加转化为较高的瘦脂肪比。除此之外,研究人员发现DSF对空腹血糖和胰岛素水平没有显着影响,而在DSF处理的大鼠中,肝脏甘油三酯呈下降趋势。总的体重和四头肌重量不受DSF补充的影响,而与对照组相比,高剂量的DSF促进肝脏体重增加和三个脂肪库的减少,这与DSF介导的脂肪质量损失一致。肝窦内皮细胞中的穿孔可介导饮食中大量营养素(如脂肪酸、肠道衍生分子)从循环中的清除,并促进基质在血液和肝细胞之间的转移。DSF明显增加了开窗的频率,而减少了开窗的平均直径。总之,这些观察结果支持了DSF治疗通过保存肝功能改善机体反应的观点。

原始出处:

Michel Bernier, Sarah J Mitchell, Devin Wah, et al.Disulfiram Treatment Normalizes Body Weight in Obese Mice.Cell Metab. 2020 Aug 4;32(2):203-214.e4. doi: 10.1016/j.cmet.2020.04.019. Epub 2020 May 14.

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    2021-04-09 爆笑小医
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    2020-10-12 一闲
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    2020-12-02 guojianrong
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    2020-08-19 ms5000000741733160

    👍🏻

    0

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    2020-08-17 CHANGE

    什么时候有懒人用的减肥神药?

    0

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