4.7 Article

Supplementation of milk polar lipids to obese dams improves neurodevelopment and cognitive function in male offspring

期刊

FASEB JOURNAL
卷 35, 期 4, 页码 -

出版社

WILEY
DOI: 10.1096/fj.202001974RRR

关键词

cognitive function; insulin resistance; maternal obesity; neurodevelopment; polar lipids‐ enriched milk fat globule membrane

资金

  1. National Natural Science Foundation of China [31871806]
  2. Beijing Dairy Industry Innovation Team [BAIC06-2020]
  3. National Key Research Development Program of China [2019YFC1605000]

向作者/读者索取更多资源

The study found that maternal MFGM-PL supplementation can promote neurodevelopment and exert long-term effects against HFD-induced cognitive impairment in offspring by alleviating hippocampal insulin resistance. Additionally, MFGM-PL supplementation suppressed body weight gain and hyperinsulinemia in both obese dams and their offspring.
Milk contains about 4% fat globules with its surface covered by polar lipids. Despite the abundant consumption of dairy products, the biological effects of dietary milk polar lipids on metabolic health have only been sparsely examined. Maternal obesity results in neurodevelopmental disorders and cognitive impairment in offspring. Considering the importance of maternal nutrition, the effects of polar lipids-enriched milk fat globule membrane (MFGM-PL) supplementation to dams during pregnancy and lactation on neurodevelopment and its long-term programming effects on offspring cognition were examined. Female Sprague-Dawley rats consumed 8-week control diet (CON) or high-fat diet (HFD) to induce obesity before mating. Then, female rats were fed CON or HFD with or without the supplementation of 400 mg/kg body weight MFGM-PL during pregnancy and lactation. The offspring were fed 11-week HFD after weaning. MFGM-PL supplementation to obese dams suppressed body weight gain and hyperinsulinemia in both dams and offspring. Offspring born to obese dams displayed delayed neurological reflexes development, impaired neurogenesis before weaning, and cognitive impairment in adulthood, which were recovered by maternal MFGM-PL supplementation. Insulin resistance and aberrant brain-derived neurotrophic factor signaling were induced in the hippocampus of neonatal and adult offspring due to maternal and progeny HFD, but recovered by maternal MFGM-PL administration. This study demonstrates that maternal MFGM-PL supplementation can promote neurodevelopment and exert long-term effects against HFD-induced cognitive impairment in offspring via alleviating hippocampal insulin resistance. Hence, MFGM-PL is a promising ingredient for exerting beneficial programming effects on the brain health of offspring.

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