A Novel Camel Milk-Derived Peptide LLPK Improves Glucose-Lipid Metabolism in db/db Mice via PPAR Signaling Pathway

文献类型： 外文期刊

第一作者： Han, Binsong

作者： Han, Binsong;Ye, Yuhui;Zhang, Cunzheng;Han, Binsong;Zhang, Lina;Zhou, Peng;Han, Binsong;Zhang, Lina;Zhou, Peng

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关键词： camel milk-derived peptide; diabetes; hepatic proteome; PPAR signaling pathway

期刊名称：NUTRIENTS （ 影响因子：5.0； 五年影响因子：6.0 ）

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年卷期： 2025 年 17 卷 10 期

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收录情况： SCI

摘要： Background: Camel milk is considered to be an important source of bioactive peptides with potential anti-diabetic effects. However, the mechanism by which these active peptides exert their anti-diabetic effects is not clear. The aim of this study was to systematically evaluate the in vivo anti-diabetic effects of Leucine-Leucine-Proline-Lysine (LLPK), a novel dipeptidyl peptidase-4 (DPP-4) inhibitory peptide identified from the in vitro gastrointestinal digestion product of camel milk. Methods: A db/db diabetic mouse model was used, and LLPK was administered to mice at doses of 50 mg/kg BW and 100 mg/kg BW as a daily oral gavage for 30 days. The effects of LLPK on fasting blood glucose (FBG), oral glucose tolerance test (OGTT), insulin tolerance test (ITT), and serum lipid levels were monitored, and possible mechanisms of action were elucidated using proteomics. Results: The results demonstrated that LLPK significantly improved diabetic symptoms, including FBG, OGTT, ITT, and serum lipid levels in db/db diabetic mice. Furthermore, significantly increased levels of serum glucagon-like peptide 1 (GLP-1) and reduced serum DPP-4 activity were observed in the LLPK-treated group compared to the control group. Hepatic proteomics indicated that LLPK improved glucose and lipid metabolism via the PPAR signaling pathway, where the key targets were Scd1, Acox1, Acaa1b, Slc27a1, Acsl1, and Ehhadh. Conclusions: In summary, this study provided new insights into the anti-diabetic mechanisms of camel milk and supported the development of camel milk-based anti-diabetic functional foods or nutraceuticals.

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