Genetic analysis of metabolic defects in the spontaneously hypertensive rat
Jazyk angličtina Země Spojené státy americké Médium print
Typ dokumentu časopisecké články, práce podpořená grantem, Research Support, U.S. Gov't, P.H.S.
Grantová podpora
P01 HL 35018
NHLBI NIH HHS - United States
R01 HL 56028
NHLBI NIH HHS - United States
- MeSH
- cholesterol krev metabolismus MeSH
- glukosa analýza metabolismus MeSH
- glukózový toleranční test MeSH
- hyperlipidemie genetika MeSH
- inzulin krev metabolismus MeSH
- inzulinová rezistence genetika MeSH
- krysa rodu Rattus MeSH
- kvantitativní znak dědičný * MeSH
- modely nemocí na zvířatech MeSH
- porucha glukózové tolerance genetika MeSH
- potkani inbrední BN MeSH
- potkani inbrední SHR genetika metabolismus MeSH
- triglyceridy krev metabolismus MeSH
- zvířata MeSH
- Check Tag
- krysa rodu Rattus MeSH
- mužské pohlaví MeSH
- ženské pohlaví MeSH
- zvířata MeSH
- Publikační typ
- časopisecké články MeSH
- práce podpořená grantem MeSH
- Research Support, U.S. Gov't, P.H.S. MeSH
- Názvy látek
- cholesterol MeSH
- glukosa MeSH
- inzulin MeSH
- triglyceridy MeSH
Abnormalities in carbohydrate and lipid metabolism are common in patients with essential hypertension and in the spontaneously hypertensive rat (SHR). To identify chromosome regions contributing to this clustering of cardiovascular risk factors in the SHR, we searched for quantitative trait loci (QTL) associated with insulin resistance, glucose intolerance, and dyslipidemia by using the HXB/BXH recombinant inbred (RI) strains. Analysis of variance in RI strains suggested significant effects of genetic factors. A genome screening of the RI strains with more than 700 markers revealed QTL significantly associated with insulin resistance on Chromosomes (Chrs) 3 and 19. The Chr 19 QTL was confirmed by testing a previously derived SHR-19 congenic strain: transfer of a Chr 19 segment delineated by markers D19Rat57 and D19Mit7 from the Brown Norway (BN/Cr) strain onto the genetic background of the SHR/Ola was associated with decreased insulin and glucose concentrations and ameliorated insulin resistance at the tissue level. These findings suggest that closely linked genes on Chr 19, or perhaps even a single gene with pleiotropic effects, influence the clustering of metabolic disturbances in the SHR-BN model.
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