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Response: Association of Vaspin with Metabolic Syndrome: The Pivotal Role of Insulin Resistance (Diabetes Metab J 2014;38:143-9)
Alireza Esteghamati, Sina Noshad, Mostafa Mousavizadeh, Ali Zandieh, Manouchehr Nakhjavani
Diabetes & Metabolism Journal 2014;38(3):242-243.
DOI: https://doi.org/10.4093/dmj.2014.38.3.242
Published online: June 17, 2014
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Endocrinology and Metabolism Research Center, Vali-Asr Hospital, Tehran University of Medical Sciences School of Medicine, Tehran, Iran.

Corresponding author: Alireza Esteghamati. Endocrinology and Metabolism Research Center, Vali-Asr Hospital, Tehran University of Medical Sciences School of Medicine, P.O. Box 13145-784, Tehran, Iran. esteghamati@tums.ac.ir

Copyright © 2014 Korean Diabetes Association

This is an Open Access article distributed under the terms of the Creative Commons Attribution Non-Commercial License (http://creativecommons.org/licenses/by-nc/3.0/) which permits unrestricted non-commercial use, distribution, and reproduction in any medium, provided the original work is properly cited.

We read with interest Dr.Choi's comments on our article titled "Association of Vaspin with Metabolic Syndrome: The Pivotal Role of Insulin Resistance" published in Diabetes & Metabolism Journal [1].
Vaspin is a novel adipokine linking adipocytes and components of metabolic syndrome, although the exact role of vaspin remains unclear [2,3]. In our study, we found that central obesity, raised triglyceride, and raised fasting blood glucose are linked to higher vaspin concentrations; meanwhile, the relationship abolished after controlling for homeostasis model assessment of insulin resistance and high sensitivity C-reactive protein revealing the leading role of insulin resistance and chronic inflammation in this regard.
Choi et al.'s reported a significant relationship between vaspin concentrations and metabolic syndrome component including obesity and raised triglyceride. However, they did not find any connection between raised fasting plasma glucose and vaspin, which is evident in our series of patients. Discrepancies observed between the two studies likely reflect the differences in glycemic status of the patients enrolled. Choi et al. included patients from a routine health examination center (Seoul National University Bundang Hospital, Seoul, Korea) whereas our sample comprised patients visited at a diabetes clinic of a teaching hospital (Valiasr Hospital, Tehran, Iran). The proportion of patients with diabetes in the Korean sample was low (16.0%). In our sample a significantly larger proportion of patients were diagnosed with type 2 diabetes (59.3%) and another 9.7% had impaired fasting glucose. We suggest the more prominent association observed between insulin resistance/chronic inflammation and vaspin is due to prolonged hyperglycemia and insulin insensitivity.
It is hypothesized that the principal event for the development of metabolic syndrome is the deposition of fat in adipose tissue, liver, muscles, and pancreas in the face of impaired triglyceride/cholesterol metabolism and central obesity. This process in turn triggers the development of insulin resistance through various pathways including oxidative stress and chronic inflammation which, in a proportion of patients, lead to type 2 diabetes mellitus [4,5]. Chronic inflammation in turn could impair insulin signaling pathways in liver and other organs [6]. Vaspin is an adipocytokine involved in early as well as late stages of metabolic syndrome. In this view, results of the present study complement Choi et al. findings by showing the unflagging contribution of vaspin to the pathogenesis of metabolic syndrome. Further investigating the mechanisms by which vaspin promotes metabolic syndrome and resultant atherosclerosis is a focus of future research. The authors would like to thank Dr.Choi for thoughtful comments which put the findings of our study in perspective and postulate possible hypotheses for future research.

No potential conflict of interest relevant to this article was reported.

  • 1. Esteghamati A, Noshad S, Mousavizadeh M, Zandieh A, Nakhjavani M. Association of vaspin with metabolic syndrome: the pivotal role of insulin resistance. Diabetes Metab J 2014;38:143-149. ArticlePubMedPMC
  • 2. Auguet T, Quintero Y, Riesco D, Morancho B, Terra X, Crescenti A, Broch M, Aguilar C, Olona M, Porras JA, Hernandez M, Sabench F, del Castillo D, Richart C. New adipokines vaspin and omentin. Circulating levels and gene expression in adipose tissue from morbidly obese women. BMC Med Genet 2011;12:60ArticlePubMedPMCPDF
  • 3. Youn BS, Kloting N, Kratzsch J, Lee N, Park JW, Song ES, Ruschke K, Oberbach A, Fasshauer M, Stumvoll M, Bluher M. Serum vaspin concentrations in human obesity and type 2 diabetes. Diabetes 2008;57:372-377. ArticlePubMedPDF
  • 4. Sattar N, Scherbakova O, Ford I, O'Reilly DS, Stanley A, Forrest E, Macfarlane PW, Packard CJ, Cobbe SM, Shepherd J. west of Scotland coronary prevention study. Elevated alanine aminotransferase predicts new-onset type 2 diabetes independently of classical risk factors, metabolic syndrome, and C-reactive protein in the west of Scotland coronary prevention study. Diabetes 2004;53:2855-2860. ArticlePubMedPDF
  • 5. Kerner A, Avizohar O, Sella R, Bartha P, Zinder O, Markiewicz W, Levy Y, Brook GJ, Aronson D. Association between elevated liver enzymes and C-reactive protein: possible hepatic contribution to systemic inflammation in the metabolic syndrome. Arterioscler Thromb Vasc Biol 2005;25:193-197. PubMed
  • 6. Vozarova B, Stefan N, Lindsay RS, Saremi A, Pratley RE, Bogardus C, Tataranni PA. High alanine aminotransferase is associated with decreased hepatic insulin sensitivity and predicts the development of type 2 diabetes. Diabetes 2002;51:1889-1895. ArticlePubMedPDF

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