AIM: Hyperglycemia status induces endothelial dysfunction, although the underlying pathogenic mechanisms are not fully understood. There are several studies connecting sugar/sweetened beverages to the cardiovascular disease. Currently, many sweeteners have been extensively introduced into lifestyle to normalize blood glucose levels without altering the sweet taste. However, there is growing concern for their impact on metabolic health. METHODS: Human endothelial cells were treated with Glucose, Fructose, Aspartame, Rebaudioside A, Stevioside, or Steviol. Morphological characteristics, in vitro angiogenesis and array gene expression were analyzed. RESULTS: High-glucose and fructose concentrations significantly decreased cell features such as angiogenic capability. Interestingly, non-caloric sweeteners did not significantly modified all cell characteristics and they did not compromised cell angiogenic ability. Array gene expression analysis revealed that the chemokine fractalkine (CX3CL1) and the enzyme transferase (HPRT1) were always significantly upregulated and downregulated respectively, after glucose and fructose treatments (P > .05), whereas they were non-differentially expressed with all the other sweeteners. Interestingly, both genes are considered as cardiovascular disease risk biomarkers. Specifically, upregulation of CX3CL1/CX3CR1 occurs in the human placenta and serum levels of the ligand are associated with markers of insulin resistance in GDM. CONCLUSIONS: Differently from glucose and fructose, steviol glycosides do not damage endothelial cells. Prospective preclinical studies and clinical trials are warranted to confirm the long-term safety of such compounds.

Non-nutritional sweeteners effects on endothelial vascular function / C. Schiano, V. Grimaldi, M. Franzese, C. Fiorito, F.D. Nigris, F. Donatelli, C. Napoli. - In: TOXICOLOGY IN VITRO. - ISSN 0887-2333. - 62:(2020 Feb). [Epub ahead of print] [10.1016/j.tiv.2019.104694]

Non-nutritional sweeteners effects on endothelial vascular function

F. Donatelli
Penultimo
Membro del Collaboration Group
;
2020

Abstract

AIM: Hyperglycemia status induces endothelial dysfunction, although the underlying pathogenic mechanisms are not fully understood. There are several studies connecting sugar/sweetened beverages to the cardiovascular disease. Currently, many sweeteners have been extensively introduced into lifestyle to normalize blood glucose levels without altering the sweet taste. However, there is growing concern for their impact on metabolic health. METHODS: Human endothelial cells were treated with Glucose, Fructose, Aspartame, Rebaudioside A, Stevioside, or Steviol. Morphological characteristics, in vitro angiogenesis and array gene expression were analyzed. RESULTS: High-glucose and fructose concentrations significantly decreased cell features such as angiogenic capability. Interestingly, non-caloric sweeteners did not significantly modified all cell characteristics and they did not compromised cell angiogenic ability. Array gene expression analysis revealed that the chemokine fractalkine (CX3CL1) and the enzyme transferase (HPRT1) were always significantly upregulated and downregulated respectively, after glucose and fructose treatments (P > .05), whereas they were non-differentially expressed with all the other sweeteners. Interestingly, both genes are considered as cardiovascular disease risk biomarkers. Specifically, upregulation of CX3CL1/CX3CR1 occurs in the human placenta and serum levels of the ligand are associated with markers of insulin resistance in GDM. CONCLUSIONS: Differently from glucose and fructose, steviol glycosides do not damage endothelial cells. Prospective preclinical studies and clinical trials are warranted to confirm the long-term safety of such compounds.
Cardiovascular; Diabetes; Endothelium; Sweetener
Settore MED/05 - Patologia Clinica
Settore MED/11 - Malattie dell'Apparato Cardiovascolare
Settore MED/23 - Chirurgia Cardiaca
feb-2020
23-ott-2019
Article (author)
File in questo prodotto:
File Dimensione Formato  
1-s2.0-S0887233319305326-main.pdf

accesso riservato

Descrizione: Articolo principale
Tipologia: Publisher's version/PDF
Dimensione 1.81 MB
Formato Adobe PDF
1.81 MB Adobe PDF   Visualizza/Apri   Richiedi una copia
Pubblicazioni consigliate

I documenti in IRIS sono protetti da copyright e tutti i diritti sono riservati, salvo diversa indicazione.

Utilizza questo identificativo per citare o creare un link a questo documento: https://hdl.handle.net/2434/686301
Citazioni
  • ???jsp.display-item.citation.pmc??? 6
  • Scopus 18
  • ???jsp.display-item.citation.isi??? 17
social impact