ABSTRACT
BACKGROUND: Epicardial adipose tissue (EAT) is in close contact with coronary vessels and therefore could alter coronary homeostasis. Glucocorticoids are pathophysiological mediators of visceral fat deposition and its associated atherogenic complications. AIM: We investigated in EAT the expression of the glucocorticoid receptor (GR) and its various (A, B, C) promoters. MATERIALS AND METHODS: Paired subcutaneous adipose tissue (SAT) and EAT biopsies were obtained from 15 patients with coronary artery disease (CAD) and 12 patients without CAD (NCAD). GR and 11ß-hydroxysteroid dehydrogenase type 1 protein (11ß-HSD-1, the enzyme which converts inactive cortisone into active cortisol) were studied by immunohistochemistry and GR and its various promoters were studied by mRNA quantitative RT-PCR. RESULTS: GR and 11ß-HSD-1 protein were expressed in adipocytes, stromal areas, isolated stromal cells close to adipocytes, and blood vessels. Total GR mRNA levels did not differ in SAT obtained from NCAD or CAD patients and were decreased in EAT, irrespectively of the coronary status, with parallel changes in promoter B- and C-, but not promoter A-associated transcripts. Total GR mRNA and adipocyte surface in EAT obtained from CAD patients were correlated negatively (p<0.035, r=0.39). CONCLUSIONS: Our findings demonstrate that in EAT, GR gene promoters could play a role in tissue- specific GR expression levels. EAT may be less sensitive to glucocorticoids than SAT, preventing the EAT mass development in CAD patients and suggesting a protective role on coronary homeostasis.
Subject(s)
Adipose Tissue, White/metabolism , Coronary Artery Disease/metabolism , Gene Expression Regulation , Promoter Regions, Genetic , Receptors, Glucocorticoid/metabolism , 11-beta-Hydroxysteroid Dehydrogenase Type 1/metabolism , Adipose Tissue, White/pathology , Adult , Aged , Biopsy , Cell Size , Coronary Artery Disease/pathology , Female , Humans , Male , Middle Aged , Organ Specificity , Pericardium , RNA Splice Sites , RNA, Messenger/metabolism , Receptors, Glucocorticoid/genetics , Stromal Cells/metabolism , Stromal Cells/pathology , Subcutaneous Fat/metabolism , Subcutaneous Fat/pathologyABSTRACT
Moderate hematologic abnormalities, like anemia or leukopenia, are frequently seen in anorexia nervosa, whereas pancytopenia and bone marrow abnormalities are uncommon. We report a case of tricytopenia with gelatinous bone marrow transformation in anorexia nervosa. Marrow gelatinous transformation (also called serous fat atrophy or starvation marrow) is characterized by the association of marrow hypoplasia and interstitial infiltration of a ground gelatinous substance (acidic mucopolysaccharides). Changes in peripheral blood cell counts are various and moderate, and do not always reflect the severity of bone marrow damage. The pathogenesis is not yet well elucidated but is certainly related to the nutritional status because gelatinous bone marrow transformation is found in anorexia nervosa and in other clinical situations with cachexia. Gelatinous transformation of the marrow is reversible with feeding.
