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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
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.
Desaturase, Elongase, High fat diet, Inflammation, PUFA
0007-1145
1-24
Losol, Purevsuren
85a3c8ff-a437-44d0-8472-9b090039cf63
Mercken, Lindert Petrus
868aca0a-cf66-41c9-b4f3-1a6215bfb374
Fisk, Helena Lucy
38c7f1f0-5dfc-4f71-aa0f-ec4f0e5839f3
Calder, Philip
1797e54f-378e-4dcb-80a4-3e30018f07a6
Holloway, John
4bbd77e6-c095-445d-a36b-a50a72f6fe1a
Torrens, Christopher
15a35713-0651-4249-8227-5901e2cfcd22
Losol, Purevsuren
85a3c8ff-a437-44d0-8472-9b090039cf63
Mercken, Lindert Petrus
868aca0a-cf66-41c9-b4f3-1a6215bfb374
Fisk, Helena Lucy
38c7f1f0-5dfc-4f71-aa0f-ec4f0e5839f3
Calder, Philip
1797e54f-378e-4dcb-80a4-3e30018f07a6
Holloway, John
4bbd77e6-c095-445d-a36b-a50a72f6fe1a
Torrens, Christopher
15a35713-0651-4249-8227-5901e2cfcd22

Losol, Purevsuren, Mercken, Lindert Petrus, Fisk, Helena Lucy, Calder, Philip, Holloway, John and Torrens, Christopher (2020) Maternal high fat diet in mice alters immune regulation and lung function in the offspring. British Journal of Nutrition, 1-24. (doi:10.1017/S0007114520004742).

Record type: Article

Abstract

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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Accepted/In Press date: 19 November 2020
e-pub ahead of print 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
ORCID for Philip Calder: ORCID iD orcid.org/0000-0002-6038-710X
ORCID for John Holloway: ORCID iD orcid.org/0000-0001-9998-0464

Catalogue record

Date deposited: 26 Nov 2020 17:30
Last modified: 26 Nov 2021 05:58

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Contributors

Author: Purevsuren Losol
Author: Lindert Petrus Mercken
Author: Helena Lucy Fisk
Author: Philip Calder ORCID iD
Author: John Holloway ORCID iD
Author: Christopher Torrens

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