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Low vitamin B12 in pregnancy is associated with adipose-derived circulating miRs targeting PPARγ and insulin resistance

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Adaikalakoteswari, Antonysunil, Vatish, Manu, Alam, Mohammad T., Ott, Sascha, Kumar, Sudhesh and Saravanan, P. (2017) Low vitamin B12 in pregnancy is associated with adipose-derived circulating miRs targeting PPARγ and insulin resistance. The Journal of Clinical Endocrinology & Metabolism, 102 (11). pp. 4200-4209. doi:10.1210/jc.2017-01155 ISSN 0021-972X.

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Official URL: http://dx.doi.org/10.1210/jc.2017-01155

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Abstract

Objective

We hypothesize that B12 plays a role in epigenetic regulation by altering circulating microRNAs (miRs) during adipocyte differentiation and results in an adverse metabolic phenotype.

Design, Settings, and Main Outcome Measure

Human preadipocyte cell line (Chub-S7) was differentiated in various B12 concentrations: control (500 nM), low B12 (0.15 nM), and no B12 (0 nM). Maternal blood samples (n = 91) and subcutaneous adipose tissue (SAT) (n = 42) were collected at delivery. Serum B12, folate, lipids, plasma one-carbon metabolites, miR profiling, miR expression, and gene expression were measured.

Results

Our in vitro model demonstrated that adipocytes in B12-deficient conditions accumulated more lipids, had higher triglyceride levels, and increased gene expression of adipogenesis and lipogenesis. MiR array screening revealed differential expression of 133 miRs involving several metabolic pathways (adjusted P < 0.05). Altered miR expressions were observed in 12 miRs related to adipocyte differentiation and function in adipocytes. Validation of these data in pregnant women with low B12 confirmed increased expression of adipogenic and lipogenic genes and altered miRs in SAT and altered levels of 11 of the 12 miRs in circulation. After adjustment for other possible confounders, multiple regression analysis revealed an independent association of B12 with body mass index (β: −0.264; 95% confidence interval, −0.469 to −0.058; P = 0.013) and was mediated by four circulating miRs targeting peroxisome proliferator–activated receptor γ and IR.

Conclusions:

Low B12 levels in pregnancy alter adipose-derived circulating miRs, which may mediate an adipogenic and IR phenotype, leading to obesity.

Item Type: Journal Article
Subjects: R Medicine > RC Internal medicine
R Medicine > RG Gynecology and obstetrics
Divisions: Faculty of Science, Engineering and Medicine > Medicine > Warwick Medical School > Biomedical Sciences > Cell & Developmental Biology
Faculty of Science, Engineering and Medicine > Medicine > Warwick Medical School > Biomedical Sciences
Faculty of Science, Engineering and Medicine > Science > Computer Science
Faculty of Science, Engineering and Medicine > Medicine > Warwick Medical School > Dean's Office & Professional Support Services
Faculty of Science, Engineering and Medicine > Medicine > Warwick Medical School > Health Sciences > Population, Evidence & Technologies (PET)
Faculty of Science, Engineering and Medicine > Medicine > Warwick Medical School > Biomedical Sciences > Translational & Experimental Medicine > Reproductive Health ( - until July 2016)
Faculty of Science, Engineering and Medicine > Medicine > Warwick Medical School
Library of Congress Subject Headings (LCSH): Vitamin B12 deficiency, Pregnancy, Insulin resistance
Journal or Publication Title: The Journal of Clinical Endocrinology & Metabolism
Publisher: The Endocrine Society
ISSN: 0021-972X
Official Date: 5 September 2017
Dates:
DateEvent
5 September 2017Published
31 August 2017Accepted
Volume: 102
Number: 11
Page Range: pp. 4200-4209
DOI: 10.1210/jc.2017-01155
Status: Peer Reviewed
Publication Status: Published
Access rights to Published version: Open Access (Creative Commons)
Date of first compliant deposit: 5 June 2018
Date of first compliant Open Access: 6 June 2018
RIOXX Funder/Project Grant:
Project/Grant IDRIOXX Funder NameFunder ID
UNSPECIFIEDDiabetes UKhttp://dx.doi.org/10.13039/501100000361
UNSPECIFIED[MRC] Medical Research Councilhttp://dx.doi.org/10.13039/501100000265
UNSPECIFIEDGeorge Eliot Hospital NHS Trusthttp://viaf.org/viaf/133956591

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