Beneficial effect of a multistrain synbiotic prodefen® plus on the systemic and vascular alterations associated with metabolic syndrome in rats: The role of the neuronal nitric oxide synthase and protein kinase A
Entity
UAM. Departamento de Cirugía; UAM. Departamento de Farmacología; UAM. Departamento de Fisiología; Instituto de Investigación Sanitaria Hospital Universitario de La Paz (IdiPAZ)Publisher
MDPI, Basel, SwitzerlandDate
2020-01-01Citation
10.3390/nu12010117
Nutrients 12.1 (2020): 117
ISSN
2072-6643DOI
10.3390/nu12010117Funded by
This research was funded by Italfarmaco, S.A (L.O.U. 83; 0138/2018), CiberCV (Grant number: CB16/11/00286), the European Regional Development Grant (FEDER) (Comunidad de Madrid, Grant number B2017/BMD-3676), and R + D projects for young researchers, Universidad Autónoma de Madrid (Comunidad de Madrid (SI1-PJI-2019-00321). R.R.-D. received a fellowship from Juan de la Cierva Program (IJCI-2017-31399).Project
Comunidad de Madrid. B2017/BMD-3676/AORTASANAEditor's Version
http://doi.org/doi:10.3390/nu12010117Subjects
Metabolic syndrome; Synbiotic; Hypertension; Mesenteric artery; Perivascular nitrergic innervation; Nitric oxide; Neuronal nitric oxide synthase; Protein kinase a; MedicinaRights
© 2020 The AuthorsAbstract
A high fat diet (HFD) intake is crucial for the development and progression of metabolic
syndrome (MtS). Increasing evidence links gut dysbiosis with the metabolic and vascular alterations
associated with MtS. Here we studied the use of a combination of various probiotic strains together
with a prebiotic (synbiotic) in a commercially available Prodefen® Plus. MtS was induced by HFD (45%)
in maleWistar rats. Half of the MtS animals received Prodefen® Plus for 4 weeks. At 12 weeks, we
observed an increase in body weight, together with the presence of insulin resistance, liver steatosis,
hypertriglyceridemia and hypertension in MtS rats. Prodefen® Plus supplementation did not a ect
the body weight gain but ameliorated all the MtS-related symptoms. Moreover, the hypertension
induced by HFD is caused by a diminished both nitric oxide (NO) functional role and release probably
due to a diminished neuronal nitric oxide synthase (nNOS) activation by protein kinase A (PKA)
pathway. Prodefen® Plus supplementation for 4 weeks recovered the NO function and release and the
systolic blood pressure was returned to normotensive values as a result. Overall, supplementation
with Prodefen® Plus could be considered an interesting non-pharmacological approach in MtS.
Files in this item
Google Scholar:Llévenes, Pablo
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Rodrigues Díez, Raquel
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Cros-Brunsó, Laia
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Prieto, Mª Isabel
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Casani, Laura
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Balfagón, Gloria
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Blanco Rivero, Javier
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