Maternal high fat diet in mice alters immune regulation and lung function in the offspring.


Br J Nutr. 2020 Nov 27:1-24. Epub 2020 Nov 27. PMID: 33243305

Abstract Title: 

Maternal high fat diet in mice alters immune regulation and lung function in the offspring.


Polyunsaturated fatty acids (PUFA) modulate immune function and have been associated with risk of childhood atopy and asthma. We investigated the effect of maternal fat intake in mice on PUFA status, elongase and desaturase gene expression, inflammatory markers and lung function in the offspring. C57BL/6J mice (n=32) were fed either standard chow (C, 21% kcal fat) or a high fat diet (HFD, 45% kcal fat) for 4 weeks prior to conception and during gestation and lactation. At 21 days of age, offspring were weaned onto either the HFD or C, generating four experimental groups: C/C, C/HF, HF/C and HF/HF. Plasma and liver fatty acid composition were measured by gas chromatography and gene expression by qPCR. Lung resistance to methacholine was assessed. Arachidonic acid concentrations in offspring plasma and liver phospholipids were increased by HFD; this effect was greater in the post-natal HFD group. Docosahexaenoic acid concentration in offspring liver phospholipids was increased in response to HFD and was higher in the post-natal HFD group. Post-natal HFD increased hepatic FADS2 and ELOVL5 expression in male offspring, whereas maternal HFD elevated expression of FADS1 and FADS2 in female offspring comparing to males. Post-natal HFD increased expression of IL-6 and CCL2 in perivascular adipose tissue. The HFD lowered lung resistance to methacholine. Excessive maternal fat intake during development modifies hepatic PUFA status in offspring through regulation of gene expression of enzymes that are involved in PUFA biosynthesis and modifies the development of the offspring lungs leading to respiratory dysfunction.

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