TY - JOUR
T1 - Metabolic syndrome components in murine models
AU - Lawson, Heather A.
AU - Cheverud, James M.
N1 - Copyright:
Copyright 2017 Elsevier B.V., All rights reserved.
PY - 2010/3
Y1 - 2010/3
N2 - Animal models have enriched understanding of the physiological basis of metabolic disorders and advanced identification of genetic risk factors underlying the metabolic syndrome (MetS). Murine models are especially appropriatefor this type of research, and are an excellent resource not only for identifying candidate genomic regions, but also for illuminating the possible molecular mechanisms or pathways affected in individual components of MetS. In this review, we briefly discuss findings from mouse models of metabolic disorders, particularly in light of issues raised by the recent flood of human genome-wide association studies (GWAS) results. We describe how mouse models are revealing that genotype interacts with environment in important ways, indicating that the underlying genetics of MetS is highly context dependant. Further we show that epistasis, imprinting and maternal effects each contribute to the genetic architecture underlying variation in metabolic traits, and mouse models provide an opportunity to dissect these aspects of the genetic architecture that are difficult if not impossible to ascertain in humans. Finally we discuss how knowledge gained from mouse models can be used in conjunction with comparative genomic methods and bioinformatic resources to inform human MetS research.
AB - Animal models have enriched understanding of the physiological basis of metabolic disorders and advanced identification of genetic risk factors underlying the metabolic syndrome (MetS). Murine models are especially appropriatefor this type of research, and are an excellent resource not only for identifying candidate genomic regions, but also for illuminating the possible molecular mechanisms or pathways affected in individual components of MetS. In this review, we briefly discuss findings from mouse models of metabolic disorders, particularly in light of issues raised by the recent flood of human genome-wide association studies (GWAS) results. We describe how mouse models are revealing that genotype interacts with environment in important ways, indicating that the underlying genetics of MetS is highly context dependant. Further we show that epistasis, imprinting and maternal effects each contribute to the genetic architecture underlying variation in metabolic traits, and mouse models provide an opportunity to dissect these aspects of the genetic architecture that are difficult if not impossible to ascertain in humans. Finally we discuss how knowledge gained from mouse models can be used in conjunction with comparative genomic methods and bioinformatic resources to inform human MetS research.
KW - Bioinformatics
KW - Cardiovascular disease
KW - Comparative genomics
KW - Genome-wide association studies
KW - Hypertension
KW - Metabolic syndrome
KW - Murine models
KW - Obesity
KW - Type-2 diabetes
UR - http://www.scopus.com/inward/record.url?scp=77950790765&partnerID=8YFLogxK
U2 - 10.2174/187153010790827948
DO - 10.2174/187153010790827948
M3 - Review article
C2 - 20088816
AN - SCOPUS:77950790765
SN - 1871-5303
VL - 10
SP - 25
EP - 40
JO - Endocrine, Metabolic and Immune Disorders - Drug Targets
JF - Endocrine, Metabolic and Immune Disorders - Drug Targets
IS - 1
ER -