{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2025,12,12]],"date-time":"2025-12-12T08:10:22Z","timestamp":1765527022851,"version":"3.48.0"},"reference-count":79,"publisher":"Walter de Gruyter GmbH","issue":"2","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":[],"published-print":{"date-parts":[[2016,5,1]]},"abstract":"<jats:title>Abstract<\/jats:title>\n                  <jats:p>\n                    <jats:bold>Background<\/jats:bold>\n                    : 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.\n                  <\/jats:p>\n                  <jats:p>\n                    <jats:bold>Materials and methods<\/jats:bold>\n                    : 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.\n                  <\/jats:p>\n                  <jats:p>\n                    <jats:bold>Results<\/jats:bold>\n                    : Hepatic p-IRS1\n                    <jats:sup>Ser307<\/jats:sup>\n                    \/IRS1 (tendency), p-IRS1\n                    <jats:sup>Ser307<\/jats:sup>\n                    , total JNK and (activated IRE1\u03b1)\/(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-eIF2\u03b1 (tendency) and total IRS1 (tendency) decreased in both fructose-fed groups. p-ERK\/ERK and total IRE1\u03b1 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.\n                  <\/jats:p>\n                  <jats:p>\n                    <jats:bold>Conclusions<\/jats:bold>\n                    : 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 IRE1\u03b1 activation, and increased unspliced-XBP1 and lipid area may protect against oxidative stress and IR development in FRUCTMIN.\n                  <\/jats:p>","DOI":"10.1515\/hmbci-2015-0033","type":"journal-article","created":{"date-parts":[[2016,1,7]],"date-time":"2016-01-07T05:17:15Z","timestamp":1452143835000},"page":"135-150","source":"Crossref","is-referenced-by-count":8,"title":["Ingestion of a natural mineral-rich water in an animal model of metabolic syndrome: effects in insulin signalling and endoplasmic reticulum stress"],"prefix":"10.1515","volume":"26","author":[{"given":"Cid\u00e1lia D.","family":"Pereira","sequence":"first","affiliation":[]},{"given":"Emanuel","family":"Passos","sequence":"additional","affiliation":[]},{"given":"Milton","family":"Severo","sequence":"additional","affiliation":[]},{"given":"Isabel","family":"Vit\u00f3","sequence":"additional","affiliation":[{"name":"Department of Pathology, Hospital S. Jo\u00e3o, Porto, Portugal"}]},{"given":"Xiaogang","family":"Wen","sequence":"additional","affiliation":[]},{"given":"F\u00e1tima","family":"Carneiro","sequence":"additional","affiliation":[]},{"given":"Pedro","family":"Gomes","sequence":"additional","affiliation":[{"name":"Faculty of Medicine, Department of Pharmacology and Therapeutics, University of Porto, Porto, Portugal"}]},{"given":"Ros\u00e1rio","family":"Monteiro","sequence":"additional","affiliation":[]},{"ORCID":"https:\/\/orcid.org\/0000-0002-3560-3261","authenticated-orcid":false,"given":"Maria J.","family":"Martins","sequence":"additional","affiliation":[]}],"member":"374","published-online":{"date-parts":[[2016,1,7]]},"reference":[{"key":"2025121207161921882_j_hmbci-2015-0033_ref_001_w2aab3b8c11b1b7b1ab2b2b1Aa","doi-asserted-by":"crossref","unstructured":"Alberti KG, Eckel RH, Grundy SM, Zimmet PZ, Cleeman JI, Donato KA, Fruchart JC, James WP, Loria CM, Smith SC, Jr. Harmonizing the metabolic syndrome: a joint interim statement of the International Diabetes Federation Task Force on Epidemiology and Prevention; National Heart, Lung, and Blood Institute; American Heart Association; World Heart Federation; International Atherosclerosis Society; and International Association for the Study of Obesity. 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