RGD Reference Report - Quantitative trait loci for cellular defects in glucose and fatty acid metabolism in hypertensive rats. - Rat Genome Database

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Quantitative trait loci for cellular defects in glucose and fatty acid metabolism in hypertensive rats.

Authors: Aitman, TJ  Gotoda, T  Evans, AL  Imrie, H  Heath, KE  Trembling, PM  Truman, H  Wallace, CA  Rahman, A  Dore, C  Flint, J  Kren, V  Zidek, V  Kurtz, TW  Pravenec, M  Scott, J 
Citation: Aitman TJ, etal., Nat Genet 1997 Jun;16(2):197-201
RGD ID: 61078
Pubmed: PMID:9171835   (View Abstract at PubMed)
DOI: DOI:10.1038/ng0697-197   (Journal Full-text)

Coronary heart disease, hypertension, non-insulin-dependent diabetes and obesity are major causes of ill health in industrial societies. Disturbances of carbohydrate and lipid metabolism are a common feature of these disorders. The bases for these disturbances and their roles in disease pathogenesis are poorly understood. The spontaneously hypertensive rat (SHR), a widely used animal model of essential hypertension, has a global defect in insulin action on glucose metabolism and shows reduced catecholamine action on lipolysis in fat cells. In our study we used cellular defects in carbohydrate and lipid metabolism to dissect the genetics of defective insulin and catecholamine action in the SHR strain. In a genome screen for loci linked to insulin and catecholamine action, we identified two quantitative trait loci (QTLs) for defective insulin action, on chromosome 4 and 12. We found that the major (and perhaps only) genetic determinant of defective control of lipolysis in SHR maps to the same region of chromosome 4. These linkage results were ascertained in at least two independent crosses. As the SHR strain manifests many of the defining features of human metabolic Syndrome X, in which hypertension associates with insulin resistance, dyslipidaemia and abdominal obesity, the identification of genes for defective insulin and catecholamine action in SHR may facilitate gene identification in this syndrome and in related human conditions, such as type-2 diabetes and familial combined hyperlipidaemia.



Disease Annotations    

Phenotype Annotations    

Objects Annotated

QTLs
Gluco16  (Glucose level QTL 16)
Gluco17  (Glucose level QTL 17)
Gluco3  (Glucose level QTL 3)
Gluco4  (Glucose level QTL 4)
Gluco5  (Glucose level QTL 5)

Strains
SHR/NCruk  (Spontaneously Hypertensive Rat)
SHR/Ola  (NA)
WKY/NCruk  (NA)

Objects referenced in this article
Marker D12Mit8 D12Mit8 Rattus norvegicus
Marker D12Mgh1 D12Mgh1 Rattus norvegicus
Marker D4Arb13 D4Arb13 Rattus norvegicus
Strain BXH/Ipcv null Rattus norvegicus
Strain HXB/Ipcv null Rattus norvegicus
Strain SHR.WKY-(D12Rat1-D12Mit3)/Tja null Rattus norvegicus
Strain SHR.WKY-(D16Rat88-D16Rat15)/Tja null Rattus norvegicus
Strain SHR.WKY-(D4Rat143-D4Rat10)/Tja null Rattus norvegicus
Gene Slc4a2 solute carrier family 4 member 2 Rattus norvegicus

Additional Information