Ingestion of a natural mineral rich water in an animal model of metabolic syndrome: effects in insulin signalling and endoplasmic reticulum stress
Abstract Background: 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 IRE1a)(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 eIF2a (tendency) and total IRS1 (tendency) decreased in both fructose fed groups. p ERK/ERK and total IRE1a 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 IRE1a activation, and increased unspliced XBP1 and lipid area may protect against oxidative stress and IR development in FRUCTMIN.
Hormone molecular biology and clinical investigation