open access

Vol 89, No 4 (2018)
Review paper
Published online: 2018-04-30
Get Citation

The role of new adipokines in gestational diabetes mellitus pathogenesis

Radzisław Mierzyński1, Elżbieta Poniedziałek-Czajkowska1, Dominik Dłuski1, Bożena Leszczyńska-Gorzelak1
·
Pubmed: 29781079
·
Ginekol Pol 2018;89(4):222-227.
Affiliations
  1. Chair and Department of Obstetrics and Perinatology, Medical University of Lublin, Poland, Jaczewskiego 8, 20-954 Lublin, Poland

open access

Vol 89, No 4 (2018)
REVIEW PAPERS Obstetrics
Published online: 2018-04-30

Abstract

Gestational diabetes mellitus (GDM) is defined as any degree of glucose intolerance with onset or first recognition dur­ing pregnancy. Explanation of the GDM pathogenesis is important due to preventing gestational complications. During pregnancy there are significant changes in maternal metabolism. Many of these changes are influenced by different adi­pokines produced in the placenta and adipose tissue. The exact role of adipokines in the pathogenesis of GDM remains still unknown. Several adipokines have been analysed throughout gestation and their levels have been suggested as biomarkers of maternal–perinatal outcomes. Some of them have been postulated as significant in the pathogenesis of pregnancy complications like GDM. This report aims to review some of the recent topics of adipokine research that may be of particular importance in patho­physiology and diagnosis of gestational diabetes mellitus. Because of manuscript length limitations, after thorough literature review and in view of the recent evidence, we focus on the one of the most well-known adipokine: adiponectin, and not so well-studied: nesfatin-1, chemerin, ghrelin, and CTRP 1.

Abstract

Gestational diabetes mellitus (GDM) is defined as any degree of glucose intolerance with onset or first recognition dur­ing pregnancy. Explanation of the GDM pathogenesis is important due to preventing gestational complications. During pregnancy there are significant changes in maternal metabolism. Many of these changes are influenced by different adi­pokines produced in the placenta and adipose tissue. The exact role of adipokines in the pathogenesis of GDM remains still unknown. Several adipokines have been analysed throughout gestation and their levels have been suggested as biomarkers of maternal–perinatal outcomes. Some of them have been postulated as significant in the pathogenesis of pregnancy complications like GDM. This report aims to review some of the recent topics of adipokine research that may be of particular importance in patho­physiology and diagnosis of gestational diabetes mellitus. Because of manuscript length limitations, after thorough literature review and in view of the recent evidence, we focus on the one of the most well-known adipokine: adiponectin, and not so well-studied: nesfatin-1, chemerin, ghrelin, and CTRP 1.

Get Citation

Keywords

gestational diabetes mellitus, adiponectin, nesfatin-1, chemerin, ghrelin, CTRP 1

About this article
Title

The role of new adipokines in gestational diabetes mellitus pathogenesis

Journal

Ginekologia Polska

Issue

Vol 89, No 4 (2018)

Article type

Review paper

Pages

222-227

Published online

2018-04-30

Page views

2626

Article views/downloads

2114

DOI

10.5603/GP.a2018.0038

Pubmed

29781079

Bibliographic record

Ginekol Pol 2018;89(4):222-227.

Keywords

gestational diabetes mellitus
adiponectin
nesfatin-1
chemerin
ghrelin
CTRP 1

Authors

Radzisław Mierzyński
Elżbieta Poniedziałek-Czajkowska
Dominik Dłuski
Bożena Leszczyńska-Gorzelak

References (37)
  1. Gestational Diabetes Mellitus. Diabetes Care. 2003; 26(Supplement 1): S103–S105.
  2. Miehle K, Stepan H, Fasshauer M. Leptin, adiponectin and other adipokines in gestational diabetes mellitus and pre-eclampsia. Clin Endocrinol (Oxf). 2012; 76(1): 2–11.
  3. Lappas M, Yee K, Permezel M, et al. Release and regulation of leptin, resistin and adiponectin from human placenta, fetal membranes, and maternal adipose tissue and skeletal muscle from normal and gestational diabetes mellitus-complicated pregnancies. J Endocrinol. 2005; 186(3): 457–465.
  4. Cawthorn WP, Scheller EL, Learman BS, et al. Bone marrow adipose tissue is an endocrine organ that contributes to increased circulating adiponectin during caloric restriction. Cell Metab. 2014; 20(2): 368–375.
  5. Rasouli N, Kern P. Adipocytokines and the metabolic complications of obesity. J Clin Endorinol Metab. 2008; 93(11_supplement_1): s64–s73.
  6. Mazaki-Tovi S, Kanety H, Pariente C, et al. Maternal serum adiponectin levels during human pregnancy. J Perinatol. 2007; 27(2): 77–81.
  7. Cseh K, Baranyi E, Melczer Z, et al. Plasma adiponectin and pregnancy-induced insulin resistance. Diabetes Care. 2004; 27(1): 274–275.
  8. Cortelazzi D, Corbetta S, Ronzoni S, et al. Maternal and foetal resistin and adiponectin concentrations in normal and complicated pregnancies. Clin Endocrinol (Oxf). 2007; 66(3): 447–453.
  9. Bao W, Baecker A, Song Y, et al. Adipokine levels during the first or early second trimester of pregnancy and subsequent risk of gestational diabetes mellitus: A systematic review. Metabolism. 2015; 64(6): 756–764.
  10. Retnakaran R, Zinman B, Connelly PW, et al. Reduced adiponectin concentration in women with gestational diabetes: a potential factor in progression to type 2 diabetes. Diabetes Care. 2004; 27(3): 799–800.
  11. Foo KS, Brismar H, Broberger C. Distribution and neuropeptide coexistence of nucleobindin-2 mRNA/nesfatin-like immunoreactivity in the rat CNS. Neuroscience. 2008; 156(3): 563–579.
  12. Li QC, Wang HY, Chen Xi, et al. Fasting plasma levels of nesfatin-1 in patients with type 1 and type 2 diabetes mellitus and the nutrient-related fluctuation of nesfatin-1 level in normal humans. Regul Pept. 2010; 159(1-3): 72–77.
  13. Aslan M, Celik O, Celik N, et al. Cord blood nesfatin-1 and apelin-36 levels in gestational diabetes mellitus. Endocrine. 2011; 41(3): 424–429.
  14. Kucukler FK, Gorkem U, Simsek Y, et al. Gynecol Endocrinol. Low level of Nesfatin-1 is associated with gestational diabetes mellitus. 2016; 6: 1–3.
  15. Su Y, Zhang J, Tang Y, et al. The novel function of nesfatin-1: anti-hyperglycemia. Biochem Biophys Res Commun. 2010; 391(1): 1039–1042.
  16. Roman AA, Parlee SD, Sinal CJ. Chemerin: a potential endocrine link between obesity and type 2 diabetes. Endocrine. 2012; 42(2): 243–251.
  17. Fatima S, Alam F, Chaudhry B, et al. Elevated levels of chemerin, leptin, and interleukin-18 in gestational diabetes mellitus. The Journal of Maternal-Fetal & Neonatal Medicine. 2016; 30(9): 1023–1028.
  18. Li XM, Ji H, Li CJ, et al. Chemerin expression in Chinese pregnant women with and without gestational diabetes mellitus. Ann Endocrinol (Paris). 2015; 76(1): 19–24.
  19. Van Poppel MNM, Zeck W, Ulrich D, et al. Cord blood chemerin: differential effects of gestational diabetes mellitus and maternal obesity. Clin Endocrinol (Oxf). 2014; 80(1): 65–72.
  20. Pfau D, Stepan H, Kratzsch J, et al. Circulating levels of the adipokine chemerin in gestational diabetes mellitus. Horm Res Paediatr. 2010; 74(1): 56–61.
  21. Ademoglu E, Berberoglu Z, Dellal FD, et al. Higher Levels of Circulating Chemerin in Obese Women with Gestational Diabetes Mellitus. Acta Endocrinologica (Bucharest). 2015; 11(1): 32–38.
  22. Barker G, Lim R, Rice GE, et al. Increased chemerin concentrations in fetuses of obese mothers and correlation with maternal insulin sensitivity. J Matern Fetal Neonatal Med. 2012; 25(11): 2274–2280.
  23. Lehrke M, Becker A, Greif M, et al. Chemerin is associated with markers of inflammation and components of the metabolic syndrome but does not predict coronary atherosclerosis. Eur J Endocrinol. 2009; 161(2): 339–344.
  24. Pradhan G, Samson SL, Sun Y. Ghrelin: much more than a hunger hormone. Curr Opin Clin Nutr Metab Care. 2013; 16(6): 619–624.
  25. Patel AD, Stanley SA, Murphy KG, et al. Ghrelin stimulates insulin-induced glucose uptake in adipocytes. Regul Pept. 2006; 134(1): 17–22.
  26. Baykus Y, Gurates B, Aydin S, et al. Changes in serum obestatin, preptin and ghrelins in patients with Gestational Diabetes Mellitus. Clin Biochem. 2012; 45(3): 198–202.
  27. Aydin S, Geckil H, Karatas F, et al. Milk and blood ghrelin level in diabetics. Nutrition. 2007; 23(11-12): 807–811.
  28. Gómez-Díaz RA, Gómez-Medina MP, Ramírez-Soriano E, et al. Lower plasma ghrelin levels are found in women with diabetes-complicated pregnancies. J Clin Res Pediatr Endocrinol. 2016; 8(4): 425–431.
  29. Riedl M, Maier C, Handisurya A, et al. Insulin resistance has no impact on ghrelin suppression in pregnancy. J Intern Med. 2007; 262(4): 458–465.
  30. Karakulak M, Saygili U, Temur M, et al. Comparison of umbilical cord ghrelin concentrations in full-term pregnant women with or without gestational diabetes. Endocr Res. 2017; 42(2): 79–85.
  31. Lappas M, Jinks D, Ugoni A, et al. Post-partum plasma C-peptide and ghrelin concentrations are predictive of type 2 diabetes in women with previous gestational diabetes mellitus. J Diabetes. 2015; 7(4): 506–511.
  32. Seldin MM, Peterson JM, Byerly MS, et al. Myonectin (CTRP15), a novel myokine that links skeletal muscle to systemic lipid homeostasis. J Biol Chem. 2012; 287(15): 11968–11980.
  33. Kim Ky, Kim HY, Kim JH, et al. Tumor necrosis factor-alpha and interleukin-1beta increases CTRP1 expression in adipose tissue. FEBS Lett. 2006; 580(16): 3953–3960.
  34. Pan X, Lu T, Wu F, et al. Circulating complement-C1q TNF-related protein 1 levels are increased in patients with type 2 diabetes and are associated with insulin sensitivity in Chinese subjects. PLoS One. 2014; 9(5): e94478.
  35. Chalupova L, Zakovska A, Adamcova K. Development of a novel enzyme-linked immunosorbent assay (ELISA) for measurement of serum CTRP1: a pilot study: measurement of serum CTRP1 in healthy donors and patients with metabolic syndrome. Clin Biochem. 2013; 46(1-2): 73–78.
  36. Xin Y, Lyu X, Wang C, et al. Elevated circulating levels of CTRP1, a novel adipokine, in diabetic patients. Endocr J. 2014; 61(9): 841–847.
  37. Han S, Kim JD, Lee S, et al. Circulating CTRP1 Levels in Type 2 Diabetes and Their Association with FGF21. Int J Endocrinol. 2016.

Regulations

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.

By VM Media Group sp. z o.o., ul. Świętokrzyska 73, 80–180 Gdańsk
tel.:+48 58 320 94 94, faks:+48 58 320 94 60, e-mail:  viamedica@viamedica.pl