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dc.creatorPereira, CD-
dc.creatorPassos, E-
dc.creatorSevero, M-
dc.creatorVito, I-
dc.creatorWen, X-
dc.creatorCarneiro, F-
dc.creatorGomes, P-
dc.creatorMonteiro, R-
dc.creatorMartins, MJ-
dc.description.abstractBACKGROUND: High-fructose and/or low-mineral diets are relevant in metabolic syndrome (MS) development. Insulin resistance (IR) represents a central mechanism in MS development. Glucocorticoid signalling dysfunction and endoplasmic reticulum (ER) and oxidative stresses strongly contribute to IR and associate with MS. We have described that natural mineral-rich water ingestion delays fructose-induced MS development, modulates fructose effects on the redox state and glucocorticoid signalling and increases sirtuin 1 expression. Here, we investigated mineral-rich water ingestion effects on insulin signalling and ER homeostasis of fructose-fed rats. MATERIALS AND METHODS: Adult male Sprague-Dawley rats had free access to standard-chow diet and different drinking solutions (8 weeks): tap water (CONT), 10%-fructose/tap water (FRUCT) or 10%-fructose/mineral-rich water (FRUCTMIN). Hepatic and adipose (visceral, VAT) insulin signalling and hepatic ER homeostasis (Western blot or PCR) as well as hepatic lipid accumulation were evaluated. RESULTS: Hepatic p-IRS1Ser307/IRS1 (tendency), p-IRS1Ser307, total JNK and (activated IRE1α)/(activated JNK) decreased with fructose ingestion, while p-JNK tended to increase; mineral-rich water ingestion, totally or partially, reverted all these effects. Total PERK, p-eIF2α (tendency) and total IRS1 (tendency) decreased in both fructose-fed groups. p-ERK/ERK and total IRE1α increasing tendencies in FRUCT became significant in FRUCTMIN (similar pattern for lipid area). Additionally, unspliced-XBP1 increased with mineral-rich water. In VAT, total ERK fructose-induced increase was partially prevented in FRUCTMIN. CONCLUSIONS: Mineral-rich water modulation of fructose-induced effects on insulin signalling and ER homeostasis matches the better metabolic profile previously reported. Increased p-ERK/ERK, adding to decreased IRE1α activation, and increased unspliced-XBP1 and lipid area may protect against oxidative stress and IR development in FRUCTMIN.-
dc.relation.ispartofHormone Molecular Biology and Clinical Investigation, vol. 26(2), p. 135-150-
dc.subjectWater - Ingestion-
dc.subjectMineral-rich water-
dc.subjectMetabolic syndrome-
dc.titleIngestion of a natural mineral-rich water in an animal model of metabolic syndrome: effects in insulin signalling and endoplasmic reticulum stress-
dc.typeArtigo em Revista Científica Internacional-
dc.contributor.uportoInstituto de Saúde Pública-
Appears in Collections:ISPUP - Artigo em Revista Científica Internacional

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