Maternal high fat diet in mice alters immune regulation and lung function in the offspring
Maternal high fat diet in mice alters immune regulation and lung function in the offspring
PUFA modulate immune function and have been associated with the 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, 20·4 % energy as fat) or a high-fat diet (HFD, 39·9 % energy as fat) for 4 weeks prior to conception and during gestation and lactation. At 21 d 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 GC and gene expression by quantitative PCR. 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. DHA 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 fatty acid desaturase (FADS) 2 and elongation of very long-chain fatty acid 5 expression in male offspring, whereas maternal HFD elevated expression of FADS1 and FADS2 in female offspring compared with males. Post-natal HFD increased expression of IL-6 and C-C motif chemokine ligand 2 (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.
Desaturase, Elongase, High fat diet, Inflammation, PUFA
844-852
Losol, Purevsuren
85a3c8ff-a437-44d0-8472-9b090039cf63
Mercken, Lindert P.
868aca0a-cf66-41c9-b4f3-1a6215bfb374
Fisk, Helena L.
38c7f1f0-5dfc-4f71-aa0f-ec4f0e5839f3
Calder, Philip C.
1797e54f-378e-4dcb-80a4-3e30018f07a6
Holloway, John W.
4bbd77e6-c095-445d-a36b-a50a72f6fe1a
Torrens, Christopher
15a35713-0651-4249-8227-5901e2cfcd22
27 November 2020
Losol, Purevsuren
85a3c8ff-a437-44d0-8472-9b090039cf63
Mercken, Lindert P.
868aca0a-cf66-41c9-b4f3-1a6215bfb374
Fisk, Helena L.
38c7f1f0-5dfc-4f71-aa0f-ec4f0e5839f3
Calder, Philip C.
1797e54f-378e-4dcb-80a4-3e30018f07a6
Holloway, John W.
4bbd77e6-c095-445d-a36b-a50a72f6fe1a
Torrens, Christopher
15a35713-0651-4249-8227-5901e2cfcd22
Losol, Purevsuren, Mercken, Lindert P., Fisk, Helena L., Calder, Philip C., Holloway, John W. and Torrens, Christopher
(2020)
Maternal high fat diet in mice alters immune regulation and lung function in the offspring.
British Journal of Nutrition, 126 (6), .
(doi:10.1017/S0007114520004742).
Abstract
PUFA modulate immune function and have been associated with the 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, 20·4 % energy as fat) or a high-fat diet (HFD, 39·9 % energy as fat) for 4 weeks prior to conception and during gestation and lactation. At 21 d 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 GC and gene expression by quantitative PCR. 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. DHA 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 fatty acid desaturase (FADS) 2 and elongation of very long-chain fatty acid 5 expression in male offspring, whereas maternal HFD elevated expression of FADS1 and FADS2 in female offspring compared with males. Post-natal HFD increased expression of IL-6 and C-C motif chemokine ligand 2 (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.
Text
Manuscript final 201117_
- Accepted Manuscript
More information
Accepted/In Press date: 19 November 2020
e-pub ahead of print date: 27 November 2020
Published date: 27 November 2020
Keywords:
Desaturase, Elongase, High fat diet, Inflammation, PUFA
Identifiers
Local EPrints ID: 445245
URI: http://eprints.soton.ac.uk/id/eprint/445245
ISSN: 0007-1145
PURE UUID: f9bb0f27-14aa-42cf-bf07-0d61f3141608
Catalogue record
Date deposited: 26 Nov 2020 17:30
Last modified: 17 Mar 2024 02:45
Export record
Altmetrics
Contributors
Author:
Purevsuren Losol
Author:
Lindert P. Mercken
Author:
Helena L. Fisk
Author:
Christopher Torrens
Download statistics
Downloads from ePrints over the past year. Other digital versions may also be available to download e.g. from the publisher's website.
View more statistics
