Genetics of nonsyndromic human obesity, with suggestions for new studies from work in mouse models

Craig H. Warden, Janis S. Fisler

Research output: Chapter in Book/Report/Conference proceedingChapter

Abstract

Most genetic human obesity is due to multiple genes interacting with each other and with environment. Sequencing exomes, genome-wide associations with single nucleotide polymorphisms, sequencing methylations, and sequencing genomic DNA have revealed hundreds of obesity-causing polymorphisms that all together account for a small percent of total heritability. Pathway analyses reveal that most body mass index genes are expressed in the brain whereas most waist-to-hip ratio fat distribution genes are expressed in adipose tissue. Most mouse obesity genes are also human obesity genes and vice versa. Studies in mice demonstrate that quantitating fat mass, individual fat depots, responses of individual fat depots to dieting and exercise, and parental effects will reveal many new obesity genes. These topics have been explored superficially or not at all in studies of humans. Genetic and randomized controlled diet data are presently inadequate for development of personalized obesity therapy.

Original languageEnglish (US)
Title of host publicationNutrition in the Prevention and Treatment of Disease
PublisherElsevier
Pages455-476
Number of pages22
ISBN (Electronic)9780128029282
DOIs
StatePublished - Jan 1 2017

Keywords

  • Clinical implications
  • Epigenetics
  • Heritability
  • Leptin-melanocortin pathway
  • Methods of detection
  • Monogenic
  • Multigenic

ASJC Scopus subject areas

  • Engineering(all)
  • Agricultural and Biological Sciences(all)

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    Warden, C. H., & Fisler, J. S. (2017). Genetics of nonsyndromic human obesity, with suggestions for new studies from work in mouse models. In Nutrition in the Prevention and Treatment of Disease (pp. 455-476). Elsevier. https://doi.org/10.1016/B978-0-12-802928-2.00021-7