on March 24, 2003
Published online before print March 24, 2003, doi: 10.1161/01.HYP.0000064347.49341.0B
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Submitted on December 19, 2002
From the Centre de recherche, Centre hospitalier de l'Université de Montréal (Z.P., L.S., J.B., P.H., J.T., M.D., D.G.), Montréal, Canada; and Charles University (M.P., V.K.) and the Institute of Physiology, Academy of Sciences (M.P., V.K., J.K.), Prague, Czech Republic. * To whom correspondence should be addressed. E-mail: zdenka.pausova{at}umontreal.ca.
Abstract--Previous linkage and association studies have suggested that a region of human chromosome 6 containing the tumor necrosis factor (TNF)-
Revised on January 13, 2003
Segment of Rat Chromosome 20 Regulates Diet-Induced Augmentations in Adiposity, Glucose Intolerance, and Blood Pressure
Zdenka Pausova*;
gene is involved in the pathogenesis of obesity and obesity-associated hypertension. The aim of the present investigation was to establish whether a segment of rat chromosome 20 (RNO20), which also contains the TNF- gene, determines diet-induced changes in adiposity and blood pressure (BP). The results showed that a transfer of the RNO20 segment from the normotensive Brown Norway (BN) rat onto the background of the spontaneously hypertensive rat (SHR) is associated with a significantly greater increase in adiposity, glucose intolerance, circulating leptin levels, and BP during 12-week, high-fat-diet feeding. In contrast, the transfer is not associated with significant changes in these variables during 12-week, normal-diet feeding. In addition, sequencing of the TNF- gene revealed differences between SHR and BN in the 5'- and 3'-regulatory regions of the gene. Subsequent analyses of TNF- gene expression in fat, muscle, and liver, however, did not provide support for the functional involvement of these differences. In summary, the investigated RNO20 segment contains 1 or more gene variants that affect adiposity, glucose tolerance, serum leptin levels, and BP, but only when the animals are exposed to a particular environment, ie, high-fat-diet feeding. Further studies are needed to identify genes mediating these effects. Considering current changes in our lifestyle involving an increased calorie and fat intake, we believe that gene-environment interactions, such as those described here, play an important role in the current epidemic of obesity and obesity-associated hypertension.
Key words: hypertension, obesity • diet • genetics • glucose • tumor necrosis factor • gene-environment interaction
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