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AmJCaseRep

Mineralocorticoid receptor expression is modulated and mitochondrial biogenesis is enhanced in colonic enterocytes of patients with ulcerative colitis and massive fluid loss

Patrick Brück, Rudolf J Wiesner, Elizabeth Ramos Lopez, Franz Xavier Huber

Med Sci Tech 2007; 48(3): RA147-151

ID: 881560

Available online:

Published: 2007-03-20


Introduction: Mineralocorticoid receptors play a central role in electrolyte and fluid regulation. Patients with ulcerative colitis (CU) are ideal for studying aldosterone dependent fluid regulation at the colorectal junction, because of the high fluid loss. Material and Methods: Beside the clinical data and steroid serum levels of three patients with CU and familial adenomatous polyposis (FAP), the expression of the mineralocorticoid (MR) and glucocorticoid receptor (GR), the mitochondrial DNA encoded cytochrome C oxidase subunit II (COX II) and the nuclear encoded human mitochondrial transcription factor A (TFAM) at the colorectal junction was measured by western blots. Results: While the mitochondrial COX II, and nuclear TFAM were clearly increased in the enterocyte layer of the proximal colorectum of patients with CU, GR and MR expression was similar in both groups, but a clear difference in the expression pattern of the MR was observed. Conclusions: Mitochondrial biogenesis in the colorectal junction is up-regulated in order to provide the surplus of energy needed to compensate the faecal fluid loss. This mechanism is independent of steroid medication. The compensation thereby is not mediated via an up-regulation of the mineralocorticoid receptor but post-translational changes in the expression pattern. (Clin Exp Med Lett 2007; 48(3):147-151)

Keywords: mineralocorticoid receptor, mitochondrial biogenesis, colonic enterocytes, ulcerative colitis, FAP



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