Metabolic syndrome is a cluster of the most dangerous cardiovascular (CV) risk factors including visceral obesity, insulin resistance, hyperglycemia, alterations in lipid metabolism and arterial hypertension (AH). In particular, AH plays a key role in the complications associated with metabolic syndrome. High salt intake is a well-known risk factor for AH and CV diseases. Vasocon-striction, impaired vasodilation, extracellular volume expansion, inflammation, and an increased sympathetic nervous system (SNS) activity are the mechanisms involved in the pathogenesis of AH, induced by Western diet. Gut dysbiosis in AH is associated with reduction of short chain fatty acid-producing bacteria: acetate, butyrate and propionate, which activate different pathways, causing vasoconstriction, impaired vasodilation, salt and water retention and a consequent high blood pressure. Moreover, increased trimethylamine N-oxide and lipopolysaccharides trigger chronic inflammation, which contributes to endothelial dysfunction and target organs damage. Additionally, a high salt-intake diet impacts negatively on gut microbiota composition. A bidirectional neuronal pathway determines the “brain–gut” axis, which, in turn, influences blood pressure levels. Then, we discuss the possible adjuvant novel treatments related to gut microbiota modulation for AH control.

Canale, M. P., Noce, A., Di Lauro, M., Marrone, G., Cantelmo, M., Cardillo, C., Federici, M., Di Daniele, N., Tesauro, M., Gut dysbiosis and western diet in the pathogenesis of essential arterial hypertension: A narrative review, <<NUTRIENTS>>, 2021; 13 (4): N/A-N/A. [doi:10.3390/nu13041162] [https://hdl.handle.net/10807/301990]

Gut dysbiosis and western diet in the pathogenesis of essential arterial hypertension: A narrative review

Cardillo, Carmine;
2021

Abstract

Metabolic syndrome is a cluster of the most dangerous cardiovascular (CV) risk factors including visceral obesity, insulin resistance, hyperglycemia, alterations in lipid metabolism and arterial hypertension (AH). In particular, AH plays a key role in the complications associated with metabolic syndrome. High salt intake is a well-known risk factor for AH and CV diseases. Vasocon-striction, impaired vasodilation, extracellular volume expansion, inflammation, and an increased sympathetic nervous system (SNS) activity are the mechanisms involved in the pathogenesis of AH, induced by Western diet. Gut dysbiosis in AH is associated with reduction of short chain fatty acid-producing bacteria: acetate, butyrate and propionate, which activate different pathways, causing vasoconstriction, impaired vasodilation, salt and water retention and a consequent high blood pressure. Moreover, increased trimethylamine N-oxide and lipopolysaccharides trigger chronic inflammation, which contributes to endothelial dysfunction and target organs damage. Additionally, a high salt-intake diet impacts negatively on gut microbiota composition. A bidirectional neuronal pathway determines the “brain–gut” axis, which, in turn, influences blood pressure levels. Then, we discuss the possible adjuvant novel treatments related to gut microbiota modulation for AH control.
2021
Inglese
Canale, M. P., Noce, A., Di Lauro, M., Marrone, G., Cantelmo, M., Cardillo, C., Federici, M., Di Daniele, N., Tesauro, M., Gut dysbiosis and western diet in the pathogenesis of essential arterial hypertension: A narrative review, <<NUTRIENTS>>, 2021; 13 (4): N/A-N/A. [doi:10.3390/nu13041162] [https://hdl.handle.net/10807/301990]
File in questo prodotto:
File Dimensione Formato  
nutrients-13-01162.pdf

accesso aperto

Tipologia file ?: Versione Editoriale (PDF)
Licenza: Creative commons
Dimensione 996.31 kB
Formato Adobe PDF
996.31 kB Adobe PDF Visualizza/Apri

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/10807/301990
Citazioni
  • ???jsp.display-item.citation.pmc??? ND
  • Scopus 29
  • ???jsp.display-item.citation.isi??? 25
social impact