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      Analysis of Postprandial Glycemia in Relation to Metabolic Compensation and Other Observed Parameters of Outpatients with Type 2 Diabetes Mellitus in the Czech Republic

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          Abstract

          Introduction

          The goal of the study was to determine the level of metabolic compensation expressed by glycosylated hemoglobin, fasting plasma glucose, and postprandial glucose as determined after a standardized breakfast; further, to evaluate interrelationships between the studied parameters and postprandial glucose levels.

          Methods

          The study included 1055 patients with type 2 diabetes mellitus. Their fasting plasma glucose and postprandial glucose were measured before and after a standardized breakfast. Attending diabetologists completed a uniform questionnaire that included demographic data, type of antidiabetic treatment, duration of diabetes, latest glycosylated hemoglobin value, presence of dyslipidemia, and organic complications.

          Results

          Glycosylated hemoglobin < 53 mmol/mol was achieved in 363 (34.2%), postprandial glucose < 7.5 mmol/l in 211 (19.9%), and fasting plasma glucose < 6 mmol/l in 251 (23.7%) patients. Excellent metabolic compensation, indicated by all the above mentioned glycosylated hemoglobin, fasting plasma glucose, and postprandial glucose values simultaneously, was achieved in only 71 (6.7%) patients. Comparable to fasting plasma glucose and postprandial glucose values, correlation with glycosylated hemoglobin levels is statistically significant; however, there is no difference at different glycosylated hemoglobin levels. There was a significant correlation between dyslipidemia and postprandial glycemia ( p = 0.013).

          Conclusion

          The objective of care for patients with diabetes mellitus is to improve their long-term metabolic compensation; to that end, both fasting plasma glucose and postprandial glucose deserve equal attention.

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          Most cited references29

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          Glucose tolerance and cardiovascular mortality: comparison of fasting and 2-hour diagnostic criteria.

          (2001)
          New diagnostic criteria for diabetes based on fasting blood glucose (FBG) level were approved by the American Diabetes Association. The impact of using FBG only has not been evaluated thoroughly. The fasting and the 2-hour glucose (2h-BG) criteria were compared with regard to the prediction of mortality. Existing baseline data on glucose level at fasting and 2 hours after a 75-g oral glucose tolerance test from 10 prospective European cohort studies including 15 388 men and 7126 women aged 30 to 89 years, with a median follow-up of 8.8 years, were analyzed. Hazards ratios for death from all causes, cardiovascular disease, coronary heart disease, and stroke were estimated. Multivariate Cox regression analyses showed that the inclusion of FBG did not add significant information on the prediction of 2h-BG alone (P>.10 for various causes), whereas the addition of 2h-BG to FBG criteria significantly improved the prediction (P<.001 for all causes and P<.005 for cardiovascular disease). In a model including FBG and 2h-BG simultaneously, hazards ratios (95% confidence intervals) in subjects with diabetes on 2h-BG were 1.73 (1.45-2.06) for all causes, 1.40 (1.02-1.92) for cardiovascular disease, 1.56 (1.03-2.36) for coronary heart disease, and 1.29 (0.66-2.54) for stroke mortality, compared with the normal 2h-BG group. Compared with the normal FBG group, the corresponding hazards ratios in subjects with diabetes on FBG were 1.21 (1.01-1.44), 1.20 (0.88-1.64), 1.09 (0.71-1.67), and 1.64 (0.88-3.07), respectively. The largest number of excess deaths was observed in subjects who had impaired glucose tolerance but normal FBG levels. The 2h-BG is a better predictor of deaths from all causes and cardiovascular disease than is FBG.
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            The loss of postprandial glycemic control precedes stepwise deterioration of fasting with worsening diabetes.

            The aim of the study was to determine whether the loss of fasting and postprandial glycemic control occurs in parallel or sequentially in the evolution of type 2 diabetes. In 130 type 2 diabetic patients, 24-h glucose profiles were obtained using a continuous glucose monitoring system. The individuals with type 2 diabetes were divided into five groups according to A1C levels: 1 ( or =9%, n = 26). The glucose profiles between the groups were compared. The overall glucose concentrations for the diurnal, nocturnal, and morning periods, which represent the postprandial, fasting, and the dawn phenomenon states, respectively, were also compared. Glucose concentrations increased steadily from group 1 to 5 in a stepwise manner. The initial differences in mean glucose concentrations reaching statistical significance occurred 1) between groups 1 and 2 (6.4 vs. 7.7 mmol/l, P = 0.0004) for daytime postprandial periods, followed by differences; 2) between groups 2 and 3 (7.5 vs. 9.3 mmol/l, P = 0.0003) for the morning periods (dawn phenomenon); and finally 3) between groups 3 and 4 (6.3 vs. 8.4 mmol/l, P < 0.0001) for nocturnal fasting periods. The deterioration of glucose homeostasis in individuals with type 2 diabetes progressed from postprandial to fasting hyperglycemia following a three-step process. The first step related to the three diurnal postmeal periods considered as a whole, the second step occurred during the morning period, and the third and final step corresponded to sustained hyperglycemia over the nocturnal fasting periods. Such a description of the key stages in the evolution of type 2 diabetes may be of interest for implementing antidiabetes treatment.
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              Effect of nateglinide on the incidence of diabetes and cardiovascular events.

              The ability of short-acting insulin secretagogues to reduce the risk of diabetes or cardiovascular events in people with impaired glucose tolerance is unknown. In a double-blind, randomized clinical trial, we assigned 9306 participants with impaired glucose tolerance and either cardiovascular disease or cardiovascular risk factors to receive nateglinide (up to 60 mg three times daily) or placebo, in a 2-by-2 factorial design with valsartan or placebo, in addition to participation in a lifestyle modification program. We followed the participants for a median of 5.0 years for incident diabetes (and a median of 6.5 years for vital status). We evaluated the effect of nateglinide on the occurrence of three coprimary outcomes: the development of diabetes; a core cardiovascular outcome that was a composite of death from cardiovascular causes, nonfatal myocardial infarction, nonfatal stroke, or hospitalization for heart failure; and an extended cardiovascular outcome that was a composite of the individual components of the core composite cardiovascular outcome, hospitalization for unstable angina, or arterial revascularization. After adjustment for multiple testing, nateglinide, as compared with placebo, did not significantly reduce the cumulative incidence of diabetes (36% and 34%, respectively; hazard ratio, 1.07; 95% confidence interval [CI], 1.00 to 1.15; P=0.05), the core composite cardiovascular outcome (7.9% and 8.3%, respectively; hazard ratio, 0.94, 95% CI, 0.82 to 1.09; P=0.43), or the extended composite cardiovascular outcome (14.2% and 15.2%, respectively; hazard ratio, 0.93, 95% CI, 0.83 to 1.03; P=0.16). Nateglinide did, however, increase the risk of hypoglycemia. Among persons with impaired glucose tolerance and established cardiovascular disease or cardiovascular risk factors, assignment to nateglinide for 5 years did not reduce the incidence of diabetes or the coprimary composite cardiovascular outcomes. (ClinicalTrials.gov number, NCT00097786.) 2010 Massachusetts Medical Society
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                Author and article information

                Contributors
                denisa.janickova.zdarska@email.cz
                Journal
                Diabetes Ther
                Diabetes Ther
                Diabetes Therapy
                Springer Healthcare (Cheshire )
                1869-6953
                1869-6961
                19 February 2018
                19 February 2018
                April 2018
                : 9
                : 2
                : 665-672
                Affiliations
                [1 ]ISNI 0000 0004 1937 116X, GRID grid.4491.8, Department of Internal Medicine, Second Faculty of Medicine, , Charles University, ; Prague, Czech Republic
                [2 ]ISNI 0000 0001 0833 2673, GRID grid.418976.5, Institute of Endocrinology, ; Prague, Czech Republic
                Article
                379
                10.1007/s13300-018-0379-3
                6104280
                29460257
                270668c7-3f38-4322-9942-0ea5d431ecdd
                © The Author(s) 2018

                Open AccessThis article is distributed under the terms of the Creative Commons Attribution 4.0 International License ( https://creativecommons.org/licenses/by/4.0), which permits use, duplication, adaptation, distribution, and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license, and indicate if changes were made.

                History
                : 23 August 2017
                Categories
                Original Research
                Custom metadata
                © Springer Healthcare Ltd., part of Springer Nature 2018

                Endocrinology & Diabetes
                diabetes mellitus,fasting glycemia,glycosylated hemoglobin,metabolic compensation,postprandial glycemia

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