RGD Reference Report - Mapping of genetic loci predisposing to hypertriglyceridaemia in the hereditary hypertriglyceridaemic rat: analysis of genetic association with related traits of the insulin resistance syndrome. - Rat Genome Database

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Mapping of genetic loci predisposing to hypertriglyceridaemia in the hereditary hypertriglyceridaemic rat: analysis of genetic association with related traits of the insulin resistance syndrome.

Authors: Klimes, I  Weston, K  Kovacs, P  Gasperikova, D  Jezova, D  Kvetnansky, R  Thompson, JR  Sebokova, E  Samani, NJ 
Citation: Klimes I, etal., Diabetologia 2003 Mar;46(3):352-8.
RGD ID: 631174
Pubmed: PMID:12687333   (View Abstract at PubMed)
DOI: DOI:10.1007/s00125-003-1035-6   (Journal Full-text)

AIMS/HYPOTHESIS. Hypertriglyceridaemia is an important risk factor for coronary heart disease, especially in the context of the insulin resistance syndrome where it often occurs with hypertension. The two phenotypes are also associated in the hereditary hypertriglyceridaemic (hHTg) rat. The aim of this study was to map quantitative trait loci that affect plasma triglyceride concentration in the hHTg rat and determine whether they co-localize with loci for blood pressure. METHODS. Second filial generation progeny ( n=189) from a cross of the hHTg rat with the Brown Norway rat were phenotyped for fasting plasma triglyceride, glucose and insulin concentrations, and direct unrestrained resting blood pressure. A partial genome-scan was conducted using 153 microsatellite markers that were polymorphic between the two strains. RESULTS. A major locus (lod score 6.5) influencing plasma triglyceride concentration in a co-dominant fashion was mapped to chromosome 4 between D1Mit 5 and D1Mit17. Chromosome 8 contained multiple peaks with a lod score greater than 4.0 influencing triglyceride concentration. Importantly, none of the triglyceride loci had an effect on blood pressure. The triglyceride locus on chromosome 4 co-localized with a locus for fasting plasma insulin (lod score 4.1), although the effect on insulin concentration was in the opposite direction to that on triglyceride. CONCLUSION/INTERPRETATION. We have mapped the major loci that affect plasma triglyceride concentration in the hHTg rat. These loci do not influence blood pressure suggesting that these commonly associated phenotypes of the insulin resistance syndrome are not be due to pleiotropic effects of the same gene(s).



RGD Manual Disease Annotations    Click to see Annotation Detail View

  
Object SymbolSpeciesTermQualifierEvidenceWithNotesSourceOriginal Reference(s)
Stl4Rathyperinsulinism  IDA  RGD 
Stl4RatHypertriglyceridemia  IDA  RGD 
Stl5RatHypertriglyceridemia  IDA  RGD 
Stl6RatHypertriglyceridemia  IDA  RGD 

Phenotype Annotations    Click to see Annotation Detail View

Mammalian Phenotype

Object SymbolSpeciesTermQualifierEvidenceWithNotesSourceOriginal Reference(s)
Stl4Ratincreased circulating insulin level  QTM  RGD 
Stl4Ratincreased circulating triglyceride level  QTM  RGD 
Stl5Ratincreased circulating triglyceride level  QTM  RGD 
Stl6Ratincreased circulating triglyceride level  QTM  RGD 

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Objects Annotated

QTLs
Stl4  (Serum triglyceride level QTL 4)
Stl5  (Serum triglyceride level QTL 5)
Stl6  (Serum triglyceride level QTL 6)

Strains
BN/OrlIcoCrlf  (NA)
HTG  (Prague hypertriglyceridemic)


Additional Information