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Administration of n-3 unsaturated fatty acids suppressed glycation and improved signaling in GDM rat pups. In this study, we investigated their effects on cranial neurons using the GDM rat model and PC12 cells derived from rat adrenal pheochromocytomas. Additionally, we examined whether n-3 and n-7 unsaturated fatty acids (cis-palmitoleic acid [CPA] and trans-palmitoleic acid [TPA]) ameliorate the detrimental effects of high glucose exposure on rats. In the neonatal cerebrum of GDM rats, increased levels of advanced glycation end products (AGEs) inhibited Akt phosphorylation; however, CPA and TPA intake during pregnancy ameliorated these abnormalities. Furthermore, exposure to high-glucose-induced apoptosis in PC12 cells compared to the cells cultured in control glucose. PC12 cells exposed to high-glucose with fatty acids exhibited reduced AGE production and apoptosis induction compared to the high-glucose group. These findings suggest that a hyperglycemic environment during pregnancy promotes AGE formation in brain neuronal proteins and induces apoptosis. Both TPA and CPA mitigated these abnormalities; however, CPA is cytotoxic, highlighting its safety in pregnant women.<\/jats:p>","DOI":"10.3390\/nu15153434","type":"journal-article","created":{"date-parts":[[2023,8,3]],"date-time":"2023-08-03T11:13:06Z","timestamp":1691061186000},"page":"3434","update-policy":"https:\/\/doi.org\/10.3390\/mdpi_crossmark_policy","source":"Crossref","is-referenced-by-count":5,"title":["Maternal n-7 Unsaturated Fatty Acids Protect the Fetal Brain from Neuronal Degeneration in an Intrauterine Hyperglycemic Animal Model"],"prefix":"10.3390","volume":"15","author":[{"given":"Haruka","family":"Okami","sequence":"first","affiliation":[{"name":"Department of General Surgical Science, Graduate School of Medicine, Gunma University, Maebashi 371-8511, Japan"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Ritsuko","family":"Kawaharada","sequence":"additional","affiliation":[{"name":"Department of Health and Nutrition, Takasaki University of Health and Welfare, Takasaki 370-0033, Japan"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Hitomi","family":"Yoshizaki","sequence":"additional","affiliation":[{"name":"Department of Bioregulatory Science (Physiology), Nippon Medical School, Tokyo 113-8602, Japan"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Akiyo","family":"Toriumi","sequence":"additional","affiliation":[{"name":"Department of Public Health, Graduate School of Medicine, Gunma University, Maebashi 371-8511, Japan"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Saki","family":"Tsutsumi","sequence":"additional","affiliation":[{"name":"Department of Neurophysiology & Neural Repair, Graduate School of Medicine, Gunma University, Maebashi 371-8511, Japan"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Akio","family":"Nakamura","sequence":"additional","affiliation":[{"name":"Department of Molecular Nutrition, Faculty of Human Life Sciences, Jissen Women\u2019s University, Hino 191-8510, Japan"}],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"1968","published-online":{"date-parts":[[2023,8,3]]},"reference":[{"key":"ref_1","doi-asserted-by":"crossref","first-page":"1111","DOI":"10.1136\/bmj.301.6761.1111","article-title":"The fetal and infant origins of adult disease","volume":"301","author":"Barker","year":"1990","journal-title":"BMJ"},{"key":"ref_2","doi-asserted-by":"crossref","first-page":"412","DOI":"10.1111\/j.1365-2796.2007.01809.x","article-title":"The origins of the developmental origins theory","volume":"261","author":"Barker","year":"2007","journal-title":"J. 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