Manaer Tabusi, Sailike Jialehasibieke, Sun Xin, Yeerjiang Baheban, Nabi Xinhua
School of Pharmacy, Xinjiang Medical University, Urumchi, China.
Xinjiang Key Laboratory of Biopharmaceuticals and Medical Devices, Urumchi, China.
Front Pharmacol. 2025 Jan 7;15:1520158. doi: 10.3389/fphar.2024.1520158. eCollection 2024.
In the Kazakh community of Xinjiang, China, fermented camel milk has been traditionally used to manage diabetes. This study evaluates the effects of composite probiotics derived from fermented camel milk (CPCM) on metabolic disturbances in a rat model of Type 2 diabetes (T2DM).
T2DM was induced in Wistar rats using streptozotocin. Experimental groups included a diabetic control, Metformin, and low- and high-dose CPCM. Measurements over 6 weeks included body weight (BW), fasting blood glucose (FBG), oral glucose tolerance test (OGTT), glycated hemoglobin (HbA1c), C-peptide (CP), lipid profiles, inflammatory markers, fecal short-chain fatty acids (SCFAs), and tight junction protein expression in colonic tissues.
High-dose CPCM significantly increased BW by 22.2% ( < 0.05) and reduced FBG by 6.5 mmol/L ( < 0.001). The OGTT AUC decreased by 40.1% ( < 0.001), and HbA1c levels fell by 22.9% ( < 0.01). CP levels rose by 21.8% ( < 0.05). Lipid profiles improved: TC decreased by 40.0%, TG by 17.1%, and LDL-C by 30.4% (all < 0.001). Fecal SCFAs, including acetate (75.4%, < 0.001), methyl acetate (18.9%, < 0.05), and butyrate (289.9%, < 0.001), increased, with total SCFAs rising by 89.7% ( < 0.001). Inflammatory markers IL-1β (12.7%, < 0.01), TNF-α (16.7%, < 0.05), and IL-6 (17.3%, < 0.01) were significantly reduced. Tight junction protein expression (ZO-1, occludin, claudin-1) and mucin (MUC2) in colonic tissues increased ( < 0.05). CPCM treatment also reduced serum total bile acids by 24.9%, while hepatic and fecal bile acids increased by 114.0% and 37.8% (all < 0.001). CPCM lowered serum DAO, D-lactate, and LPS levels (all < 0.001). mRNA levels of TGR5 and CYP7A1 in the liver, and TGR5 and FXR in the colon, were markedly elevated (all < 0.001). Histological examinations revealed reduced pancreatic inflammation and hepatic steatosis, with restored colonic structure.
CPCM treatment significantly improved metabolic dysregulation in the T2DM rat model, reducing blood glucose and lipid levels, enhancing intestinal barrier function, and increasing insulin secretion. These findings highlight the therapeutic potential of CPCM in T2DM management and probiotics' role in metabolic health.
在中国新疆的哈萨克族社区，发酵驼奶传统上用于管理糖尿病。本研究评估了源自发酵驼奶的复合益生菌（CPCM）对2型糖尿病（T2DM）大鼠模型代谢紊乱的影响。
使用链脲佐菌素诱导Wistar大鼠患T2DM。实验组包括糖尿病对照组、二甲双胍组以及低剂量和高剂量CPCM组。6周内的测量指标包括体重（BW）、空腹血糖（FBG）、口服葡萄糖耐量试验（OGTT）、糖化血红蛋白（HbA1c）、C肽（CP）、血脂谱、炎症标志物、粪便短链脂肪酸（SCFAs）以及结肠组织中紧密连接蛋白的表达。
高剂量CPCM使BW显著增加22.2%（P<0.05），FBG降低6.5 mmol/L（P<0.001）。OGTT曲线下面积（AUC）下降40.1%（P<0.001），HbA1c水平下降22.9%（P<0.01）。CP水平升高21.8%（P<0.05）。血脂谱得到改善：总胆固醇（TC）降低40.0%，甘油三酯（TG）降低17.1%，低密度脂蛋白胆固醇（LDL-C）降低30.4%（均P<0.001）。粪便SCFAs增加，包括乙酸（增加75.4%，P<0.001）、乙酸甲酯（增加18.9%，P<0.05）和丁酸（增加289.9%，P<0.001），总SCFAs增加89.7%（P<0.001）。炎症标志物白细胞介素-1β（IL-1β，降低12.7%，P<0.01）、肿瘤坏死因子-α（TNF-α，降低16.7%，P<0.05）和白细胞介素-6（IL-6，降低17.3%，P<0.01）显著降低。结肠组织中紧密连接蛋白表达（闭合蛋白1、闭锁蛋白、Claudin-1）和黏蛋白（MUC2）增加（P<0.05）。CPCM治疗还使血清总胆汁酸降低24.9%，而肝脏和粪便胆汁酸分别增加114.0%和37.8%（均P<0.001）。CPCM降低血清二胺氧化酶（DAO）、D-乳酸和脂多糖（LPS）水平（均P<0.001）。肝脏中TGR5和CYP7A1以及结肠中TGR5和法尼醇X受体（FXR）的mRNA水平显著升高（均P<0.001）。组织学检查显示胰腺炎症减轻、肝脏脂肪变性改善，结肠结构恢复。
CPCM治疗显著改善了T2DM大鼠模型的代谢失调，降低血糖和血脂水平，增强肠道屏障功能，并增加胰岛素分泌。这些发现凸显了CPCM在T2DM管理中的治疗潜力以及益生菌在代谢健康中的作用。
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