title: Baboons as a model to study genetics and epigenetics of human disease.
abstract: A major challenge for understanding susceptibility to common human diseases is determining genetic and environmental factors that influence mechanisms underlying variation in disease-related traits. The most common diseases afflicting the US population are complex diseases that develop as a result of defects in multiple genetically controlled systems in response to environmental challenges. Unraveling the etiology of these diseases is exceedingly difficult because of the many genetic and environmental factors involved. Studies of complex disease genetics in humans are challenging because it is not possible to control pedigree structure and often not practical to control environmental conditions over an extended period of time. Furthermore, access to tissues relevant to many diseases from healthy individuals is quite limited. The baboon is a well-established research model for the study of a wide array of common complex diseases, including dyslipidemia, hypertension, obesity, and osteoporosis. It is possible to acquire tissues from healthy, genetically characterized baboons that have been exposed to defined environmental stimuli. In this review, we describe the genetic and physiologic similarity of baboons with humans, the ability and usefulness of controlling environment and breeding, and current genetic and genomic resources. We discuss studies on genetics of heart disease, obesity, diabetes, metabolic syndrome, hypertension, osteoporosis, osteoarthritis, and intrauterine growth restriction using the baboon as a model for human disease. We also summarize new studies and resources under development, providing examples of potential translational studies for targeted interventions and therapies for human disease.
authors.forename: Laura A
authors.initials: LA
authors.lastname: Cox
authors.forename: Anthony G
authors.initials: AG
authors.lastname: Comuzzie
authors.forename: Lorena M
authors.initials: LM
authors.lastname: Havill
authors.forename: Genesio M
authors.initials: GM
authors.lastname: Karere
authors.forename: Kimberly D
authors.initials: KD
authors.lastname: Spradling
authors.forename: Michael C
authors.initials: MC
authors.lastname: Mahaney
authors.forename: Peter W
authors.initials: PW
authors.lastname: Nathanielsz
authors.forename: Daniel P
authors.initials: DP
authors.lastname: Nicolella
authors.forename: Robert E
authors.initials: RE
authors.lastname: Shade
authors.forename: Saroja
authors.initials: S
authors.lastname: Voruganti
authors.forename: John L
authors.initials: JL
authors.lastname: VandeBerg
mesh_terms: D000818:Animals; D002318:Cardiovascular Diseases / Q000235:genetics* / Q000503:physiopathology; D004195:Disease Models, Animal; D044127:Epigenesis, Genetic / Q000235:genetics* / Q000502:physiology; D005260:Female; D005317:Fetal Growth Retardation / Q000235:genetics* / Q000503:physiopathology; D006801:Humans; D006973:Hypertension / Q000235:genetics* / Q000503:physiopathology; D009765:Obesity / Q000235:genetics* / Q000503:physiopathology; D010215:Papio / Q000235:genetics* / Q000502:physiology; D011247:Pregnancy
keywords: cardiovascular disease; diabetes; genomics resources; hypertension; intrauterine growth restriction; metabolic syndrome; obesity; osteoporosis