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Diabetes Obes Metab:利拉鲁肽对膳食脂质诱导的胰岛素抵抗的影响!

2017-06-19 xing.T MedSci原创

由此可见,利拉鲁肽能够减弱富含SFA饮食诱导的胰岛素抵抗。这种效应可能与改善微血管功能和调节骨骼肌中的TxNIP和AMPK通路相关。

高饱和脂肪酸(SFA)饮食会抑制外周胰岛素的作用。GLP-1受体激动剂抑制餐后血脂和内皮功能障碍,其可能对抗SFA诱导的胰岛素抵抗。近日,代谢内分泌疾病领域权威杂志Diabetes Obesity & Metabolism上发表了一篇研究文章,这项研究旨在检验利拉鲁肽能否抑制餐后血脂升高,从而防止高SFA饮食诱导的胰岛素抵抗。

在这项随机安慰剂对照交叉研究中,32例正常或轻度糖耐量受损的接受利拉鲁肽和安慰剂治疗3周的患者被纳入研究。每一次治疗后,在基线和24小时富含SFA的饮食后进行胰岛素抑制试验(IST)。血糖、胰岛素、甘油三酯和非酯化脂肪酸(NEFA)在SFA饮食最初的8小时内(早餐和午餐)进行检测。一组受试者在体外测量胰岛素介导的脂肪组织小动脉血管舒张和骨骼肌葡萄糖代谢调节蛋白。

研究人员发现利拉鲁肽可以降低SFA饮食期间的血糖、甘油三酯和NEFA浓度(分别为50、25和9%),并且SFA饮食增加IST期间的血糖水平(36%)(所有P<0.01,vs. 安慰剂)。在安慰剂组SFA饮食诱导的血管舒损伤(-9.4% vs. 基线,P<0.01)可被利拉鲁肽(-4.8%,P=0.1  vs. 基线)明显减轻。在骨骼肌中,利拉鲁肽废除了SFA诱导的硫氧还蛋白相互作用蛋白(TxNIP)的表达增加(减少了75%,P<0.01 vs. 安慰剂)并增加了5'AMP-激活的蛋白激酶(AMPK)磷酸化(50% vs. 3%,P=0.04 vs. 安慰剂)。

由此可见,利拉鲁肽能够减弱富含SFA饮食诱导的胰岛素抵抗。这种效应可能与改善微血管功能和调节骨骼肌中的TxNIP和AMPK通路相关。

原始出处:

Juraj Koska,et al. The Effect of Liraglutide on Dietary Lipid Induced Insulin Resistance in Humans. Diabetes Obesity & Metabolism.2017. http://onlinelibrary.wiley.com/doi/10.1111/dom.13037/full

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    2017-10-15 baoya
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    2018-04-19 一闲
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    2017-10-02 guojianrong
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    2017-06-21 zhaojie88
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    2017-06-19 1e0f8808m18(暂无匿称)

    利拉鲁肽的应用,学习了。

    0

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Diabetes Care:利拉鲁肽治疗的2型糖尿病患者淀粉酶、脂肪酶以及急性胰腺炎如何变化?

在2型糖尿病患者心血管疾病高风险的人群中,利拉鲁肽治疗的患者中(无论胰腺炎病史)与安慰剂组相比发生急性胰腺炎的事件数量较少。利拉鲁肽和血清淀粉酶和脂肪酶升高有关,但这并不能预测随后的急性胰腺炎事件。

J Clin Endoc Metab:利拉鲁肽能否减少控制不佳2型糖尿病患者肝脏脂肪生成?

利拉鲁肽是一种人胰高糖素样肽-1(GLP-1)类似物,用于治疗糖尿病。肝脏是人体重要的消化器官,对脂肪的消化、吸收、氧化、分解、合成、转运等起着十分重要的作用。

Diabetes Obes Metab:早期2型糖尿病患者使用利拉鲁肽或增强内源性GLP-1分泌应答

特定激素受体的持续外源性刺激会对内源激素调节产生影响。在这种情况下,胰高血糖素样肽-1(GLP-1)激动剂长期治疗对内源性GLP-1应答的影响相关研究较少。2017年5月,发表在《Diabetes Obes Metab.》的一项研究评价了利拉鲁肽长期药物疗法对内源性GLP-1的影响,以及葡萄糖依赖性促胰岛素多肽(GIP)对口服葡萄糖负荷的应答。

Diabetes:胰高血糖素样肽-1受体激活可增加心输出量和心脏效率!

这些数据支持GLP-1激动剂增强心脏的效率,通过减弱肥胖和心肌梗死的不良交感神经信号。

Diabetes Care:利拉鲁肽和西格列汀对超重的2型糖尿病患者的胰腺有何影响?

GLP-1受体激动利拉鲁肽和DPP4抑制剂西格列汀不改变胰腺的形态。

JAMA Psychiatry:利拉鲁肽可降低抗精神病药导致的心血管风险

利拉鲁肽可显著改善服用氯氮平或奥氮平的精神病患者的糖耐量水平、体重和心脏代谢紊乱的病情

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