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首页> 外文期刊>Cell metabolism >Muramyl Dipeptide-Based Postbiotics Mitigate Obesity-Induced Insulin Resistance via IRF4
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Muramyl Dipeptide-Based Postbiotics Mitigate Obesity-Induced Insulin Resistance via IRF4

机译：基于Muramyl二肽的晚期性植物通过IRF4减轻肥胖症诱导的胰岛素抗性

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摘要

Intestinal dysbiosis contributes to obesity and insulin resistance, but intervening with antibiotics, prebiotics, or probiotics can be limited by specificity or sustained changes in microbial composition. Postbiotics include bacterial components such as lipopolysaccharides, which have been shown to promote insulin resistance during metabolic endotoxemia. We found that bacterial cell wall-derived muramyl dipeptide (MDP) is an insulin-sensitizing postbiotic that requires NOD2. Injecting MDP lowered adipose inflammation and reduced glucose intolerance in obese mice without causing weight loss or altering the composition of the microbiome. MDP reduced hepatic insulin resistance during obesity and lowlevel endotoxemia. NOD1-activating muropeptides worsened glucose tolerance. IRF4 distinguished opposing glycemic responses to different types of peptidoglycan and was required for MDP/NOD2-induced insulin sensitization and lower metabolic tissue inflammation during obesity and endotoxemia. IRF4 was dispensable for exacerbated glucose intolerance via NOD1. Mifamurtide, an MDP-based drug with orphan drug status, was an insulin sensitizer at clinically relevant doses in obese mice.
机译：肠脱敏症有助于肥胖和胰岛素抵抗力，但抗生素，益生元或益生菌的干预可以受到微生物组合物的特异性或持续变化的限制。产后药包括脂多糖等细菌组分，已经显示出在代谢内毒性期间促进胰岛素抗性。我们发现细菌细胞壁衍生的蛋白质二肽（MDP）是需要NOD2的胰岛素敏化分娩。注射MDP降低脂肪炎症并降低肥胖小鼠的葡萄糖不耐受，而不会导致体重减轻或改变微生物组的组成。 MDP在肥胖期间降低了肝胰岛素抗性和肺内毒素血症。 NOD1激活的杂物肽恶化葡萄糖耐量。 IRF4可区分对不同类型的肽聚糖的反对血糖反应，并且是MDP / NOD2诱导的胰岛素敏化和肥胖症期间代谢组织炎症所必需的。 IRF4可通过NOD1加剧葡萄糖不耐受。 Mifamurtide是一种基于MDP的药物，具有孤儿药物状态，是肥胖小鼠临床相关剂量的胰岛素敏感剂。

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