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妊娠和哺乳期代谢及肠道微生物反应对瘦型和饮食诱导肥胖大鼠后代肥胖风险的潜在影响。

Potential Impact of Metabolic and Gut Microbial Response to Pregnancy and Lactation in Lean and Diet-Induced Obese Rats on Offspring Obesity Risk.

机构信息

Department of Biochemistry and Molecular Biology, Cumming School of Medicine, University of Calgary, Calgary, AB, Canada.

Biomedical Engineering, Schulich School of Engineering, University of Calgary, Calgary, AB, Canada.

出版信息

Mol Nutr Food Res. 2018 Feb;62(4). doi: 10.1002/mnfr.201700820. Epub 2018 Jan 22.

Abstract

SCOPE

Maternal obesity programs metabolic dysfunction in offspring, increasing their susceptibility to obesity and metabolic diseases in later life. Moreover, pregnancy and lactation are associated with many metabolic adaptations, yet it is unclear how diet-induced maternal obesity may interrupt these processes.

METHODS AND RESULTS

H NMR serum metabolomics analysis was performed on samples collected pre-pregnancy and in pregnant and lactating lean and high fat/sucrose (HFS) diet-induced obese Sprague-Dawley rats to identify maternal metabolic pathways associated with developmental programming of offspring obesity. Gut microbial composition was assessed using qPCR. Offspring of HFS dams had nearly 40% higher adiposity at weaning compared to offspring of lean dams. While pregnancy and lactation were associated with distinct maternal metabolic changes common to both lean and obese dams, we identified several metabolic differences, potentially implicating dysregulated one-carbon and mammary gland metabolism in the metabolic programming of obesity. Gut microbial composition was significantly altered with obesity, and both gestation and lactation were accompanied by changes in gut microbiota.

CONCLUSION

Diet-induced maternal obesity and consumption of an obesogenic maternal diet results in differential metabolic and gut microbial adaptations to pregnancy and lactation; these maladaptations may be directly involved in maternal programming of offspring susceptibility to obesity.

摘要

范围

母体肥胖会导致后代代谢功能障碍,增加其在以后生活中肥胖和代谢疾病的易感性。此外,妊娠和哺乳期与许多代谢适应有关,但目前尚不清楚饮食诱导的母体肥胖如何中断这些过程。

方法和结果

对孕前和妊娠及哺乳期瘦鼠和高脂肪/蔗糖(HFS)饮食诱导肥胖的 Sprague-Dawley 大鼠的血清进行 1H-NMR 代谢组学分析,以鉴定与后代肥胖发育编程相关的母体代谢途径。使用 qPCR 评估肠道微生物组成。与瘦鼠的后代相比,HFS 鼠的后代在断奶时的肥胖程度高近 40%。虽然妊娠和哺乳期与瘦鼠和肥胖鼠共有的母体代谢变化有关,但我们发现了一些代谢差异,这可能表明在肥胖的代谢编程中,一碳和乳腺代谢失调。肥胖会导致肠道微生物组成发生显著变化,妊娠和哺乳期都伴随着肠道微生物群的变化。

结论

饮食诱导的母体肥胖和食用致肥胖的母体饮食会导致妊娠和哺乳期的代谢和肠道微生物适应性出现差异;这些适应不良可能直接参与母体对后代肥胖易感性的编程。

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