Abstract
This study investigated the incidence of cafeteria-diet induced hypertension on hypothalamic tyrosine hydroxylase (TH) and α2-adrenoceptor subtype gene expression in male, female, and neonatally testosterone-imprinted female rats. After 10 weeks of cafeteria diet, all these rats were hyperleptinemic. In contrast, males and testosterone-treated females developed hypertension, whereas intact females remained normotensive. In these rats, cafeteria diet up-regulated TH gene expression only in males and testosterone-treated females. On the other hand, cafeteria diet differentially affected hypothalamic gene expression of α2-adrenoceptor subtypes. In fact, this diet increased α2A-adrenoceptor mRNA levels only in intact normotensive females. In contrast, gene expression of the α2B-adrenoceptor was up-regulated only in male and testosterone-treated female cafeteria-fed rats. Furthermore, an α2C-adrenoceptor gene over-expression was also induced, but only in male cafeteria-fed rats. If one assumes that the up-regulations in TH and α2B-adrenoceptor gene expression are indicative of increased sympathetic nervous activity, then, these altered gene expressions could be responsible for the maintenance of high blood pressure in male and testosterone-treated female cafeteria-fed rats. Conversely, in intact females, the absence of these over-expressions and the up-regulation of the α2A-adrenoceptor gene expression could reflect an adaptive response to the diet and, consequently, could be protective against cafeteria diet-induced hypertension. Moreover, neonatal testosterone imprinting in females could have induced an irreversible android susceptibility to the cafeteria diet, leading to the onset of hypertension.
Footnotes
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This article is available online at http://jpet.aspetjournals.org
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This work was supported by grants from the University René Descartes.
- Abbreviations:
- TH
- tyrosine hydroxylase
- PCR
- polymerase chain reaction
- bp
- base pair(s)
- RT-PCR
- reverse transcription-polymerase chain reaction
- Received December 26, 2001.
- Accepted April 2, 2002.
- The American Society for Pharmacology and Experimental Therapeutics
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