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Negative Effects of Chronic High Intake of Fructose on Lung Diseases.
Hernández-Díazcouder, Adrián; González-Ramírez, Javier; Sanchez, Fausto; Leija-Martínez, José J; Martínez-Coronilla, Gustavo; Amezcua-Guerra, Luis M; Sánchez-Muñoz, Fausto.
  • Hernández-Díazcouder A; Department of Immunology, Instituto Nacional de Cardiología Ignacio Chávez, Mexico City 14080, Mexico.
  • González-Ramírez J; Cellular Biology Laboratory, Faculty of Nursing, Universidad Autónoma de Baja California Campus Mexicali, Mexicali 21100, Mexico.
  • Sanchez F; Department of Agricultural and Animal Production, Universidad Autónoma Metropolitana Xochimilco, Mexico City 04960, Mexico.
  • Leija-Martínez JJ; Master and Doctorate Program in Medical, Dental, and Health Sciences, Faculty of Medicine, Universidad Nacional Autónoma de México Campus Ciudad Universitaria, Mexico City 04510, Mexico.
  • Martínez-Coronilla G; Research Laboratory of Pharmacology, Hospital Infantil de Mexico Federico Gómez, Mexico City 06720, Mexico.
  • Amezcua-Guerra LM; Histology Laboratory, Faculty of Medicine, Universidad Autónoma de Baja California Campus Mexicali, Mexicali 21100, Mexico.
  • Sánchez-Muñoz F; Department of Immunology, Instituto Nacional de Cardiología Ignacio Chávez, Mexico City 14080, Mexico.
Nutrients ; 14(19)2022 Oct 01.
Article in English | MEDLINE | ID: covidwho-2066298
ABSTRACT
In the modern diet, excessive fructose intake (>50 g/day) had been driven by the increase, in recent decades, of the consumption of sugar-sweetened beverages. This phenomenon has dramatically increased within the Caribbean and Latin American regions. Epidemiological studies show that chronic high intake of fructose related to sugar-sweetened beverages increases the risk of developing several non-communicable diseases, such as chronic obstructive pulmonary disease and asthma, and may also contribute to the exacerbation of lung diseases, such as COVID-19. Evidence supports several mechanisms-such as dysregulation of the renin-angiotensin system, increased uric acid production, induction of aldose reductase activity, production of advanced glycation end-products, and activation of the mTORC1 pathway-that can be implicated in lung damage. This review addresses how these pathophysiologic and molecular mechanisms may explain the lung damage resulting from high intake of fructose.
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Full text: Available Collection: International databases Database: MEDLINE Main subject: Fructose / Lung Diseases Type of study: Experimental Studies / Observational study / Prognostic study Limits: Humans Language: English Year: 2022 Document Type: Article Affiliation country: Nu14194089

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Full text: Available Collection: International databases Database: MEDLINE Main subject: Fructose / Lung Diseases Type of study: Experimental Studies / Observational study / Prognostic study Limits: Humans Language: English Year: 2022 Document Type: Article Affiliation country: Nu14194089