Advanced search×

Effect of hyperlipidemia on 11@b-hydroxysteroid-dehydrogenase, glucocorticoid receptor, and leptin expression in insulin-sensitive tissues of cats

Nadja S NS Sieber-Ruckstuhl, Eric E Zini, Melanie M Osto, Marco M Franchini, Felicitas S FS Boretti, Marina L ML Meli, Brigitte B Sigrist, Thomas A TA Lutz, and Claudia E CE Reusch

Domest Anim Endocrinol 39(4):9 (2010) PMID 20688460

Glucocorticoid (GC) action depends on GC plasma concentration, cellular GC receptor expression, and the pre-receptor hormone metabolism catalyzed by 11@b-hydroxysteroid dehydrogenase (11@b-HSD). 11@b-Hydroxysteroid dehydrogenase exists in 2 isoforms; 11@b-HSD1 converts inactive cortisone to cortisol, and 11@b-HSD2 converts cortisol to cortisone. Increasing evidence in humans and experimental animals suggests that altered tissue cortisol metabolism may predispose to diabetes mellitus (DM). Once DM is established, hyperglycemia and hyperlipidemia may further maintain the abnormal metabolism of cortisol. To gain further insight in this regard, healthy cats were infused for 10 d with lipids (n = 6) or saline (n = 5). At the end of the infusion period, tissue samples from adipose tissue (visceral, subcutaneous), liver, and muscle were collected to determine mRNA expression of 11@b-HSD1, 11@b-HSD2, and GC receptor by real-time reverse-transcriptase polymerase chain reaction; blood samples were collected to determine plasma cortisol and leptin concentrations. Lipid infusion resulted in greater 11@b-HSD1 expression and lower GC receptor expression in visceral and subcutaneous adipose tissue, and lower 11@b-HSD2 expression in visceral adipose tissue and liver. Plasma cortisol did not differ. Leptin and body weight increased in lipid-infused cats. In spite of comparable circulating cortisol levels, up-regulation of 11@b-HSD1 and down-regulation of 11@b-HSD2 expression may result in increased tissue cortisol concentrations in fat depots of hyperlipidemic cats. Down-regulation of GC receptor may represent a self-protective mechanism against increased tissue cortisol levels. In conclusion, hyperlipidemia has a profound effect on 11@b-HSD expression and supports the connection between high lipid concentrations and tissue cortisol metabolism.

Copyright © 2010 Elsevier Ltd. All rights reserved.

DOI: 10.1016/j.domaniend.2010.06.003
Version: za2963e q8za2 q8zbf q8zcc q8zda q8zee q8zf5 q8zg6
Buy PDF

Similar articles you may find interesting…

  1. Erythrocyte nitric oxide synthase as a surrogate marker for mercury-induced vascular damage: The modulatory effects of naringin.
    Gamaleldin I Harisa, Amr D Mariee, and Sabry M Attiaa

    Environ Toxicol (2013) PMID 23650045

    These results indicate that mercury exposure decreased both erythrocyte NOS activity and nitrite production, and that these parameters might be indicative of mercury exposure. The data also suggest that concomitant treatment with NAR can restore NO bioavailability through either its metal-chelating...
    Buy PDF
  2. Heterochromatin protein Sir3 induces contacts between the amino terminus of histone H4 and nucleosomal DNA.
    Feng Wang, Geng Li, and Danesh Moazed

    Proc Natl Acad Sci U S A (2013) PMID 23650358

    We provide evidence that association of the budding yeast silent information regulator 3 (Sir3) silencing protein with the nucleosome induces a conformational change in the amino terminus of histone H4 that promotes interactions between the conserved H4 arginines 17 and 19 (R17 and R19) and nucleoso...
    Buy PDF
  3. Consumers mediate the effects of experimental ocean acidification and warming on primary producers.
    Christian Alsterberg, Johan S Eklöf, and Kristina Sundbäck

    Proc Natl Acad Sci U S A (2013) PMID 23630263

    We know little about the direct and indirect effects of ocean acidification and also how these effects interact with other features of environmental change such as warming and declining consumer pressure. In this study, we tested whether the presence of consumers (invertebrate mesograzers) influence...
    Buy PDF