Abstract
Fructose-sweetened liquid consumption is associated with fatty liver and oxidative stress. In rodent models of fructose-mediated fatty liver, protein consumption is decreased. Additionally, decreased sulfur amino acid intake is known to cause oxidative stress. Studies were designed to test whether oxidative stress in fructose-sweetened liquid-induced fatty liver is caused by decreased ad libitum solid food intake with associated inadequate sulfur amino acid intake. C57BL6 mice were grouped as: control (ad libitum water), fructose (ad libitum 30% fructose-sweetened liquid), glucose (ad libitum 30% glucose-sweetened water) and pair-fed (ad libitum water and sulfur amino acid intake same as the fructose group). Hepatic and plasma thiol-disulfide antioxidant status were analyzed after five weeks. Fructose- and glucose-fed mice developed fatty liver. The mitochondrial antioxidant protein, thioredoxin-2, displayed decreased abundance in the liver of fructose and glucose-fed mice compared to controls. Glutathione/glutathione disulfide redox potential (EhGSSG) and abundance of the cytoplasmic antioxidant protein, peroxiredoxin-2, were similar among groups. We conclude that both fructose and glucose-sweetened liquid consumption results in fatty liver and upregulated thioredoxin-2 expression, consistent with mitochondrial oxidative stress; however, inadequate sulfur amino acid intake was not the cause of this oxidative stress.
Highlights
Consumption of refined sugars has increased over the past decades [1,2] and fructose, in particular, has been implicated as a contributing factor in the development of metabolic diseases [3]
The results show that fructose- or glucose-induced fatty liver is not an artefact due to oxidative stress caused by insufficient protein intake
Results from fructose-fed mice confirmed fatty liver; samples from glucose-treated mice were not available, but glucose-induced fatty liver has been previously established [29,51] and confirmed in the present study by the TG measurements. These data show that both fructose and glucose cause fatty liver
Summary
Consumption of refined sugars has increased over the past decades [1,2] and fructose, in particular, has been implicated as a contributing factor in the development of metabolic diseases [3]. These diseases include conditions such as obesity, dyslipidemia, insulin resistance, diabetes, high blood pressure [4,5,6,7,8,9,10,11,12,13], and non-alcoholic fatty liver disease [14,15,16,17,18]. Inadequate ingestion of macronutrients and energy from solid foods may be important in the metabolic alterations attributed to fructose-sweetened beverages [20,37,38,39,40,41,42,43]
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