PMID- 27408648
OWN - NLM
STAT- MEDLINE
DCOM- 20180117
LR  - 20220331
IS  - 1868-7083 (Electronic)
IS  - 1868-7075 (Print)
IS  - 1868-7075 (Linking)
VI  - 7
DP  - 2015
TI  - Recent developments on the role of epigenetics in obesity and metabolic disease.
PG  - 66
LID - 10.1186/s13148-015-0101-5 [doi]
LID - 66
AB  - The increased prevalence of obesity and related comorbidities is a major public 
      health problem. While genetic factors undoubtedly play a role in determining 
      individual susceptibility to weight gain and obesity, the identified genetic 
      variants only explain part of the variation. This has led to growing interest in 
      understanding the potential role of epigenetics as a mediator of gene-environment 
      interactions underlying the development of obesity and its associated 
      comorbidities. Initial evidence in support of a role of epigenetics in obesity 
      and type 2 diabetes mellitus (T2DM) was mainly provided by animal studies, which 
      reported epigenetic changes in key metabolically important tissues following 
      high-fat feeding and epigenetic differences between lean and obese animals and by 
      human studies which showed epigenetic changes in obesity and T2DM candidate genes 
      in obese/diabetic individuals. More recently, advances in epigenetic 
      methodologies and the reduced cost of epigenome-wide association studies (EWAS) 
      have led to a rapid expansion of studies in human populations. These studies have 
      also reported epigenetic differences between obese/T2DM adults and healthy 
      controls and epigenetic changes in association with nutritional, weight loss, and 
      exercise interventions. There is also increasing evidence from both human and 
      animal studies that the relationship between perinatal nutritional exposures and 
      later risk of obesity and T2DM may be mediated by epigenetic changes in the 
      offspring. The aim of this review is to summarize the most recent developments in 
      this rapidly moving field, with a particular focus on human EWAS and studies 
      investigating the impact of nutritional and lifestyle factors (both pre- and 
      postnatal) on the epigenome and their relationship to metabolic health outcomes. 
      The difficulties in distinguishing consequence from causality in these studies 
      and the critical role of animal models for testing causal relationships and 
      providing insight into underlying mechanisms are also addressed. In summary, the 
      area of epigenetics and metabolic health has seen rapid developments in a short 
      space of time. While the outcomes to date are promising, studies are ongoing, and 
      the next decade promises to be a time of productive research into the complex 
      interactions between the genome, epigenome, and environment as they relate to 
      metabolic disease.
FAU - van Dijk, Susan J
AU  - van Dijk SJ
AD  - CSIRO Food and Nutrition Flagship, PO Box 52, North Ryde, NSW 1670 Australia.
FAU - Tellam, Ross L
AU  - Tellam RL
AD  - CSIRO Agriculture Flagship, 306 Carmody Road, St Lucia, QLD 4067 Australia.
FAU - Morrison, Janna L
AU  - Morrison JL
AD  - Early Origins of Adult Health Research Group, School of Pharmacy and Medical 
      Sciences, Sansom Institute for Health Research, University of South Australia, 
      GPO Box 2471, Adelaide, SA 5001 Australia.
FAU - Muhlhausler, Beverly S
AU  - Muhlhausler BS
AD  - FOODplus Research Centre, Waite Campus, The University of Adelaide, PMB 1, Glen 
      Osmond, SA 5064 Australia.
AD  - Women's and Children's Health Research Institute, 72 King William Road, North 
      Adelaide, SA 5006 Australia.
FAU - Molloy, Peter L
AU  - Molloy PL
AD  - CSIRO Food and Nutrition Flagship, PO Box 52, North Ryde, NSW 1670 Australia.
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
PT  - Review
DEP - 20150711
PL  - Germany
TA  - Clin Epigenetics
JT  - Clinical epigenetics
JID - 101516977
SB  - IM
MH  - Adolescent
MH  - Animals
MH  - Child
MH  - Child, Preschool
MH  - Comorbidity
MH  - DNA Methylation/genetics
MH  - Diabetes Mellitus, Type 2/epidemiology/genetics/physiopathology
MH  - Environmental Exposure
MH  - *Epigenomics
MH  - Female
MH  - Gene-Environment Interaction
MH  - Genome
MH  - Genome-Wide Association Study
MH  - Humans
MH  - Infant, Newborn
MH  - Life Style
MH  - Male
MH  - Metabolic Diseases/epidemiology/*genetics/physiopathology
MH  - Mice
MH  - Models, Animal
MH  - Nutritional Physiological Phenomena/genetics
MH  - Obesity/epidemiology/*genetics/physiopathology
MH  - Pregnancy
MH  - Pregnancy Complications
MH  - Prevalence
MH  - Weight Gain/genetics
PMC - PMC4940755
OTO - NOTNLM
OT  - DNA methylation
OT  - Developmental programming
OT  - Epigenetics
OT  - Obesity
OT  - Type 2 diabetes
EDAT- 2015/01/01 00:00
MHDA- 2015/01/01 00:01
PMCR- 2015/07/11
CRDT- 2016/07/14 06:00
PHST- 2015/03/09 00:00 [received]
PHST- 2015/06/29 00:00 [accepted]
PHST- 2016/07/14 06:00 [entrez]
PHST- 2015/01/01 00:00 [pubmed]
PHST- 2015/01/01 00:01 [medline]
PHST- 2015/07/11 00:00 [pmc-release]
AID - 101 [pii]
AID - 10.1186/s13148-015-0101-5 [doi]
PST - epublish
SO  - Clin Epigenetics. 2015 Jul 11;7:66. doi: 10.1186/s13148-015-0101-5. eCollection 
      2015.