Exp Clin Endocrinol Diabetes 2008; 116(1): 47-52
DOI: 10.1055/s-2007-990275
Article

© J. A. Barth Verlag in Georg Thieme Verlag KG Stuttgart · New York

Interfering Effects of Insulin, Growth Hormone and Glucose on Adipokine Secretion

B. Wölfing 1 , M. Neumeier 1 , C. Buechler 1 , C. Aslanidis 2 , J. Schölmerich 1 , A. Schäffler 1 , 2
  • 1Department of Internal Medicine I, Regensburg University Medical Center, Germany
  • 2Institute of Clinical Chemistry and Laboratory Medicine, Regensburg University Medical Center, Germany
Further Information

Publication History

received 12.06.2007 first decision 11.07.2007

accepted 23.08.2007

Publication Date:
31 October 2007 (online)

Abstract

Introduction: Cell culture media with high glucose concentration are normally used. Data on the secretion of the adipokines adiponectin and resistin from adipocytes in response to insulin and growth hormone (GH) both under normo- and hyperglycemic conditions are not available. It was the aim of the study to investigate the impact of standard metabolic conditions (normo-/hyperglycemia, normo-/hyperinsulinemia) and of GH on the secretion of adiponectin and resistin.

Material and Methods: 3T3-L1 preadipocytes were differentiated into adipocytes and then incubated under normoglycemia (100 mg/dl), hyperglycemia (450 mg/dl), in combination with insulin (0, 0.2, 2.0 nM) and/or GH (1 nM). Adiponectin and resistin secretion was measured by ELISA.

Results: Insulin significantly stimulates adiponectin and resistin secretion under normo- and hyperglycemia. Hyperglycemia per se stimulates adiponectin and resistin secretion both in the absence and presence of low or high insulin concentrations. GH stimulates adiponectin secretion both under normoglycemic and hyperglycemic conditions. Whereas insulin does not modulate GH-induced adiponectin secretion under normoglycemia, insulin augments adiponectin release under hyperglycemia. GH stimulates resistin secretion only under normoglycemia, but not under hyperglycemic conditions. Since scavenger receptor B-I expression did not change, these effects are specific and not caused by a simple enhancement of adipocyte differentiation.

Discussion: Glucose, insulin and growth hormone have significant and interfering effects on the secretion of resistin and adiponectin. Several of the well-known in vivo phenomena such as diurnal variation or effects of re-feeding and weight-loss might be explained by direct effects of these hormones on adipocytes. Finally, when effects of hormones on adipocyte function are investigated, it is a prerequisite to take glucose levels of the cell culture media into account.

References

  • 1 Whitehead JP. et al . Adiponectin - a key adipokine in the metabolic syndrome.  Diabetes Obes Metab. 2006;  8 264-280
  • 2 Okamoto Y. et al . Adiponectin: a key adipocytokine in metabolic syndrome.  Clin Sci (Lond). 2006;  110 267-278
  • 3 Vasseur F. Adiponectin and its receptors: partners contributing to the “vicious circle” leading to the metabolic syndrome?.  Pharmacol Res. 2006;  53 478-481
  • 4 Rea R, Donnelly R. Resistin: an adipocyte-derived hormone. Has it a role in diabetes and obesity?.  Diabetes Obes Metab. 2004;  6 163-170
  • 5 Pang SS, Le YY. Role of resistin in inflammation and inflammation-related diseases.  Cell Mol Immunol. 2006;  3 29-34
  • 6 Arner P. Resistin: yet another adipokine tells us that men are not mice.  Diabetologia. 2005;  48 2203-2205
  • 7 Green H, Kehinde O. An established preadipose cell line and its differentiation in culture. II. Factors affecting the adipose conversion.  Cell. 1975;  5 19-27
  • 8 Zaitsu H, Serrero G. Pedersen fetuin contains three adipogenic factors with distinct biochemical characteristics.  J Cell Physiol. 1990;  144 485-491
  • 9 Bachmeier M, Loffler G. Adipogenic activities in commercial preparations of fetuin.  Horm Metab Res. 1994;  26 92-96
  • 10 Green H, Kehinde O. Formation of normally differentiated subcutaneous fat pads by an established preadipose cell line.  J Cell Physiol. 1979;  101 169-171
  • 11 Green H, Meuth M. An established pre-adipose cell line and its differentiation in culture.  Cell. 1974;  3 127-133
  • 12 Cornelius P. et al . Regulation of adipocyte development.  Annu Rev Nutr. 1994;  14 99-129
  • 13 MacDougald OA, Lane MD. Transcriptional regulation of gene expression during adipocyte differentiation.  Annu Rev Biochem. 1995;  64 345-373
  • 14 Scherer PE. et al . A novel serum protein similar to C1q, produced exclusively in adipocytes.  J Biol Chem. 1995;  270 26746-26749
  • 15 Bogan JS, Lodish HF. Two compartments for insulin-stimulated exocytosis in 3T3-L1 adipocytes defined by endogenous ACRP30 and GLUT4.  J Cell Biol. 1999;  146 609-620
  • 16 Fasshauer M. et al . Hormonal regulation of adiponectin gene expression in 3T3-L1 adipocytes.  Biochem Biophys Res Commun. 2002;  290 1084-1089
  • 17 Richards AA. et al . Adiponectin multimerization is dependent on conserved lysines in the collagenous domain: evidence for regulation of multimerization by alterations in posttranslational modifications.  Mol Endocrinol. 2006;  20 1673-1687
  • 18 Gavrila A. et al . Diurnal and ultradian dynamics of serum adiponectin in healthy men: comparison with leptin, circulating soluble leptin receptor, and cortisol patterns.  J Clin Endocrinol Metab. 2003;  88 2838-2843
  • 19 Hotta K. et al . Plasma concentrations of a novel, adipose-specific protein, adiponectin, in type 2 diabetic patients.  Arterioscler Thromb Vasc Biol. 2000;  20 1595-1599
  • 20 Calvani M. et al . Restoration of adiponectin pulsatility in severely obese subjects after weight loss.  Diabetes. 2004;  53 939-947
  • 21 Xu A. et al . Chronic treatment with growth hormone stimulates adiponectin gene expression in 3T3-L1 adipocytes.  FEBS Lett. 2004;  572 129-134
  • 22 Shojima N. et al . Humoral regulation of resistin expression in 3T3-L1 and mouse adipose cells.  Diabetes. 2002;  51 1737-1744
  • 23 Haugen F. et al . Inhibition by insulin of resistin gene expression in 3T3-L1 adipocytes.  FEBS Lett. 2001;  507 105-108
  • 24 Kawashima J. et al . Insulin down-regulates resistin mRNA through the synthesis of protein(s) that could accelerate the degradation of resistin mRNA in 3T3-L1 adipocytes.  Diabetologia. 2003;  46 231-240
  • 25 Kim KH. et al . A cysteine-rich adipose tissue-specific secretory factor inhibits adipocyte differentiation.  J Biol Chem. 2001;  276 11252-11256
  • 26 Zhong Q. et al . Endothelin-1 inhibits resistin secretion in 3T3-L1 adipocytes.  Biochem Biophys Res Commun. 2002;  296 383-387
  • 27 Rajala MW. et al . Cell type-specific expression and coregulation of murine resistin and resistin-like molecule-alpha in adipose tissue.  Mol Endocrinol. 2002;  16 1920-1930
  • 28 Schaffler A. et al . Acute hyperglycaemia causes severe disturbances of mesenteric microcirculation in an in vivo rat model.  Eur J Clin Invest. 1998;  28 886-893
  • 29 Delhanty PJ. et al . Growth hormone rapidly induces resistin gene expression in white adipose tissue of spontaneous dwarf (SDR) rats.  Endocrinology. 2002;  143 2445-2244

Correspondence

A. SchäfflerMD 

Department of Internal Medicine I

University of Regensburg

93042 Regensburg

Germany

Phone: +49/941/944 70 09

Fax: +49/941/944 70 19

Email: andreas.schaeffler@klinik.uni-regensburg.de

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