High salt intake causes leptin resistance and obesity in mice by stimulating endogenous fructose production and metabolism.
Proc Natl Acad Sci U S A
; 115(12): 3138-3143, 2018 03 20.
Article
em En
| MEDLINE
| ID: mdl-29507217
ABSTRACT
Dietary guidelines for obesity typically focus on three food groups (carbohydrates, fat, and protein) and caloric restriction. Intake of noncaloric nutrients, such as salt, are rarely discussed. However, recently high salt intake has been reported to predict the development of obesity and insulin resistance. The mechanism for this effect is unknown. Here we show that high intake of salt activates the aldose reductase-fructokinase pathway in the liver and hypothalamus, leading to endogenous fructose production with the development of leptin resistance and hyperphagia that cause obesity, insulin resistance, and fatty liver. A high-salt diet was also found to predict the development of diabetes and nonalcoholic fatty liver disease in a healthy population. These studies provide insights into the pathogenesis of obesity and diabetes and raise the potential for reduction in salt intake as an additional interventional approach for reducing the risk for developing obesity and metabolic syndrome.
Palavras-chave
Texto completo:
1
Base de dados:
MEDLINE
Assunto principal:
Cloreto de Sódio na Dieta
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Leptina
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Hepatopatia Gordurosa não Alcoólica
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Frutose
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Obesidade
Tipo de estudo:
Etiology_studies
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Prognostic_studies
Limite:
Adult
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Aged
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Aged80
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Animals
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Humans
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Middle aged
Idioma:
En
Revista:
Proc Natl Acad Sci U S A
Ano de publicação:
2018
Tipo de documento:
Article