Prevalence of melanocortin system transcripts in rat salt homeostasis endocrine tissues
Melanocortin receptors have been implicated in the confounding factors of cardiovascular diseases such as obesity, insulin resistance and salt-sensitive hypertension. The aim of this study was determine how increased dietary salt intake affects the expression profiles of melanocortin system genes in...
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Published in: | Cellular and molecular biology (Noisy-le-Grand, France) Vol. 53; no. 4; p. 8 |
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Main Authors: | , , , |
Format: | Journal Article |
Language: | English |
Published: |
France
15-05-2007
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Subjects: | |
Online Access: | Get more information |
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Summary: | Melanocortin receptors have been implicated in the confounding factors of cardiovascular diseases such as obesity, insulin resistance and salt-sensitive hypertension. The aim of this study was determine how increased dietary salt intake affects the expression profiles of melanocortin system genes in relevant endocrine tissues. Total RNA was isolated from the pituitary and adrenal glands of Wistar Kyoto (WKY) and stroke-prone spontaneously hypertensive rats (SP-SHR) and subjected to real-time PCR analysis. Expression levels of pro-opiomelanocortin (POMC), POMC processing enzymes prohormone convertases 1 and 2 (PC1/PC2), melanocortin 3 receptor (MC3R) and melanocortin 5 receptor (MC5R) were not significantly affected by high dietary salt intake in either WKY or SP-SHR tissues. Consistent with known endocrine relationship between the pituitary and adrenal glands, the expression levels of the ACTH receptor, MC2R, were five orders of magnitude higher in adrenal tissues whereas those of POMC were three orders of magnitude higher in the pituitary. MC3R, PC1 and PC2 transcripts were expressed at similar levels in both tissues while MC5R was expressed at a higher level in the adrenal tissues. These results are therefore inconsistent with an endocrine pathway that involves pituitary derived gamma-MSH modulating adrenal function in response to high dietary salt intake. |
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ISSN: | 1165-158X |
DOI: | 10.1170/T802 |