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      Correlation of Serum Vaspin, Omentin-1, and adiponectin with metabolic phenotypes in Type-2 diabetes mellitus patients

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          Abstract

          Objectives:

          To investigate adipocytokines’ (vaspin, omentin-1, and adiponectin) correlation with metabolic phenotypes in type 2 diabetes mellitus (T2DM) patients.

          Methods:

          This case-control research was done at the Diabetic Clinic in Jeddah, Kingdom of Saudi Arabia (KSA), from November 2018 to March 2019. Seventy-five T2DM patients and 75 gender, age, and BMI-matched healthy subjects were recruited for this research.

          Results:

          In DM patients, the concentrations of serum vaspin and omentin-1 were substantially lower (p<0.001) than in the control group. A significant positive relationship between vaspin concentration and DBP (p<0.001), BMI (p<0.001), and waist circumference (p<0.001) was found in patients and control subjects, while FPG (p<0.016), serum insulin (p<0.001), HOMA-IR (p<0.001), TC (p<0.001), TG (p<0.001), and LDLc (p<0.001) were significantly interrelated among patients. Serum concentrations of omentin-1 and ADN were significantly negatively correlated with serum insulin, HOMA-IR, and TG among the DM group. Serum vaspin and ADN levels were significantly higher in the cases and control groups with BMI>25, and no gender-wise variance was observed in adipocytokines levels. Binary logistic regression analysis showed a significantly negative predictive relationship of vaspin and omentin-1 with DM.

          Conclusion:

          The DM group displayed substantially lower serum vaspin and omentin-1 levels. However, there was no consistent relationship observed between these adipocytokines and metabolic phenotypes.

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          Most cited references30

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          Homeostasis model assessment: insulin resistance and beta-cell function from fasting plasma glucose and insulin concentrations in man.

          The steady-state basal plasma glucose and insulin concentrations are determined by their interaction in a feedback loop. A computer-solved model has been used to predict the homeostatic concentrations which arise from varying degrees beta-cell deficiency and insulin resistance. Comparison of a patient's fasting values with the model's predictions allows a quantitative assessment of the contributions of insulin resistance and deficient beta-cell function to the fasting hyperglycaemia (homeostasis model assessment, HOMA). The accuracy and precision of the estimate have been determined by comparison with independent measures of insulin resistance and beta-cell function using hyperglycaemic and euglycaemic clamps and an intravenous glucose tolerance test. The estimate of insulin resistance obtained by homeostasis model assessment correlated with estimates obtained by use of the euglycaemic clamp (Rs = 0.88, p less than 0.0001), the fasting insulin concentration (Rs = 0.81, p less than 0.0001), and the hyperglycaemic clamp, (Rs = 0.69, p less than 0.01). There was no correlation with any aspect of insulin-receptor binding. The estimate of deficient beta-cell function obtained by homeostasis model assessment correlated with that derived using the hyperglycaemic clamp (Rs = 0.61, p less than 0.01) and with the estimate from the intravenous glucose tolerance test (Rs = 0.64, p less than 0.05). The low precision of the estimates from the model (coefficients of variation: 31% for insulin resistance and 32% for beta-cell deficit) limits its use, but the correlation of the model's estimates with patient data accords with the hypothesis that basal glucose and insulin interactions are largely determined by a simple feed back loop.
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            Serum vaspin concentrations in human obesity and type 2 diabetes.

            Vaspin was identified as an adipokine with insulin-sensitizing effects, which is predominantly secreted from visceral adipose tissue in a rat model of type 2 diabetes. We have recently shown that vaspin mRNA expression in adipose tissue is related to parameters of obesity and glucose metabolism. However, the regulation of vaspin serum concentrations in human obesity and type 2 diabetes is unknown. For the measurement of vaspin serum concentrations, we developed an enzyme-linked immunosorbent assay (ELISA). Using this ELISA, we assessed circulating vaspin in a cross-sectional study of 187 subjects with a wide range of obesity, body fat distribution, insulin sensitivity, and glucose tolerance and in 60 individuals with normal glucose tolerance (NGT), impaired glucose tolerance (IGT), or type 2 diabetes before and after a 4-week physical training program. Vaspin serum concentrations were significantly higher in female compared with male subjects. There was no difference in circulating vaspin between individuals with NGT and type 2 diabetes. In the normal glucose-tolerant group, circulating vaspin significantly correlated with BMI and insulin sensitivity. Moreover, physical training for 4 weeks resulted in significantly increased circulating vaspin levels. We found a sexual dimorphism in circulating vaspin. Elevated vaspin serum concentrations are associated with obesity and impaired insulin sensitivity, whereas type 2 diabetes seems to abrogate the correlation between increased circulating vaspin, higher body weight, and decreased insulin sensitivity. Low circulating vaspin correlates with a high fitness level, whereas physical training in untrained individuals causes increased vaspin serum concentrations.
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              The role of leptin/adiponectin ratio in metabolic syndrome and diabetes.

              The metabolic syndrome comprises a cluster of cardiometabolic risk factors, with insulin resistance and adiposity as its central features. Identifying individuals with metabolic syndrome is important due to its association with an increased risk of coronary heart disease and type 2 diabetes mellitus. Attention has focused on the visceral adipose tissue production of cytokines (adipokines) in metabolic syndrome and type 2 diabetes mellitus, as the levels of the anti-inflammatory adipokine adiponectin are decreased, while proinflammatory cytokines are elevated, creating a proinflammatory state associated with insulin resistance and endothelial dysfunction. In this review, we will give special attention to the role of the leptin/adiponectin ratio. We have previously demonstrated that in individuals with severe coronary artery disease, abdominal obesity was uniquely related to decreased plasma concentrations of adiponectin and increased leptin levels. Leptin/adiponectin imbalance was associated with increased waist circumference and a decreased vascular response to acetylcholine and increased vasoconstriction due to angiotensin II. Leptin and adiponectin have opposite effects on subclinical inflammation and insulin resistance. Leptin upregulates proinflammatory cytokines such as tumor necrosis factor-α and interleukin-6; these are associated with insulin resistance and type 2 diabetes mellitus. In contrast, adiponectin has anti-inflammatory properties and downregulates the expression and release of a number of proinflammatory immune mediators. Therefore, it appears that interactions between angiotensin II and leptin/adiponectin imbalance may be important mediators of the elevated risk of developing type 2 diabetes mellitus and cardiovascular diseases associated with abdominal obesity.
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                Author and article information

                Journal
                Pak J Med Sci
                Pak J Med Sci
                Pakistan Journal of Medical Sciences
                Professional Medical Publications (Pakistan )
                1682-024X
                1681-715X
                Nov-Dec 2021
                : 37
                : 7
                : 1762-1767
                Affiliations
                [1 ]Dr. Mukhtiar Baig, Ph.D. Department of Clinical Biochemistry, Faculty of Medicine, Rabigh, King Abdulaziz University, Jeddah, Saudi Arabia
                [2 ]Dr. Zohair J Gazzaz, Ph.D. Department of Internal Medicine, Faculty of Medicine, Rabigh, King Abdulaziz University, Jeddah, Saudi Arabia
                [3 ]Dr. Marwan A Bakarman, FFCM. Department of Family and Community Medicine, Faculty of Medicine, Rabigh, King Abdulaziz University, Jeddah, Saudi Arabia
                [4 ]Dr. Sami H Alzahrani, SBFM Department of Family Medicine, Faculty of Medicine, King Abdulaziz University, Jeddah, Saudi Arabia.
                Author notes
                Correspondence: Dr. Mukhtiar Baig Department of Clinical Biochemistry, Faculty of Medicine, Rabigh, King Abdulaziz University, Jeddah-22431, Saudi Arabia. E-mail: drmukhtiarbaig@ 123456yahoo.com
                Article
                PJMS-37-1762
                10.12669/pjms.37.7.4330
                8613014
                34912392
                b77a99ae-6873-4a47-b9f4-698c13e74436
                Copyright: © Pakistan Journal of Medical Sciences

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

                History
                : 24 February 2021
                : 29 May 2021
                : 15 June 2021
                Categories
                Original Article

                diabetes mellitus,adipokines,vaspin,omentin-1,adiponectin
                diabetes mellitus, adipokines, vaspin, omentin-1, adiponectin

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