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      Relationship between serum levels of fetuin-A with apo-A1, apo-B100, body composition and insulin resistance in patients with type 2 diabetes

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          Abstract

          Background: Some results exist on fetuin-A as marker for vascular disease in type 2diabetes. We examined the relationship between serum fetuin-A with some factors, in patients with type 2 diabetes mellitus (T2DM).

          Methods: From October 2012 to June 2013, a total of 131 T2DM patients were recruited and evaluated for various parameters including HOMA-IR, Apo-A1, Apo-B100, body fat percentage and waist circumference. Serum fetuin-A levels were measured by enzyme-linkedimmunosorbent assay (ELISA), and Serum glucose with a Cobas MIRA analyzer by enzymatic method. Apo-B100 and apo-A1 were measured by immunoturbidimetry with a Cobas MIRA analyzer. HOMA-IR was calculated by the following formula: [fasting insulin (uIU/mL) × fasting blood glucose (mmol/L)]/22.5.

          Results: The mean levels of HOMA-IR were significantly increased progressively across fetuin-A tertiles (p for trend=0.04) in women but not men. Fetuin-A had just a significant positive correlation with Apo- A1(r=0.22, p=0.02).

          Conclusion: This present study showed that levels of serum fetuin-A are significantly associated with insulin resistance in women with T2DM.

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          Retinol-binding protein 4 and insulin resistance in lean, obese, and diabetic subjects.

          Timothy Graham, Qin Yang, Matthias Blüher … (2006)
          Insulin resistance has a causal role in type 2 diabetes. Serum levels of retinol-binding protein 4 (RBP4), a protein secreted by adipocytes, are increased in insulin-resistant states. Experiments in mice suggest that elevated RBP4 levels cause insulin resistance. We sought to determine whether serum RBP4 levels correlate with insulin resistance and change after an intervention that improves insulin sensitivity. We also determined whether elevated serum RBP4 levels are associated with reduced expression of glucose transporter 4 (GLUT4) in adipocytes, an early pathological feature of insulin resistance. We measured serum RBP4, insulin resistance, and components of the metabolic syndrome in three groups of subjects. Measurements were repeated after exercise training in one group. GLUT4 protein was measured in isolated adipocytes. Serum RBP4 levels correlated with the magnitude of insulin resistance in subjects with obesity, impaired glucose tolerance, or type 2 diabetes and in nonobese, nondiabetic subjects with a strong family history of type 2 diabetes. Elevated serum RBP4 was associated with components of the metabolic syndrome, including increased body-mass index, waist-to-hip ratio, serum triglyceride levels, and systolic blood pressure and decreased high-density lipoprotein cholesterol levels. Exercise training was associated with a reduction in serum RBP4 levels only in subjects in whom insulin resistance improved. Adipocyte GLUT4 protein and serum RBP4 levels were inversely correlated. RBP4 is an adipocyte-secreted molecule that is elevated in the serum before the development of frank diabetes and appears to identify insulin resistance and associated cardiovascular risk factors in subjects with varied clinical presentations. These findings provide a rationale for antidiabetic therapies aimed at lowering serum RBP4 levels. Copyright 2006 Massachusetts Medical Society.
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            Adiponectin and protection against type 2 diabetes mellitus.

            Joachim Spranger, Anja Kroke, Matthias Möhlig … (2003)
            Adiponectin is an adipocyte-derived peptide, which has anti-inflammatory and insulin-sensitising properties. We designed a nested case-control study to assess whether baseline adiponectin concentrations in plasma are independently associated with risk of type 2 diabetes. We found that adiponectin concentrations in plasma were lower among individuals who later developed type 2 diabetes than among controls (mean 5.34 microg/mL [SD 3.49] vs 6.87 microg/mL [4.58], p<0.0001). High concentrations of adiponectin were associated with a substantially reduced relative risk of type 2 diabetes after adjustment for age, sex, waist-to-hip ratio, body-mass index, smoking, exercise, alcohol consumption, education, and glycosylated haemoglobin A(1c) (odds ratio 4th vs 1st quartile 0.3 [95% CI 0.2-0.7], p=0.0051). We conclude that adiponectin is independently associated with a reduced risk of type 2 diabetes in apparently healthy individuals.
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              The serum protein alpha 2-Heremans-Schmid glycoprotein/fetuin-A is a systemically acting inhibitor of ectopic calcification.

              Cora Schäfer, Alexander Heiss, Anke Schwarz … (2003)
              Ectopic calcification is a frequent complication of many degenerative diseases. Here we identify the serum protein alpha2-Heremans-Schmid glycoprotein (Ahsg, also known as fetuin-A) as an important inhibitor of ectopic calcification acting on the systemic level. Ahsg-deficient mice are phenotypically normal, but develop severe calcification of various organs on a mineral and vitamin D-rich diet and on a normal diet when the deficiency is combined with a DBA/2 genetic background. This phenotype is not associated with apparent changes in calcium and phosphate homeostasis, but with a decreased inhibitory activity of the Ahsg-deficient extracellular fluid on mineral formation. The same underlying principle may contribute to many calcifying disorders including calciphylaxis, a syndrome of severe systemic calcification in patients with chronic renal failure. Taken together, our data demonstrate a critical role of Ahsg as an inhibitor of unwanted mineralization and provide a novel therapeutic concept to prevent ectopic calcification accompanying various diseases.
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                Author and article information

                Journal
                Journal ID (nlm-ta): Med J Islam Repub Iran
                Journal ID (iso-abbrev): Med J Islam Repub Iran
                Journal ID (publisher-id): MJIRI
                Journal ID (publisher-id): Med J Islam Repub Iran
                Title: Medical Journal of the Islamic Republic of Iran
                Publisher: Iran University of Medical Sciences
                ISSN (Print): 1016-1430
                ISSN (Electronic): 2251-6840
                Publication date Collection: 2014
                Publication date (Electronic): 20 September 2014
                Volume: 28
                Page: 100
                Affiliations
                1. PhD. Professor of Nutrition, Institute of Endocrinology and Metabolism Research and Training Center, Iran University of Medical Sciences, Tehran, Iran. shidfar.f@ 123456iums.ac.ir
                2. PhD, Institute of Endocrinology and Metabolism Research and Training Center, Iran University of Medical Sciences, Tehran, Iran. zarrati_ms@ 123456yahoo.com
                3. Professor of Endocrinology, Institute of Endocrinology and Metabolism Research and Training Center, Iran University of Medical Sciences, Tehran, Iran. khamseh.m@ 123456iums.ac.ir
                4. Master, Institute of Endocrinology and Metabolism Research and Training Center, Iran University of Medical Sciences, Tehran, Iran. neda.hag@ 123456gmail.com
                5. Master, Institute of Endocrinology and Metabolism Research and Training Center, Iran University of Medical Sciences, Tehran, Iran. ali.rostami.nut@ 123456gmail.com
                6. Master, Institute of Endocrinology and Metabolism Research and Training Center, Iran University of Medical Sciences, Tehran, Iran. h.z.7025@ 123456gmail.com
                Author notes
                (Corresponding author) Master, Institute of Endocrinology and Metabolism Research and Training Center, Iran University of Medical Sciences, Tehran, Iran. h.z.7025@ 123456gmail.com
                Article
                PMC ID: 4301224
                SO-VID: 347d84bc-f50d-4aa8-b724-96c11e29024d
                Copyright © © 2014 Iran University of Medical Sciences
                License:

                This is an open-access article distributed under the terms of the Creative Commons Attribution NonCommercial 3.0 License (CC BY-NC 3.0), which allows users to read, copy, distribute and make derivative works for non-commercial purposes from the material, as long as the author of the original work is cited properly.

                History
                Date received : 08 December 2013
                Date accepted : 01 February 2014
                Page count
                Tables: 5, References: 32, Pages: 7
                Categories
                Subject: Original Article

                Keywords: fetuin-a,apo-a1,apo-b100,body fat percentage,insulin resistance,type 2 diabetes
                Data availability:
                Keywords: fetuin-a, apo-a1, apo-b100, body fat percentage, insulin resistance, type 2 diabetes

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