open access

Vol 70, No 2 (2019)
Original papers
Published online: 2018-11-27
Submitted: 2018-06-25
Accepted: 2018-10-27
Get Citation

Comparison of adipose tissue derived genes in endogenous Cushing’s syndrome versus diet-induced obesity

Judit Denes, Adrienn Zsippai, Laszlo Kovacs, Zoltan Gorombey, Gabor L. Kovacs, Miklos Goth, Peter Igaz, Erika Hubina
DOI: 10.5603/EP.a2018.0091
·
Pubmed: 30480750
·
Endokrynologia Polska 2019;70(2):131-134.

open access

Vol 70, No 2 (2019)
Original papers
Published online: 2018-11-27
Submitted: 2018-06-25
Accepted: 2018-10-27

Abstract

Introduction: Dysregulation of adipokine secretion and action is a characteristic feature of obesity and a key clinical feature of Cushing’s syndrome (CS). We have investigated whether endogenous glucocorticoid excess influences adipose tissue-derived gene expression.

Material and methods: mRNA expression of adipokines; adiponectin, resistin, tumour necrosis factor-a, interleukin-6 (IL-6), angiotensinogen (AGT), plasminogen activator inhibitor type 1, retinol binding protein 4, visfatin, and cystatin C was assessed by quantitative real-time RT-PCR in visceral adipose tissue removed during abdominal surgery of eight patients with CS, and six control patients.

Results: We did not find any significant difference in the investigated genes; however, the almost significant overexpression of AGT and underexpression of IL-6 might be noteworthy (p = 0.06 in both cases).

Conclusions: No significant differences were found in the expression of the investigated genes known as cardiometabolic risk factors. This indicates that there are no major differences between endogenous hypercortisolism or diet-induced obesity regarding the expression of adipokines involved in cardiometabolic disorders. However, the difference in AGT and IL-6 expression might be included in pathways affecting fat distribution in CS

Abstract

Introduction: Dysregulation of adipokine secretion and action is a characteristic feature of obesity and a key clinical feature of Cushing’s syndrome (CS). We have investigated whether endogenous glucocorticoid excess influences adipose tissue-derived gene expression.

Material and methods: mRNA expression of adipokines; adiponectin, resistin, tumour necrosis factor-a, interleukin-6 (IL-6), angiotensinogen (AGT), plasminogen activator inhibitor type 1, retinol binding protein 4, visfatin, and cystatin C was assessed by quantitative real-time RT-PCR in visceral adipose tissue removed during abdominal surgery of eight patients with CS, and six control patients.

Results: We did not find any significant difference in the investigated genes; however, the almost significant overexpression of AGT and underexpression of IL-6 might be noteworthy (p = 0.06 in both cases).

Conclusions: No significant differences were found in the expression of the investigated genes known as cardiometabolic risk factors. This indicates that there are no major differences between endogenous hypercortisolism or diet-induced obesity regarding the expression of adipokines involved in cardiometabolic disorders. However, the difference in AGT and IL-6 expression might be included in pathways affecting fat distribution in CS

Get Citation

Keywords

Cushing’s syndrome; obesity; adipokines; visceral adipose tissue, glucocorticoids

About this article
Title

Comparison of adipose tissue derived genes in endogenous Cushing’s syndrome versus diet-induced obesity

Journal

Endokrynologia Polska

Issue

Vol 70, No 2 (2019)

Pages

131-134

Published online

2018-11-27

DOI

10.5603/EP.a2018.0091

Pubmed

30480750

Bibliographic record

Endokrynologia Polska 2019;70(2):131-134.

Keywords

Cushing’s syndrome
obesity
adipokines
visceral adipose tissue
glucocorticoids

Authors

Judit Denes
Adrienn Zsippai
Laszlo Kovacs
Zoltan Gorombey
Gabor L. Kovacs
Miklos Goth
Peter Igaz
Erika Hubina

References (31)
  1. Walker GE, Marzullo P, Ricotti R, et al. The pathophysiology of abdominal adipose tissue depots in health and disease. Horm Mol Biol Clin Investig. 2014; 19(1): 57–74.
  2. Dallman MF, Warne JP, Foster MT, et al. Glucocorticoids and insulin both modulate caloric intake through actions on the brain. J Physiol. 2007; 583(Pt 2): 431–436.
  3. Hauner H, Schmid P, Pfeiffer EF. Glucocorticoids and insulin promote the differentiation of human adipocyte precursor cells into fat cells. J Clin Endocrinol Metab. 1987; 64(4): 832–835.
  4. Lee MJ, Pramyothin P, Karastergiou K, et al. Deconstructing the roles of glucocorticoids in adipose tissue biology and the development of central obesity. Biochim Biophys Acta. 2014; 1842(3): 473–481.
  5. Valassi E, Biller BMK, Klibanski A, et al. Adipokines and cardiovascular risk in Cushing's syndrome. Neuroendocrinology. 2012; 95(3): 187–206.
  6. Hochberg I, Harvey I, Tran QT, et al. Gene expression changes in subcutaneous adipose tissue due to Cushing's disease. J Mol Endocrinol. 2015; 55(2): 81–94.
  7. Umemura S, Nyui N, Tamura K, et al. Plasma angiotensinogen concentrations in obese patients. Am J Hypertens. 1997; 10(6): 629–633.
  8. van Harmelen V, Elizalde M, Ariapart P, et al. The association of human adipose angiotensinogen gene expression with abdominal fat distribution in obesity. Int J Obes Relat Metab Disord. 2000; 24(6): 673–678.
  9. Lijnen HR. Angiogenesis and obesity. Cardiovasc Res. 2008; 78(2): 286–293.
  10. Cao Y. Adipose tissue angiogenesis as a therapeutic target for obesity and metabolic diseases. Nat Rev Drug Discov. 2010; 9(2): 107–115.
  11. Vincent F, Bonnin P, Clemessy M, et al. Angiotensinogen delays angiogenesis and tumor growth of hepatocarcinoma in transgenic mice. Cancer Res. 2009; 69(7): 2853–2860.
  12. Corvol P, Lamandé N, Cruz A, et al. Inhibition of angiogenesis: a new function for angiotensinogen and des(angiotensin I)angiotensinogen. Curr Hypertens Rep. 2003; 5(2): 149–154.
  13. Coppack SW. Pro-inflammatory cytokines and adipose tissue. Proc Nutr Soc. 2001; 60(3): 349–356.
  14. Barahona MJ, Sucunza N, Resmini E, et al. Persistent body fat mass and inflammatory marker increases after long-term cure of Cushing's syndrome. J Clin Endocrinol Metab. 2009; 94(9): 3365–3371.
  15. Papanicolaou DA, Tsigos C, Oldfield EH, et al. Acute glucocorticoid deficiency is associated with plasma elevations of interleukin-6: does the latter participate in the symptomatology of the steroid withdrawal syndrome and adrenal insufficiency? J Clin Endocrinol Metab. 1996; 81(6): 2303–2306.
  16. Górska R, Gregorek H, Kowalski J, et al. Relationship between clinical parameters and cytokine profiles in inflamed gingival tissue and serum samples from patients with chronic periodontitis. J Clin Periodontol. 2003; 30(12): 1046–1052.
  17. Fried SK, Bunkin DA, Greenberg AS. Omental and subcutaneous adipose tissues of obese subjects release interleukin-6: depot difference and regulation by glucocorticoid. J Clin Endocrinol Metab. 1998; 83(3): 847–850.
  18. Hoppmann J, Perwitz N, Meier B, et al. The balance between gluco- and mineralo-corticoid action critically determines inflammatory adipocyte responses. J Endocrinol. 2010; 204(2): 153–164.
  19. Erem C, Nuhoglu I, Yilmaz M, et al. Blood coagulation and fibrinolysis in patients with Cushing's syndrome: increased plasminogen activator inhibitor-1, decreased tissue factor pathway inhibitor, and unchanged thrombin-activatable fibrinolysis inhibitor levels. J Endocrinol Invest. 2009; 32(2): 169–174.
  20. Patrassi GM, Sartori MT, Viero ML, et al. The fibrinolytic potential in patients with Cushing's disease: a clue to their hypercoagulable state. Blood Coagul Fibrinolysis. 1992; 3(6): 789–793.
  21. Fatti LM, Bottasso B, Invitti C, et al. Markers of activation of coagulation and fibrinolysis in patients with Cushing's syndrome. J Endocrinol Invest. 2000; 23(3): 145–150.
  22. Moraes-Vieira PM, Yore MM, Dwyer PM, et al. RBP4 activates antigen-presenting cells, leading to adipose tissue inflammation and systemic insulin resistance. Cell Metab. 2014; 19(3): 512–526.
  23. Lee MJ, Gong DW, Burkey BF, et al. Pathways regulated by glucocorticoids in omental and subcutaneous human adipose tissues: a microarray study. Am J Physiol Endocrinol Metab. 2011; 300(3): E571–E580.
  24. Fallo F, Scarda A, Sonino N, et al. Effect of glucocorticoids on adiponectin: a study in healthy subjects and in Cushing's syndrome. Eur J Endocrinol. 2004; 150(3): 339–344.
  25. Libè R, Morpurgo PS, Cappiello V, et al. Ghrelin and adiponectin in patients with Cushing's disease before and after successful transsphenoidal surgery. Clin Endocrinol (Oxf). 2005; 62(1): 30–36.
  26. Krsek M, Silha JV, Jezková J, et al. Adipokine levels in Cushing's syndrome; elevated resistin levels in female patients with Cushing's syndrome. Clin Endocrinol (Oxf). 2004; 60(3): 350–357.
  27. Klaasen R, Herenius MMJ, Wijbrandts CA, et al. Treatment-specific changes in circulating adipocytokines: a comparison between tumour necrosis factor blockade and glucocorticoid treatment for rheumatoid arthritis. Ann Rheum Dis. 2012; 71(9): 1510–1516.
  28. Fried SK, Russell CD, Grauso NL, et al. Lipoprotein lipase regulation by insulin and glucocorticoid in subcutaneous and omental adipose tissues of obese women and men. J Clin Invest. 1993; 92(5): 2191–2198.
  29. Russell CD, Petersen RN, Rao SP, et al. Leptin expression in adipose tissue from obese humans: depot-specific regulation by insulin and dexamethasone. Am J Physiol. 1998; 275(3 Pt 1): E507–E515.
  30. Kola B, Christ-Crain M, Lolli F, et al. Changes in adenosine 5'-monophosphate-activated protein kinase as a mechanism of visceral obesity in Cushing's syndrome. J Clin Endocrinol Metab. 2008; 93(12): 4969–4973.
  31. Bujalska IJ, Kumar S, Stewart PM. Does central obesity reflect "Cushing's disease of the omentum"? Lancet. 1997; 349(9060): 1210–1213.

Important: This website uses cookies. More >>

The cookies allow us to identify your computer and find out details about your last visit. They remembering whether you've visited the site before, so that you remain logged in - or to help us work out how many new website visitors we get each month. Most internet browsers accept cookies automatically, but you can change the settings of your browser to erase cookies or prevent automatic acceptance if you prefer.

Via MedicaWydawcą serwisu jest  "Via Medica sp. z o.o." sp.k., ul. Świętokrzyska 73, 80–180 Gdańsk

tel.:+48 58 320 94 94, faks:+48 58 320 94 60, e-mail:  viamedica@viamedica.pl