Altered oxidant and antioxidant levels are associated with vascular stiffness and diabetic kidney disease in type 1 diabetes after exposure to acute and chronic hyperglycemia.


Journal

Cardiovascular diabetology
ISSN: 1475-2840
Titre abrégé: Cardiovasc Diabetol
Pays: England
ID NLM: 101147637

Informations de publication

Date de publication:
28 Sep 2024
Historique:
received: 13 05 2024
accepted: 30 08 2024
medline: 29 9 2024
pubmed: 29 9 2024
entrez: 28 9 2024
Statut: epublish

Résumé

Hyperglycemia-induced oxidative stress is a well-established pathological mediator of vascular complications in diabetes. We assessed plasma oxidant and antioxidant levels in response to acute and chronic hyperglycemia in relation to vascular stiffness and varying degrees of kidney disease in type 1 diabetes individuals. The acute hyperglycemia study included 22 type 1 diabetic individuals with normal albumin excretion rate (AER) and 13 non-diabetic controls. These individuals received an acute glucose challenge during a 120-minute hyperglycemic clamp. The chronic hyperglycemia study included 118 type 1 diabetic individuals with chronically low (n = 60) or high (n = 58) HbA1c concentrations and varying degrees of diabetic kidney disease (DKD) classified as normal, moderate, or severe albuminuria (AER). Levels of malondialdehyde (MDA), reactive oxygen metabolites (ROMs), total antioxidant capacity (TAC), biological antioxidant potential (BAP) and superoxide dismutase (SOD) were measured from plasma or serum samples in the FinnDiane study. Levels of MDA (p < 0.01) and ROMs (p < 0.01) were elevated in type 1 diabetes individuals compared to non-diabetic controls at baseline. Acute hyperglycemia further increased MDA levels (p < 0.05) and sustained the elevation of ROMs in type 1 diabetes individuals. Acute hyperglycemic challenge impaired TAC in both non-diabetic (p < 0.05) and type 1 diabetes (p < 0.01) individuals compared to baseline whereas BAP was increased (p < 0.05) with no difference observed in non-diabetic controls. There was a positive association between high circulating MDA and AIx (r2 = 0.611, p = 0.05), and between delta ROMs and delta AIx (r2 = 0.955, p = 0.014) in combined analysis of individuals with type 1 diabetes and non-diabetic controls. Type 1 diabetes individuals with varying status of DKD, showed elevated levels of ROMs in those with high HbA1c compared to their counterpart with low HbA1c (p < 0.05). Individuals with severe albuminuria showed elevated ROM levels (p < 0.01) and depressed antioxidant capacity (p < 0.01) compared to those with normal AER of comparable HbA1c concentrations. Biomarkers of oxidative stress are associated with vascular stiffness and DKD following acute and chronic hyperglycemic exposure and may provide added value to HbA1c in understanding disease pathology, predicting risk and assessing the status of secondary complications of type 1 diabetes.

Sections du résumé

BACKGROUND BACKGROUND
Hyperglycemia-induced oxidative stress is a well-established pathological mediator of vascular complications in diabetes. We assessed plasma oxidant and antioxidant levels in response to acute and chronic hyperglycemia in relation to vascular stiffness and varying degrees of kidney disease in type 1 diabetes individuals.
METHODS METHODS
The acute hyperglycemia study included 22 type 1 diabetic individuals with normal albumin excretion rate (AER) and 13 non-diabetic controls. These individuals received an acute glucose challenge during a 120-minute hyperglycemic clamp. The chronic hyperglycemia study included 118 type 1 diabetic individuals with chronically low (n = 60) or high (n = 58) HbA1c concentrations and varying degrees of diabetic kidney disease (DKD) classified as normal, moderate, or severe albuminuria (AER). Levels of malondialdehyde (MDA), reactive oxygen metabolites (ROMs), total antioxidant capacity (TAC), biological antioxidant potential (BAP) and superoxide dismutase (SOD) were measured from plasma or serum samples in the FinnDiane study.
RESULTS RESULTS
Levels of MDA (p < 0.01) and ROMs (p < 0.01) were elevated in type 1 diabetes individuals compared to non-diabetic controls at baseline. Acute hyperglycemia further increased MDA levels (p < 0.05) and sustained the elevation of ROMs in type 1 diabetes individuals. Acute hyperglycemic challenge impaired TAC in both non-diabetic (p < 0.05) and type 1 diabetes (p < 0.01) individuals compared to baseline whereas BAP was increased (p < 0.05) with no difference observed in non-diabetic controls. There was a positive association between high circulating MDA and AIx (r2 = 0.611, p = 0.05), and between delta ROMs and delta AIx (r2 = 0.955, p = 0.014) in combined analysis of individuals with type 1 diabetes and non-diabetic controls. Type 1 diabetes individuals with varying status of DKD, showed elevated levels of ROMs in those with high HbA1c compared to their counterpart with low HbA1c (p < 0.05). Individuals with severe albuminuria showed elevated ROM levels (p < 0.01) and depressed antioxidant capacity (p < 0.01) compared to those with normal AER of comparable HbA1c concentrations.
CONCLUSIONS CONCLUSIONS
Biomarkers of oxidative stress are associated with vascular stiffness and DKD following acute and chronic hyperglycemic exposure and may provide added value to HbA1c in understanding disease pathology, predicting risk and assessing the status of secondary complications of type 1 diabetes.

Identifiants

pubmed: 39342285
doi: 10.1186/s12933-024-02427-4
pii: 10.1186/s12933-024-02427-4
doi:

Substances chimiques

Antioxidants 0
Biomarkers 0
Blood Glucose 0
hemoglobin A1c protein, human 0
Malondialdehyde 4Y8F71G49Q
Glycated Hemoglobin 0
Reactive Oxygen Species 0
Oxidants 0
Superoxide Dismutase EC 1.15.1.1

Types de publication

Journal Article

Langues

eng

Sous-ensembles de citation

IM

Pagination

350

Informations de copyright

© 2024. The Author(s).

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Auteurs

Krishna Adeshara (K)

Folkhälsan Research Center, Biomedicum Helsinki, Haartmaninkatu 8, FIN-00290, Helsinki, Finland.
Research Program for Clinical and Molecular Metabolism, University of Helsinki, Helsinki, Finland.

Elyse Di Marco (E)

Folkhälsan Research Center, Biomedicum Helsinki, Haartmaninkatu 8, FIN-00290, Helsinki, Finland.
Research Program for Clinical and Molecular Metabolism, University of Helsinki, Helsinki, Finland.
Department of Diabetes, Central Clinical School, Monash University, Melbourne, VIC, Australia.

Marco Bordino (M)

Folkhälsan Research Center, Biomedicum Helsinki, Haartmaninkatu 8, FIN-00290, Helsinki, Finland.
Research Program for Clinical and Molecular Metabolism, University of Helsinki, Helsinki, Finland.

Daniel Gordin (D)

Department of Nephrology, University of Helsinki and Helsinki University Hospital, Helsinki, Finland.
Minerva Foundation Institute for Medical Research, Helsinki, Finland.
Joslin Diabetes Center, Harvard Medical School, Boston, MA, USA.

Luciano Bernardi (L)

Folkhälsan Research Center, Biomedicum Helsinki, Haartmaninkatu 8, FIN-00290, Helsinki, Finland.
Research Program for Clinical and Molecular Metabolism, University of Helsinki, Helsinki, Finland.

Mark E Cooper (ME)

Department of Diabetes, Central Clinical School, Monash University, Melbourne, VIC, Australia.

Per-Henrik Groop (PH)

Folkhälsan Research Center, Biomedicum Helsinki, Haartmaninkatu 8, FIN-00290, Helsinki, Finland. per-henrik.groop@helsinki.fi.
Research Program for Clinical and Molecular Metabolism, University of Helsinki, Helsinki, Finland. per-henrik.groop@helsinki.fi.
Department of Diabetes, Central Clinical School, Monash University, Melbourne, VIC, Australia. per-henrik.groop@helsinki.fi.
Department of Nephrology, University of Helsinki and Helsinki University Hospital, Helsinki, Finland. per-henrik.groop@helsinki.fi.
Baker Heart and Diabetes Institute, Melbourne, VIC, Australia. per-henrik.groop@helsinki.fi.

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Classifications MeSH