Concetta Schiano1, Vincenzo Grimaldi2, Monica Franzese3, Carmela Fiorito2, Filomena De Nigris4, Francesco Donatelli5, Andrea Soricelli3, Marco Salvatore3, Claudio Napoli6. 1. Department of Advanced Clinical and Surgical Sciences, University of Campania "L. Vanvitelli", Naples, Italy. Electronic address: concetta.schiano@unicampania.it. 2. Department of Advanced Clinical and Surgical Sciences, University of Campania "L. Vanvitelli", Naples, Italy. 3. IRCCS SDN, Naples, Italy. 4. Department of Precision Medicine, University of Campania "L. Vanvitelli", Naples, Italy. 5. Department of Clinical and Community Sciences, University of Milan, Milan, Italy. 6. Department of Advanced Clinical and Surgical Sciences, University of Campania "L. Vanvitelli", Naples, Italy; IRCCS SDN, Naples, Italy.
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.
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.
Authors: V A Chavushyan; K V Simonyan; M H Danielyan; L G Avetisyan; L V Darbinyan; A S Isoyan; A G Lorikyan; L E Hovhannisyan; M A Babakhanyan; L M Sukiasyan Journal: Metab Brain Dis Date: 2022-10-22 Impact factor: 3.655