Postprandial oxidative stress and gastrointestinal hormones: is there a link?

Hana Malinska, Hana Kahleova, Ondrej Topolcan, Jindra Vrzalova, Olena Oliyarnyk, Ludmila Kazdova, Lenka Belinova, Martin Hill, Terezie Pelikanova, Hana Malinska, Hana Kahleova, Ondrej Topolcan, Jindra Vrzalova, Olena Oliyarnyk, Ludmila Kazdova, Lenka Belinova, Martin Hill, Terezie Pelikanova

Abstract

Background: Abnormal postprandial elevation of plasma glucose and lipids plays an important role in the pathogenesis of diabetes and strongly predicts cardiovascular mortality. In patients suffering from type 2 diabetes (T2D) postprandial state is associated with oxidative stress, cardiovascular risk and, probably, with impairment of both secretion and the effect of gastrointestinal peptides. Evaluating postprandial changes of gastrointestinal hormones together with changes in oxidative stress markers may help to understand the mechanisms behind the postprandial state in diabetes as well as suggest new preventive and therapeutical strategies.

Methods: A standard meal test has been used for monitoring the postprandial concentrations of gastrointestinal hormones and oxidative stress markers in patients with T2D (n = 50) compared to healthy controls (n = 50). Blood samples were drawn 0, 30, 60, 120 and 180 minutes after the standard meal.

Results: Both basal and postprandial plasma concentrations of glucose and insulin proved to be significantly higher in patients with T2D, whereas plasma concentrations of ghrelin showed significantly lower values during the whole meal test. In comparison with healthy controls, both basal and postprandial concentrations of almost all other gastrointestinal hormones and lipoperoxidation were significantly increased while ascorbic acid, reduced glutathione and superoxide dismutase activity were decreased in patients with T2D. A positive relationship was found between changes in GIP and those of glucose and immunoreactive insulin in diabetic patients (p<0.001 and p<0.001, respectively) and between changes in PYY and those of glucose (p<0.01). There was a positive correlation between changes in GIP and PYY and changes in ascorbic acid in patients with T2D (p<0.05 and p<0.001, respectively).

Conclusion/interpretation: Apart from a positive relationship of postprandial changes in GIP and PYY with changes in ascorbic acid, there was no direct link observed between gastrointestinal hormones and oxidative stress markers in diabetic patients.

Trial registration: ClinicalTrials.gov NCT01572402.

Conflict of interest statement

Competing Interests: The authors have declared that no competing interests exist.

Figures

Figure 1. Enrollment of the participants and…
Figure 1. Enrollment of the participants and completion of the study.
Figure 2. Postprandial changes in plasma concentrations…
Figure 2. Postprandial changes in plasma concentrations of glucose, lipids and insulin in diabetic (circles, full line) (n = 48) and control subjects (triangles, dashed line) (n = 49) after the standard meal test.
Data are expressed as mean with 95% CI. A: Plasma glucose: Factors time p

Figure 3. Postprandial changes in plasma concentrations…

Figure 3. Postprandial changes in plasma concentrations of gastrointestinal hormones in diabetic (circles, full line)…

Figure 3. Postprandial changes in plasma concentrations of gastrointestinal hormones in diabetic (circles, full line) (n = 48) and control subjects (triangles, dashed line) (n = 49) after the standard meal test.
Data are expressed as mean with 95% CI. A: – GIP: Factors time p

Figure 4. Postprandial changes in plasma concentrations…

Figure 4. Postprandial changes in plasma concentrations of oxidative stress markers in diabetic (circles, full…

Figure 4. Postprandial changes in plasma concentrations of oxidative stress markers in diabetic (circles, full line) (n = 45) and control subjects (triangles, dashed line) (n = 49) after the standard meal test.
Data are expressed as mean with 95% CI. A: TBARS: Factors time p
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References
    1. Bonora E, Muggeo M (2001) Postprandial blood glucose as a risk factor for cardiovascular disease in Type II diabetes: the epidemiological evidence. Diabetologia 44: 2107–2114. - PubMed
    1. Ceriello A, Esposito K, Testa R, Bonfigli AR, Marra M, et al. (2011) The possible protective role of glucagon-like peptide 1 on endothelium during the meal and evidence for an “endothelial resistance” to glucagon-like peptide 1 in diabetes. Diabetes Care 34: 697–702. - PMC - PubMed
    1. Wajchenberg BL (2007) beta-cell failure in diabetes and preservation by clinical treatment. Endocr Rev 28: 187–218. - PubMed
    1. Drucker DJ, Sherman SI, Gorelick FS, Bergenstal RM, Sherwin RS, et al. (2010) Incretin-based therapies for the treatment of type 2 diabetes: evaluation of the risks and benefits. Diabetes Care 33: 428–433. - PMC - PubMed
    1. Meier JJ, Nauck MA (2006) Incretins and the development of type 2 diabetes. Curr Diab Rep 6: 194–201. - PubMed
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This work was supported by Ministry of Health, Czech Republic, conceptual development of research organisation (“Institute for Clinical and Experimental Medicine – IKEM, IN 00023001”), by the Internal Grant Agency of the Ministry of Health of the Czech Republic (NT/11238-4) and by the Grant Agency of Charles University – GAUK No 702312. The funders had no role in study design, data collection and analysis, decision to publish, or preparation of the manuscript.
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Figure 3. Postprandial changes in plasma concentrations…
Figure 3. Postprandial changes in plasma concentrations of gastrointestinal hormones in diabetic (circles, full line) (n = 48) and control subjects (triangles, dashed line) (n = 49) after the standard meal test.
Data are expressed as mean with 95% CI. A: – GIP: Factors time p

Figure 4. Postprandial changes in plasma concentrations…

Figure 4. Postprandial changes in plasma concentrations of oxidative stress markers in diabetic (circles, full…

Figure 4. Postprandial changes in plasma concentrations of oxidative stress markers in diabetic (circles, full line) (n = 45) and control subjects (triangles, dashed line) (n = 49) after the standard meal test.
Data are expressed as mean with 95% CI. A: TBARS: Factors time p
Similar articles
Cited by
References
    1. Bonora E, Muggeo M (2001) Postprandial blood glucose as a risk factor for cardiovascular disease in Type II diabetes: the epidemiological evidence. Diabetologia 44: 2107–2114. - PubMed
    1. Ceriello A, Esposito K, Testa R, Bonfigli AR, Marra M, et al. (2011) The possible protective role of glucagon-like peptide 1 on endothelium during the meal and evidence for an “endothelial resistance” to glucagon-like peptide 1 in diabetes. Diabetes Care 34: 697–702. - PMC - PubMed
    1. Wajchenberg BL (2007) beta-cell failure in diabetes and preservation by clinical treatment. Endocr Rev 28: 187–218. - PubMed
    1. Drucker DJ, Sherman SI, Gorelick FS, Bergenstal RM, Sherwin RS, et al. (2010) Incretin-based therapies for the treatment of type 2 diabetes: evaluation of the risks and benefits. Diabetes Care 33: 428–433. - PMC - PubMed
    1. Meier JJ, Nauck MA (2006) Incretins and the development of type 2 diabetes. Curr Diab Rep 6: 194–201. - PubMed
Show all 41 references
Publication types
MeSH terms
Associated data
Grant support
This work was supported by Ministry of Health, Czech Republic, conceptual development of research organisation (“Institute for Clinical and Experimental Medicine – IKEM, IN 00023001”), by the Internal Grant Agency of the Ministry of Health of the Czech Republic (NT/11238-4) and by the Grant Agency of Charles University – GAUK No 702312. The funders had no role in study design, data collection and analysis, decision to publish, or preparation of the manuscript.
[x]
Cite
Copy Download .nbib
Format: AMA APA MLA NLM
Figure 4. Postprandial changes in plasma concentrations…
Figure 4. Postprandial changes in plasma concentrations of oxidative stress markers in diabetic (circles, full line) (n = 45) and control subjects (triangles, dashed line) (n = 49) after the standard meal test.
Data are expressed as mean with 95% CI. A: TBARS: Factors time p

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