Serum concentration and vascular expression of adiponectin are differentially associated with the diabetic calcifying peripheral arteriopathy.

Adiponectin Peripheral arterial disease Type 2 diabetes Vascular calcification

Journal

Diabetology & metabolic syndrome
ISSN: 1758-5996
Titre abrégé: Diabetol Metab Syndr
Pays: England
ID NLM: 101488958

Informations de publication

Date de publication:
2019
Historique:
received: 05 03 2019
accepted: 17 04 2019
entrez: 7 6 2019
pubmed: 7 6 2019
medline: 7 6 2019
Statut: epublish

Résumé

Medial calcification in diabetes contributes to the arterial occlusive process occurring below the knee level. Adiponectin is an adipokine with atheroprotective properties and possible protective role against arterial calcification. The aim of the study was to investigate, in type 2 diabetes, the link between vascular expression and serum concentration of adiponectin and (1) peripheral arterial calcification and (2) lower limb occlusive arterial disease. Scoring of peripheral vascular calcification and peripheral arterial occlusive disease, using CT-scan and color-duplex ultrasonography respectively, were conducted and explored in relation to serum adiponectin level in a cross sectional study of 197 patients with type 2 diabetes. Vascular adiponectin expression in the arterial wall of diabetic patients with and without medial calcification was evaluated by immunohistochemistry. Peripheral arterial calcification score was higher in patients with the highest adiponectin concentration. In a multivariate logistic regression analysis, an increase of 1 µg/mL of adiponectin was associated with a 22% increase of arterial calcification (adjusted OR = 1.22; 95% CI 1.03-1.44; p = 0.02). Arterial occlusive score was also higher in patients with adiponectin concentration > median (2.8 ± 4.8 vs 4.2 ± 5.7, p = 0.034). Immunohistochemical analyses showed a strong and specific staining of adiponectin in smooth muscle cells in calcified arteries, with a more pronounced expression of adiponectin in early stages of medial calcification. Peripheral arterial calcification is positively associated with circulating adiponectin levels in patients with type 2 diabetes, but vascular adiponectin expression is already observed at early stages of calcification. Adiponectin secretion could be a compensatory mechanism against the calcification process.

Sections du résumé

BACKGROUND BACKGROUND
Medial calcification in diabetes contributes to the arterial occlusive process occurring below the knee level. Adiponectin is an adipokine with atheroprotective properties and possible protective role against arterial calcification. The aim of the study was to investigate, in type 2 diabetes, the link between vascular expression and serum concentration of adiponectin and (1) peripheral arterial calcification and (2) lower limb occlusive arterial disease.
METHODS METHODS
Scoring of peripheral vascular calcification and peripheral arterial occlusive disease, using CT-scan and color-duplex ultrasonography respectively, were conducted and explored in relation to serum adiponectin level in a cross sectional study of 197 patients with type 2 diabetes. Vascular adiponectin expression in the arterial wall of diabetic patients with and without medial calcification was evaluated by immunohistochemistry.
RESULTS RESULTS
Peripheral arterial calcification score was higher in patients with the highest adiponectin concentration. In a multivariate logistic regression analysis, an increase of 1 µg/mL of adiponectin was associated with a 22% increase of arterial calcification (adjusted OR = 1.22; 95% CI 1.03-1.44; p = 0.02). Arterial occlusive score was also higher in patients with adiponectin concentration > median (2.8 ± 4.8 vs 4.2 ± 5.7, p = 0.034). Immunohistochemical analyses showed a strong and specific staining of adiponectin in smooth muscle cells in calcified arteries, with a more pronounced expression of adiponectin in early stages of medial calcification.
CONCLUSIONS CONCLUSIONS
Peripheral arterial calcification is positively associated with circulating adiponectin levels in patients with type 2 diabetes, but vascular adiponectin expression is already observed at early stages of calcification. Adiponectin secretion could be a compensatory mechanism against the calcification process.

Identifiants

DOI: 10.1186/s13098-019-0429-7 PMID: 31168327 PMC: PMC6489190
pubmed: 31168327
doi: 10.1186/s13098-019-0429-7
pii: 429
pmc: PMC6489190
doi:

Banques de données

ClinicalTrials.gov
['NCT02431234']

Types de publication

Journal Article

Langues

eng

Pagination

32

Déclaration de conflit d'intérêts

A patent has been filed on a method using circulating Matrix Gla protein measurement for diagnosis and treating peripheral neuropathies by Assistance Publique Hôpitaux de Paris—APHP). Olivier Bourron, Joe-Elie Salem and Agnès Hartemann are the inventors. The application number is 18306503.6–1118. The other authors declare that they have no competing interests.

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Auteurs

Carole E Aubert (CE)

2Assistance Publique-Hôpitaux de Paris (APHP), Diabetology Department, Pitié Salpêtrière Hospital, 47-83 Boulevard de l'Hôpital, Paris, France.

Sophie Liabeuf (S)

5INSERM U1088, UFR de Médecine et Pharmacie, Jules Verne University of Picardy, Amiens, France.
6Clinical Research Centre, Division of Clinical Pharmacology, Amiens University Hospital and the Jules Verne University of Picardy, Amiens, France.

Chloé Amouyal (C)

1Sorbonne Université, UPMC Univ, Paris 06, France.
2Assistance Publique-Hôpitaux de Paris (APHP), Diabetology Department, Pitié Salpêtrière Hospital, 47-83 Boulevard de l'Hôpital, Paris, France.
10Institute of Cardiometabolism and Nutrition ICAN, Paris, France.

Salim Kemel (S)

3Cardiovascular and Interventional Radiology Department, AP-HP, Pitié-Salpêtrière Hospital, Paris, France.

Frédérique Lajat-Kiss (F)

4Vascular Surgery Department, AP-HP, Pitié-Salpêtrière Hospital, Paris, France.

Jean-Marc Lacorte (JM)

1Sorbonne Université, UPMC Univ, Paris 06, France.
8Department of Endocrine and Oncologic Biochemistry, AP-HP, Pitié-Salpêtrière Hospital, Paris, France.
10Institute of Cardiometabolism and Nutrition ICAN, Paris, France.
INSERM U1166, Paris, France.

Marine Halbron (M)

2Assistance Publique-Hôpitaux de Paris (APHP), Diabetology Department, Pitié Salpêtrière Hospital, 47-83 Boulevard de l'Hôpital, Paris, France.
10Institute of Cardiometabolism and Nutrition ICAN, Paris, France.

Aurélie Carlier (A)

1Sorbonne Université, UPMC Univ, Paris 06, France.
2Assistance Publique-Hôpitaux de Paris (APHP), Diabetology Department, Pitié Salpêtrière Hospital, 47-83 Boulevard de l'Hôpital, Paris, France.
10Institute of Cardiometabolism and Nutrition ICAN, Paris, France.

Joe-Elie Salem (JE)

1Sorbonne Université, UPMC Univ, Paris 06, France.
10Institute of Cardiometabolism and Nutrition ICAN, Paris, France.
11Department of Pharmacology and CIC-1421, AP-HP, AP-HP, Pitié-Salpêtrière Hospital, Paris, France.
12INSERM, CIC-1421, Paris, France.

Christian Funck-Brentano (C)

1Sorbonne Université, UPMC Univ, Paris 06, France.
10Institute of Cardiometabolism and Nutrition ICAN, Paris, France.
11Department of Pharmacology and CIC-1421, AP-HP, AP-HP, Pitié-Salpêtrière Hospital, Paris, France.
12INSERM, CIC-1421, Paris, France.

Ljubica Perisic Matic (L)

15Division of Vascular Surgery, Department of Molecular Medicine and Surgery, Karolinska Institutet, Stockholm, Sweden.
16Center for Molecular Medicine, Karolinska Institutet, Stockholm, Sweden.

Anna Witasp (A)

16Center for Molecular Medicine, Karolinska Institutet, Stockholm, Sweden.
17Division of Renal Medicine, Department of Clinical Science, Intervention and Technology, Karolinska Institutet, Stockholm, Sweden.

Peter Stenvinkel (P)

17Division of Renal Medicine, Department of Clinical Science, Intervention and Technology, Karolinska Institutet, Stockholm, Sweden.

Franck Phan (F)

1Sorbonne Université, UPMC Univ, Paris 06, France.
2Assistance Publique-Hôpitaux de Paris (APHP), Diabetology Department, Pitié Salpêtrière Hospital, 47-83 Boulevard de l'Hôpital, Paris, France.
10Institute of Cardiometabolism and Nutrition ICAN, Paris, France.

Ziad A Massy (ZA)

7Division of Nephrology, Ambroise Paré Hospital, AP-HP, Boulogne-Billancourt, France.
13INSERM U1018, Research Centre in Epidemiology and Population Health (CESP) Team 5, University of Paris Saclay-Versailles-St-Quentin-en-Yvelines (UVSQ), Villejuif, France.

Agnès Hartemann (A)

1Sorbonne Université, UPMC Univ, Paris 06, France.
2Assistance Publique-Hôpitaux de Paris (APHP), Diabetology Department, Pitié Salpêtrière Hospital, 47-83 Boulevard de l'Hôpital, Paris, France.
9INSERM, UMR_S 1138, Centre de Recherche des Cordeliers, Paris 06, France.
10Institute of Cardiometabolism and Nutrition ICAN, Paris, France.

Olivier Bourron (O)

1Sorbonne Université, UPMC Univ, Paris 06, France.
2Assistance Publique-Hôpitaux de Paris (APHP), Diabetology Department, Pitié Salpêtrière Hospital, 47-83 Boulevard de l'Hôpital, Paris, France.
9INSERM, UMR_S 1138, Centre de Recherche des Cordeliers, Paris 06, France.
10Institute of Cardiometabolism and Nutrition ICAN, Paris, France.
ORCID: 0000-0001-7348-7161

Classifications MeSH