Impaired colonic motility in high-glycemic diet-induced diabetic mice is associated with disrupted gut microbiota and neuromuscular function.

Impaired colonic motility in high-glycemic diet-induced diabetic mice is associated with disrupted gut microbiota and neuromuscular function.
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DOI:
10.1530/ec-23-0078
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发表时间:
2023-08-03
影响因子:
2.9
通讯作者:
--
中科院分区:
医学3区
文献类型:
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文献摘要

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与高脂肪饮食(HFD)相似,高血糖饮食(HGD)有助于2型糖尿病(T2DM)的发生和进展。然而,HGD对T2DM患者胃肠运动的影响及其潜在机制尚不清楚。将30只C57BL/6J小鼠随机分为正常饲粮(NFD)组、HFD组和HGD组。检测血糖、胰岛素、胃肠蠕动。同时,计算离体结肠平滑肌环的张力,并通过16s rDNA高通量测序分析肠道菌群。饲喂HGD 16周后,HGD小鼠出现肥胖、高血糖、胰岛素抵抗和便秘。HGD小鼠结肠神经肌肉系统的自主收缩频率和电场刺激引起的收缩减少。相反,神经元一氧化氮合酶活性和神经肌肉松弛被发现增强。最后,肠道菌群分析显示,在HGD小鼠中,红螺旋菌科在科水平上的丰度显著增加。在属水平上,HGD小鼠中,太阳螺旋菌的丰度显著增加,而Turicibacter的丰度显著降低。HGD诱导肥胖糖尿病小鼠便秘,我们推测其可能与神经肌肉运动障碍和肠道菌群失调有关。
Similar to the high-fat diet (HFD), the high-glycemic diet (HGD) contributes to the development and progression of type 2 diabetes mellitus (T2DM). However, the effect of HGD on gastrointestinal motility in T2DM and its underlying mechanisms remain unclear. Thirty C57BL/6J mice were randomly designated into the normal-feeding diet (NFD) group, HFD group, and HGD group. The plasma glucose, plasma insulin, and gastrointestinal motility were examined. Meanwhile, the tension of isolated colonic smooth muscle rings was calculated, and the gut microbiota was analyzed by 16s rDNA high-throughput sequencing. After 16 weeks of HGD feeding, obesity, hyperglycemia, insulin resistance, and constipation were observed in HGD mice. Autonomic contraction frequency of the colonic neuromuscular system and electrical field stimulation-induced contractions were reduced in HGD mice. On the contrary, neuronal nitric oxide synthase activity and neuromuscular relaxation were found to be enhanced. Finally, gut microbiota analysis revealed that Rhodospirillaceae abundance significantly increased at the family level in HGD mice. At the genus level, the abundance of Insolitispirillum increased remarkably, whereas Turicibacter abundance decreased significantly in HGD mice. HGD induced constipation in obese diabetic mice, which we speculated that it may be related to neuromuscular dysmotility and intestinal microbiota dysbiosis.