Trans Fatty Acid Intake Induces Intestinal Inflammation and Impaired Glucose Tolerance.
Animals
Blood Glucose
/ drug effects
CD36 Antigens
/ metabolism
Diet, High-Fat
/ adverse effects
Dietary Sucrose
/ toxicity
Dysbiosis
Enteritis
/ chemically induced
Gastrointestinal Microbiome
/ drug effects
Glucose Intolerance
/ blood
Immunity, Innate
/ drug effects
Interleukins
/ metabolism
Intestine, Small
/ drug effects
Liver
/ drug effects
Lymphocytes
/ drug effects
Macrophages
/ drug effects
Male
Mice
Mice, Inbred C57BL
Non-alcoholic Fatty Liver Disease
/ chemically induced
RAW 264.7 Cells
Trans Fatty Acids
/ toxicity
Interleukin-22
ILC
gut microbiota
innate lymphoid cells
small intestine
trans fatty acid
Journal
Frontiers in immunology
ISSN: 1664-3224
Titre abrégé: Front Immunol
Pays: Switzerland
ID NLM: 101560960
Informations de publication
Date de publication:
2021
2021
Historique:
received:
19
02
2021
accepted:
15
04
2021
entrez:
17
5
2021
pubmed:
18
5
2021
medline:
21
10
2021
Statut:
epublish
Résumé
Many nutritional and epidemiological studies have shown that high consumption of trans fatty acids can cause several adverse effects on human health, including cardiovascular disease, diabetes, and cancer. In the present study, we investigated the effect of trans fatty acids on innate immunity in the gut by observing mice fed with a diet high in trans fatty acids, which have been reported to cause dysbiosis. We used C57BL6/J mice and fed them with normal diet (ND) or high-fat, high-sucrose diet (HFHSD) or high-trans fatty acid, high-sucrose diet (HTHSD) for 12 weeks. 16S rRNA gene sequencing was performed on the mice stool samples, in addition to flow cytometry, real-time PCR, and lipidomics analysis of the mice serum and liver samples. RAW264.7 cells were used for the Mice fed with HTHSD displayed significantly higher blood glucose levels and advanced fatty liver and intestinal inflammation, as compared to mice fed with HFHSD. Furthermore, compared to mice fed with HFHSD, mice fed with HTHSD displayed a significant elevation in the expression of CD36 in the small intestine, along with a reduction in the expression of IL-22. Furthermore, there was a significant increase in the populations of ILC1s and T-bet-positive ILC3s in the lamina propria in mice fed with HTHSD. Finally, the relative abundance of the family This study revealed that compared to saturated fatty acid intake, trans fatty acid intake significantly exacerbated metabolic diseases such as diabetes and fatty liver.
Sections du résumé
Background and Aims
Many nutritional and epidemiological studies have shown that high consumption of trans fatty acids can cause several adverse effects on human health, including cardiovascular disease, diabetes, and cancer. In the present study, we investigated the effect of trans fatty acids on innate immunity in the gut by observing mice fed with a diet high in trans fatty acids, which have been reported to cause dysbiosis.
Methods
We used C57BL6/J mice and fed them with normal diet (ND) or high-fat, high-sucrose diet (HFHSD) or high-trans fatty acid, high-sucrose diet (HTHSD) for 12 weeks. 16S rRNA gene sequencing was performed on the mice stool samples, in addition to flow cytometry, real-time PCR, and lipidomics analysis of the mice serum and liver samples. RAW264.7 cells were used for the
Results
Mice fed with HTHSD displayed significantly higher blood glucose levels and advanced fatty liver and intestinal inflammation, as compared to mice fed with HFHSD. Furthermore, compared to mice fed with HFHSD, mice fed with HTHSD displayed a significant elevation in the expression of CD36 in the small intestine, along with a reduction in the expression of IL-22. Furthermore, there was a significant increase in the populations of ILC1s and T-bet-positive ILC3s in the lamina propria in mice fed with HTHSD. Finally, the relative abundance of the family
Conclusions
This study revealed that compared to saturated fatty acid intake, trans fatty acid intake significantly exacerbated metabolic diseases such as diabetes and fatty liver.
Identifiants
pubmed: 33995404
doi: 10.3389/fimmu.2021.669672
pmc: PMC8117213
doi:
Substances chimiques
Blood Glucose
0
CD36 Antigens
0
Cd36 protein, mouse
0
Dietary Sucrose
0
Interleukins
0
Trans Fatty Acids
0
Banques de données
figshare
['10.6084/m9.figshare.14370035.v1']
Types de publication
Journal Article
Research Support, Non-U.S. Gov't
Langues
eng
Sous-ensembles de citation
IM
Pagination
669672Informations de copyright
Copyright © 2021 Okamura, Hashimoto, Majima, Senmaru, Ushigome, Nakanishi, Asano, Yamazaki, Takakuwa, Hamaguchi and Fukui.
Déclaration de conflit d'intérêts
HT was employed by Agilent Technologies. YH has received grants from Asahi Kasei Pharma, personal fees from Daiichi Sankyo Co., Ltd., personal fees from Mitsubishi Tanabe Pharma Corp., personal fees from Sanofi K.K., personal fees from Novo Nordisk Pharma Ltd., outside the submitted work. TS has received personal fees from Ono Pharma Co., Ltd., Mitsubishi Tanabe Pharma Co, Astellas Pharma Inc., Kyowa Hakko Kirin Co., Ltd., Sanofi K.K., MSD K.K., Kowa Pharma Co., Ltd., Taisho Toyama Pharma Co., Ltd., Takeda Pharma Co., Ltd., Kissei Pharma Co., Ltd., Novo Nordisk Pharma Ltd., Eli Lilly Japan K.K. outside the submitted work. MH has received grants from Asahi Kasei Pharma, Nippon Boehringer Ingelheim Co., Ltd., Mitsubishi Tanabe Pharma Corporation, Daiichi Sankyo Co., Ltd., Sanofi K.K., Takeda Pharmaceutical Company Limited, Astellas Pharma Inc., Kyowa Kirin Co., Ltd., Sumitomo Dainippon Pharma Co., Ltd., Novo Nordisk Pharma Ltd., and Eli Lilly Japan K.K., outside the submitted work. MA received personal fees from Novo Nordisk Pharma Ltd., Abbott Japan Co., Ltd., AstraZeneca plc, Kowa Pharmaceutical Co., Ltd., Ono Pharmaceutical Co., Ltd., Takeda Pharmaceutical Co., Ltd., outside the submitted work. MY reports personal fees from MSD K.K., Sumitomo Dainippon Pharma Co., Ltd., Kowa Company, Limited, AstraZeneca PLC, Takeda Pharmaceutical Company Limited, Kyowa Hakko Kirin Co., Ltd., Daiichi Sankyo Co., Ltd., Kowa Pharmaceutical Co., Ltd., Ono Pharma Co., Ltd., outside the submitted work. MF has received grants from Nippon Boehringer Ingelheim Co., Ltd., Kissei Pharma Co., Ltd., Mitsubishi Tanabe Pharma Co, Daiichi Sankyo Co., Ltd., Sanofi K.K., Takeda Pharma Co., Ltd., Astellas Pharma Inc., MSD K.K., Kyowa Hakko Kirin Co., Ltd., Sumitomo Dainippon Pharma Co., Ltd., Kowa Pharmaceutical Co., Ltd., Novo Nordisk Pharma Ltd., Ono Pharma Co., Ltd., Sanwa Kagaku Kenkyusho Co., Ltd. Eli Lilly Japan K.K., Taisho Pharma Co., Ltd., Terumo Co., Teijin Pharma Ltd., Nippon Chemiphar Co., Ltd., and Johnson & Johnson K.K. Medical Co., Abbott Japan Co., Ltd., and received personal fees from Nippon Boehringer Ingelheim Co., Ltd., Kissei Pharma Co., Ltd., Mitsubishi Tanabe Pharma Corp., Daiichi Sankyo Co., Ltd., Sanofi K.K., Takeda Pharma Co., Ltd., Astellas Pharma Inc., MSD K.K., Kyowa Kirin Co., Ltd., Sumitomo Dainippon Pharma Co., Ltd., Kowa Pharma Co., Ltd., Novo Nordisk Pharma Ltd., Ono Pharma Co., Ltd., Sanwa Kagaku Kenkyusho Co., Ltd., Eli Lilly Japan K.K., Taisho Pharma Co., Ltd., Bayer Yakuhin, Ltd., AstraZeneca K.K., Mochida Pharma Co., Ltd., Abbott Japan Co., Ltd., Medtronic Japan Co., Ltd., Arkley Inc., Teijin Pharma Ltd. and Nipro Cor., outside the submitted work. The remaining authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest.
Références
Diabetes. 2008 Jun;57(6):1470-81
pubmed: 18305141
Nat Med. 2008 Mar;14(3):282-9
pubmed: 18264109
ISME J. 2012 Oct;6(10):1848-57
pubmed: 22495068
Hepatology. 2005 Jun;41(6):1313-21
pubmed: 15915461
Endocrinology. 2016 Sep;157(9):3493-504
pubmed: 27384305
J Biol Chem. 2000 Oct 20;275(42):32523-9
pubmed: 10913136
J Nutr Biochem. 2017 Jan;39:77-85
pubmed: 27816763
Am J Physiol Gastrointest Liver Physiol. 2020 Jun 1;318(6):G989-G999
pubmed: 32363890
Curr Pharm Des. 2009;15(13):1528-36
pubmed: 19442170
Bioinformatics. 2005 Oct 1;21(19):3748-54
pubmed: 16091409
Proc Natl Acad Sci U S A. 2010 Aug 17;107(33):14691-6
pubmed: 20679230
Eur J Clin Nutr. 2011 May;65(5):553-64
pubmed: 20978530
Nat Methods. 2010 May;7(5):335-6
pubmed: 20383131
J Biol Chem. 2017 May 19;292(20):8174-8185
pubmed: 28360100
Nat Immunol. 2011 May;12(5):383-90
pubmed: 21502992
Immunity. 2015 Jul 21;43(1):146-60
pubmed: 26187413
Immunity. 2010 Nov 24;33(5):736-51
pubmed: 21093318
Br J Nutr. 2009 Nov;102(9):1254-66
pubmed: 19664299
J Lipid Res. 2010 May;51(5):1101-12
pubmed: 20040631
Exp Anim. 2011;60(5):481-7
pubmed: 22041285
Microbiome. 2018 Aug 2;6(1):134
pubmed: 30071904
N Engl J Med. 2006 Apr 13;354(15):1601-13
pubmed: 16611951
Am J Physiol Gastrointest Liver Physiol. 2008 Nov;295(5):G987-95
pubmed: 18772365
Gastroenterology. 2009 Nov;137(5):1716-24.e1-2
pubmed: 19706296
Bioinformatics. 2010 Oct 1;26(19):2460-1
pubmed: 20709691
Annu Rev Microbiol. 2016 Sep 8;70:395-411
pubmed: 27607555
J Immunol. 2017 Jan 1;198(1):452-460
pubmed: 27895169
Eur J Nutr. 2019 Oct;58(7):2625-2638
pubmed: 30120538
Life Sci. 2017 Nov 15;189:29-38
pubmed: 28912045
Science. 2019 Jul 26;365(6451):
pubmed: 31346040
Sci Rep. 2018 May 25;8(1):8171
pubmed: 29802255
Trends Mol Med. 2016 Mar;22(3):190-199
pubmed: 26852376
Endocr J. 2021 Apr 28;68(4):421-428
pubmed: 33361692
Nature. 2013 Feb 14;494(7436):261-5
pubmed: 23334414
Front Immunol. 2019 Sep 19;10:2233
pubmed: 31608059
ISME J. 2014 Feb;8(2):295-308
pubmed: 24030595
Immunity. 2013 Apr 18;38(4):769-81
pubmed: 23453631
Algorithms Mol Biol. 2008 Jun 26;3:8
pubmed: 18578891
Physiol Rev. 2010 Jul;90(3):859-904
pubmed: 20664075
Nat Rev Immunol. 2009 May;9(5):313-23
pubmed: 19343057
Immunity. 2008 Dec 19;29(6):958-70
pubmed: 19084435
Atherosclerosis. 2012 Sep;224(1):66-74
pubmed: 22809447
Nature. 2015 Jan 15;517(7534):293-301
pubmed: 25592534