Organic chromium is of great interest and has become an important chromium supplement resource in recent years because of its low toxicity and easy absorption. In our previous study, we synthesized a novel organic chromium [GLP-Cr] through the chelation of Ganoderma lucidum polysaccharide and chromium (III). The purpose of this study was to investigate the beneficial effects of GLP-Cr on the improvement of metabolic syndromes (MetS) in mice fed with a high-fat and high-fructose diet (HFHFD) and its mechanism of action. The results indicated that oral administration of GLP-Cr inhibited the excessive exaltation of body weight, glucose tolerance, fasting blood glucose and lipid levels, hepatic total cholesterol (TC), triglyceride (TG) levels caused by HFHFD. Besides, 16S rRNA amplicon sequencing showed that GLP-Cr intervention evidently ameliorated intestinal microbiota dysbiosis by changing the proportions of some intestinal microbial phylotypes. In addition, correlation network-based analysis indicated that the key intestinal microbial phylotypes were closely related to biochemical parameters associated with MetS under GLP-Cr intervention. Liver metabolomics analysis suggested that GLP-Cr intervention significantly regulated the levels of some biomarkers involved in alpha-linolenic acid metabolism, fatty acid biosynthesis, steroid hormone biosynthesis, glycerophospholipid metabolism, glycerolipid metabolism, steroid hormone biosynthesis, primary bile acid biosynthesis, and so on. Moreover, GLP-Cr intervention regulated liver mRNA levels of key genes associated with glucose and lipid metabolism. The mRNA level of glucose transporter type 4 (Glut4) was markedly increased by GLP-Cr intervention, and the mRNA levels of phosphoenolpyruvate carboxykinase (Pepck) and glucose-6-phosphatase (G6Pase) in the liver were significantly decreased. Meanwhile, GLP-Cr intervention significantly decreased hepatic mRNA levels of cluster of differentiation 36 (Cd36), acetyl-CoA carboxylase 1 (Acc1) and sterol regulatory element binding protein-1c (Srebp-1c), indicating that GLP-Cr intervention inhibited the excessive accumulation of free fatty acids in the liver. These findings suggest that the prevention of hyperglycemia and dyslipidemia by GLP-Cr may be closely related to the regulation of gut microbial composition and hepatic metabolic pathways, thus GLP-Cr can be serving as a functional component in the prevention of MetS.

有机铬因其低毒、易吸收等优点而备受关注，近年来已成为重要的铬补充资源。在我们之前的研究中，我们通过螯合灵芝合成了一种新型有机铬[GLP-Cr]多糖和铬（III）。本研究的目的是研究 GLP-Cr 对改善高脂高果糖饮食 (HFHFD) 小鼠代谢综合征 (MetS) 的有益作用及其作用机制。结果表明，口服 GLP-Cr 可抑制 HHFD 引起的体重、糖耐量、空腹血糖和血脂水平、肝总胆固醇（TC）、甘油三酯（TG）水平的过度升高。此外，16S rRNA 扩增子测序表明，GLP-Cr 干预通过改变一些肠道微生物系统型的比例，显着改善了肠道微生物群失调。此外，基于相关网络的分析表明，关键的肠道微生物系统发育型与 GLP-Cr 干预下与 MetS 相关的生化参数密切相关。肝脏代谢组学分析表明，GLP-Cr干预显着调节了参与α-亚麻酸代谢、脂肪酸生物合成、类固醇激素生物合成、甘油磷脂代谢、甘油脂代谢、类固醇激素生物合成、初级胆汁酸生物合成等的一些生物标志物的水平。 . 此外，GLP-Cr 干预调节与糖脂代谢相关的关键基因的肝脏 mRNA 水平。葡萄糖转运蛋白 4 型的 mRNA 水平 ( 肝脏代谢组学分析表明，GLP-Cr干预显着调节了参与α-亚麻酸代谢、脂肪酸生物合成、类固醇激素生物合成、甘油磷脂代谢、甘油脂代谢、类固醇激素生物合成、初级胆汁酸生物合成等的一些生物标志物的水平。 . 此外，GLP-Cr 干预调节与糖脂代谢相关的关键基因的肝脏 mRNA 水平。葡萄糖转运蛋白 4 型的 mRNA 水平 ( 肝脏代谢组学分析表明，GLP-Cr干预显着调节了参与α-亚麻酸代谢、脂肪酸生物合成、类固醇激素生物合成、甘油磷脂代谢、甘油脂代谢、类固醇激素生物合成、初级胆汁酸生物合成等的一些生物标志物的水平。 . 此外，GLP-Cr 干预调节与糖脂代谢相关的关键基因的肝脏 mRNA 水平。葡萄糖转运蛋白 4 型的 mRNA 水平 (GLP-Cr干预后Glut4显着升高，肝脏中磷酸烯醇丙酮酸羧激酶（Pepck）和葡萄糖6磷酸酶（G6Pase）的mRNA水平显着降低。同时，GLP-Cr 干预显着降低肝脏分化簇 36 ( Cd36 )、乙酰辅酶 A 羧化酶 1 ( Acc1 ) 和甾醇调节元件结合蛋白-1c ( Srebp-1c ) mRNA 水平)，表明 GLP-Cr 干预抑制了肝脏中游离脂肪酸的过度积累。这些发现表明，GLP-Cr对高血糖和血脂异常的预防可能与肠道微生物组成和肝脏代谢途径的调节密切相关，因此GLP-Cr可作为预防MetS的功能成分。