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      Increased serum cystatin C levels and responses of pancreatic α- and β-cells in type 2 diabetes


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          Increased serum cystatin C (CysC) can predict the onset of type 2 diabetes (T2D). Meanwhile, impaired pancreatic α- and β-cell functions get involved in the pathophysiological processes of T2D. So this study was to explore the relationships between serum CysC levels and pancreatic α- and β-cell functions in T2D.


          In this cross-sectional observational study, a total of 2634 patients with T2D were consecutively recruited. Each recruited patient received a serum CysC test and oral glucose tolerance test for synchronous detection of serum C-peptide and plasma glucagon. As components of pancreatic β-cell function, insulin secretion and sensitivity indices were evaluated by C-peptide area under the curve (AUC-CP) and C-peptide-substituted Matsuda’s index (Matsuda-CP), respectively. Fasting glucagon (F-GLA) and post-challenge glucagon calculated by glucagon area under the curve (AUC-GLA) were used to assess pancreatic α-cell function. These skewed indices and were further natural log-transformed (ln).


          With quartiles of serum CysC levels ascending, AUC-CP, F-GLA and AUC-GLA were increased, while Matsuda-CP was decreased ( P for trend <0.001). Moreover, serum CysC levels were positively related to lnAUC-CP, lnF-GLA and lnAUC-GLA ( r= 0.241, 0.131 and 0.208, respectively, P < 0.001), and inversely related to lnMatsuda-CP ( r= –0.195, P  < 0.001). Furthermore, after controlling for other relevant variables via multivariable linear regression analysis, serum CysC levels were identified to account for lnAUC-CP ( β= 0.178, t= 10.518, P  < 0.001), lnMatsuda-CP ( β= –0.137, t= –7.118, P  < 0.001), lnF-GLA ( β= 0.049, t= 2.263, P = 0.024) and lnAUC-GLA ( β= 0.121, t= 5.730, P  < 0.001).


          Increased serum CysC levels may be partly responsible for increased insulin secretion from β-cells, decreased systemic insulin sensitivity, and elevated fasting and postprandial glucagon secretion from α-cells in T2D.

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          Most cited references54

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          Glomerular filtration rate (GFR) estimates facilitate detection of chronic kidney disease but require calibration of the serum creatinine assay to the laboratory that developed the equation. The 4-variable equation from the Modification of Diet in Renal Disease (MDRD) Study has been reexpressed for use with a standardized assay. To describe the performance of the revised 4-variable MDRD Study equation and compare it with the performance of the 6-variable MDRD Study and Cockcroft-Gault equations. Comparison of estimated and measured GFR. 15 clinical centers participating in a randomized, controlled trial. 1628 patients with chronic kidney disease participating in the MDRD Study. Serum creatinine levels were calibrated to an assay traceable to isotope-dilution mass spectrometry. Glomerular filtration rate was measured as urinary clearance of 125I-iothalamate. Mean measured GFR was 39.8 mL/min per 1.73 m2 (SD, 21.2). Accuracy and precision of the revised 4-variable equation were similar to those of the original 6-variable equation and better than in the Cockcroft-Gault equation, even when the latter was corrected for bias, with 90%, 91%, 60%, and 83% of estimates within 30% of measured GFR, respectively. Differences between measured and estimated GFR were greater for all equations when the estimated GFR was 60 mL/min per 1.73 m2 or greater. The MDRD Study included few patients with a GFR greater than 90 mL/min per 1.73 m2. Equations were not compared in a separate study sample. The 4-variable MDRD Study equation provides reasonably accurate GFR estimates in patients with chronic kidney disease and a measured GFR of less than 90 mL/min per 1.73 m2. By using the reexpressed MDRD Study equation with the standardized serum creatinine assay, clinical laboratories can report more accurate GFR estimates.
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                Author and article information

                Endocr Connect
                Endocr Connect
                Endocrine Connections
                Bioscientifica Ltd (Bristol )
                18 February 2022
                01 March 2022
                : 11
                : 3
                : e210597
                [1 ]Department of Endocrinology , Affiliated Hospital 2 of Nantong University, and First People’s Hospital of Nantong City, Nantong, China
                [2 ]Department of Clinical Laboratory , Affiliated Hospital 2 of Nantong University, and First People’s Hospital of Nantong City, Nantong, China
                [3 ]Medical Research Center , Affiliated Hospital 2 of Nantong University, and First People’s Hospital of Nantong City, Nantong, China
                Author notes
                Correspondence should be addressed to J Su or D Zhang: sujbzjx@ 123456163.com or zdm_ntyy@ 123456163.com

                *(H Yuan and J Miao contributed equally to this work)

                Author information
                © The authors

                This work is licensed under a Creative Commons Attribution-NonCommercial-NoDerivatives 4.0 International License.

                : 03 February 2022
                : 18 February 2022

                cystatin c,c-peptide,glucagon,type 2 diabetes
                cystatin c, c-peptide, glucagon, type 2 diabetes


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