Dietary glycerol monolaurate mitigates heat stress-induced disruption of intestinal homeostasis and hepatic lipid metabolism in laying hens.

IF 5.8
Jiang Gao, Hongrui Ren, Xuanfu Wu, Cunzhi Zou, Bin He, Wenqiang Ma
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Abstract

Heat stress (HS) disrupts intestinal homeostasis and hepatic lipid metabolism in poultry, yet effective interventions remain limited. We investigate the protective effects of dietary glycerol monolaurate (GML) supplementation in laying hens under HS conditions. In a 10-week trial, 504 Hy-Line Brown hens were assigned to four groups (control and GML at 65, 195, and 325 mg/kg) with six replicates per group. Hens receiving 325 mg/kg GML exhibited significantly higher egg production and egg weight (P < 0.05), alongside improved egg quality metrics, including increased shell strength and Haugh units by week 8 (P < 0.05). Histological analysis revealed that GML (325 mg/kg) improved duodenal and ileal villus height and duodenal villus-to-crypt ratios while reducing duodenal crypt depth (P < 0.05), thereby restoring gut barrier integrity. These findings were supported by reduced plasma D-lactate (D-LA) levels and upregulated expression of tight-junction proteins ZO-1 and Occludin in the ileum and jejunum (P < 0.05). In the liver, GML supplementation alleviated HS-induced steatosis, reducing lipid droplet accumulation (P < 0.05), plasma low-density lipoprotein cholesterol (LDL-C), aspartate aminotransferase (AST), and alanine aminotransferase (ALT) levels, and hepatic triglyceride content, while elevating high density lipoprotein cholesterol (HDL-C). Integrated plasma metabolomics and hepatic transcriptomics identified 36 differential metabolites (enriched in sphingolipid metabolism) and 1,176 differentially expressed genes (enriched in PPAR signaling and Fatty acid degradation), with ACSL1 as a central regulatory gene. Key genes (ACSL1, CPT1 A) and metabolites correlated positively with production performance and gut-liver health, while SCD and Probucol showed negative associations. These findings indicate that GML supplementation enhances intestinal barrier function, promotes hepatic fatty acid β-oxidation, and reinforces sphingolipid metabolism, thereby mitigating HS-induced oxidative stress and lipid dysregulation. Our results identify 325 mg/kg GML as the optimal dosage, proposing a practical strategy to enhance poultry resilience during heat stress.

饲粮单月桂酸甘油可减轻热应激对蛋鸡肠道稳态和肝脏脂质代谢的破坏。
热应激(HS)会破坏家禽肠道内稳态和肝脏脂质代谢,但有效的干预措施仍然有限。本试验研究了HS条件下饲粮中添加单月桂酸甘油(GML)对蛋鸡的保护作用。试验10周,将504只海兰褐鸡分为4组(对照组和GML水平分别为65、195和325 mg/kg),每组6个重复。饲喂325 mg/kg GML的蛋鸡产蛋量和蛋重显著提高(P < 0.05),第8周蛋壳强度和哈夫单位均显著提高(P < 0.05)。组织学分析显示,GML (325 mg/kg)可改善十二指肠和回肠绒毛高度及绒毛/隐窝比(P < 0.05),降低十二指肠隐窝深度(P < 0.05),从而恢复肠道屏障完整性。回肠和空肠中血浆d -乳酸(D-LA)水平降低,紧密连接蛋白ZO-1和Occludin表达上调(P < 0.05)也支持了这一发现。在肝脏中,添加GML可减轻hs诱导的脂肪变性,降低脂滴积累(P < 0.05),降低血浆低密度脂蛋白胆固醇(LDL-C)、天冬氨酸转氨酶(AST)和丙氨酸转氨酶(ALT)水平,降低肝脏甘油三酯含量,同时升高高密度脂蛋白胆固醇(HDL-C)。整合血浆代谢组学和肝脏转录组学鉴定出36种差异代谢物(富集于鞘脂代谢)和1176种差异表达基因(富集于PPAR信号和脂肪酸降解),其中ACSL1为中心调控基因。关键基因(ACSL1、CPT1 A)和代谢物与生产性能和肝肠健康呈正相关,而SCD和Probucol呈负相关。上述结果表明,添加GML可增强肠道屏障功能,促进肝脏脂肪酸β-氧化,增强鞘脂代谢,从而减轻hs诱导的氧化应激和脂质失调。我们的研究结果确定325 mg/kg GML为最佳剂量,提出了提高家禽热应激恢复能力的实用策略。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
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