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Developmental Origins of Common Disease: Epigenetic Contributions to Obesity.

Developmental Origins of Common Disease: Epigenetic Contributions to Obesity.

http://www.wikidata.org/entity/Q37300945

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DNA-Methylation and Body Composition in Preschool Children: Epigenome-Wide-Analysis in the European Childhood Obesity Project (CHOP)-Study.Insulinotropic Effect of S-Allyl Cysteine in Rat Pups.Epigenetic control of variation and stochasticity in metabolic disease.

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P2860

Developmental Origins of Common Disease: Epigenetic Contributions to Obesity.

http://www.wikidata.org/entity/Q37300945

description

article científic

@ca

article scientifique

@fr

articolo scientifico

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artigo científico

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bilimsel makale

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scientific article published on 11 May 2016

@en

vedecký článok

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vetenskaplig artikel

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videnskabelig artikel

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vědecký článek

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name

Developmental Origins of Common Disease: Epigenetic Contributions to Obesity.

@en

Developmental Origins of Common Disease: Epigenetic Contributions to Obesity.

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type

label

Developmental Origins of Common Disease: Epigenetic Contributions to Obesity.

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Developmental Origins of Common Disease: Epigenetic Contributions to Obesity.

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prefLabel

Developmental Origins of Common Disease: Epigenetic Contributions to Obesity.

@en

Developmental Origins of Common Disease: Epigenetic Contributions to Obesity.

@nl

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ANNUREV-GENOM-090314-050057

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Annual Review of Genomics and Human Genetics

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Developmental Origins of Common Disease: Epigenetic Contributions to Obesity.

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Robert O Wright

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P2860

Ten putative contributors to the obesity epidemic

Assessment of cardiometabolic risk in children in population studies: underpinning developmental origins of health and disease mother-offspring cohort studies

Pesticide methoxychlor promotes the epigenetic transgenerational inheritance of adult-onset disease through the female germline

Personal genomes: The case of the missing heritability

Exercise prevents maternal high-fat diet-induced hypermethylation of the Pgc-1α gene and age-dependent metabolic dysfunction in the offspring.

Maternal high folic acid supplement promotes glucose intolerance and insulin resistance in male mouse offspring fed a high-fat diet.

Transcriptional control of preadipocyte determination by Zfp423.

Maternal obesity downregulates microRNA let-7g expression, a possible mechanism for enhanced adipogenesis during ovine fetal skeletal muscle development

Prenatal polycyclic aromatic hydrocarbon, adiposity, peroxisome proliferator-activated receptor (PPAR) γ methylation in offspring, grand-offspring mice.

High blood pressure trends in children and adolescents in national surveys, 1963 to 2002.

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177-192

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scholarly article

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10.1146/ANNUREV-GENOM-090314-050057

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17

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