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Differential methylation in inflammation and type 2 diabetes genes in siblings born before and after maternal bariatric surgery
Author(s) -
Berglind Daniel,
Müller Patrick,
Willmer Mikaela,
Sinha Indranil,
Tynelius Per,
Näslund Erik,
DahlmanWright Karin,
Rasmussen Finn
Publication year - 2016
Publication title -
obesity
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.438
H-Index - 199
eISSN - 1930-739X
pISSN - 1930-7381
DOI - 10.1002/oby.21340
Subject(s) - epigenetics , dna methylation , medicine , cpg site , type 2 diabetes , methylation , leptin , leptin receptor , obesity , sibling , adipokine , diabetes mellitus , bioinformatics , endocrinology , gene , genetics , biology , psychology , developmental psychology , gene expression
Objective Siblings born before (BMS) and after (AMS) maternal biliopancreatic diversion (BPD) show differences in the methylome. The objective was to use a sibling‐pair design to examine the effects from interpregnancy weight loss as a consequence of maternal bariatric surgery, other than BPD, on the methylome comparing BMS and AMS. Methods Women with at least one child born before and one after bariatric surgery were identified in Swedish national registers. Whole blood samples from BMS ( N = 31) and AMS ( N = 31) siblings were collected for epigenetic methylation analysis while maternal information was collected from antenatal medical records. Results In total 3,074 genes, with corresponding 23,449 CpG methylation sites, were differently methylated and associated with an overrepresentation of differently methylated CpG sites in genes involved with insulin receptor signaling, type 2 diabetes signaling, and leptin signaling in obesity, while the most significant differently methylated genes were HLA‐DQA1, HLA‐DQB1, and TSPAN18, when comparing BMS and AMS siblings. Conclusions These results suggest that maternal bariatric surgery, with subsequent weight loss between pregnancies, is associated with alterations in the methylome of genes involved in insulin receptor signaling, type 2 diabetes signaling, and leptin signaling in obesity in a comparison of BMS and AMS siblings.