Key Laboratory of Dairy Biotechnology and Engineering, Ministry of Education, Inner Mongolia Agricultural University, Hohhot, China.
Key Laboratory of Dairy Products Processing, Ministry of Agriculture and Rural Affairs, Inner Mongolia Agricultural University, Hohhot, China.
Eur J Nutr. 2022 Jun;61(4):2003-2014. doi: 10.1007/s00394-021-02764-0. Epub 2022 Jan 4.
Obesity is a major risk factor for various metabolic diseases, including metabolic syndrome and type-2 diabetes. Glucose transporter 1 (GLUT1) impairment has been proposed as a mechanism of fat accumulation and glucose tolerance. Our aims were to determine the role of intestinal epithelial glut1 activity in obesity and the mechanism of anti-obesity effect of Lactobacillus casei Zhang (LCZ) intervention in the absence of gut villi-specific glut1 expression.
This study compared the body weight, intestinal microbiota perturbations, fat mass accumulation, and glucose tolerance (by oral glucose tolerance test) between high-fat diet fed villi-specific glut1 knockout (KO) mice and control mice (glut1 flox/flox) with/without LCZ intervention. The intestinal microbiota was evaluated by metagenomic sequencing.
Our results showed that villi-specific glut1 KO mice had more fat deposition at the premetaphase stage, impaired glucose tolerance, and obvious alterations in gut microbiota compared to control mice. Probiotic administration significantly lowered the body weight, the weights of mesenteric and perirenal white adipose tissues (WAT), and mediated gut microbiota modulation in both types of KO and control mice. The species Barnesiella intestinihominis and Faecalibaculum rodentium might contribute to fasting fat mass accumulation associated with gut-specific glut1 inactivation, while the probiotic-mediated anti-obesity effect was linked to members of the Bacteroides genera, Odoribacter genera and Alistipes finegoldii.
Our study demonstrated that abrogating gut epithelial GLUT1 activity affected the gut microbiota, fat mass accumulation, and glucose tolerance; and LCZ administration reduced fat mass accumulation and central obesity.
肥胖是多种代谢性疾病的主要危险因素，包括代谢综合征和 2 型糖尿病。葡萄糖转运蛋白 1（GLUT1）功能障碍被认为是脂肪积累和葡萄糖耐量的机制。我们的目的是确定肠上皮细胞 glut1 活性在肥胖中的作用，以及在没有肠道绒毛特异性 glut1 表达的情况下，干酪乳杆菌 Zhang（LCZ）干预的抗肥胖作用的机制。
本研究比较了高脂肪饮食喂养的绒毛特异性 glut1 敲除（KO）小鼠和对照小鼠（glut1 flox/flox）在有/无 LCZ 干预时的体重、肠道微生物群扰动、脂肪量积累和葡萄糖耐量（通过口服葡萄糖耐量试验）。通过宏基因组测序评估肠道微生物群。
我们的结果表明，与对照小鼠相比，绒毛特异性 glut1 KO 小鼠在前期有更多的脂肪沉积，葡萄糖耐量受损，肠道微生物群明显改变。益生菌给药显著降低了两种 KO 和对照小鼠的体重、肠系膜和肾周白色脂肪组织（WAT）的重量，并介导了肠道微生物群的调节。Barnesiella intestinihominis 和 Faecalibaculum rodentium 可能与绒毛特异性 glut1 失活相关的空腹脂肪量积累有关，而益生菌介导的抗肥胖作用与拟杆菌属、Odoribacter 属和 Alistipes finegoldii 的成员有关。
本研究表明，阻断肠上皮细胞 GLUT1 活性会影响肠道微生物群、脂肪量积累和葡萄糖耐量；而 LCZ 给药可减少脂肪量积累和中心性肥胖。
