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Epidemiologic and Mechanistic Studies of Sucrose and Fructose in Beverages and Their Relation to Obesity and Cardiovascular Risk
Published in Nathalie Bergeron, Patty W. Siri-Tarino, George A. Bray, Ronald M. Krauss, Nutrition and Cardiometabolic Health, 2017
George A. Bray, Nathalie Bergeron, Patty W. Siri-Tarino, Ronald M. Krauss
Fructose also has interesting effects at the cellular level by inducing inflammatory markers in human kidney cells (Cirillo et al. 2009). Incubation of HK-2 (human kidney cells) with fructose increases monocyte chemotactic protein-1. Knock-down of ketohexokinase, the enzyme that phosphorylates fructose, blocks this effect as do antioxidants. Fructose also increased intracellular uric acid (Johnson et al. 2010).
The effect of evening primrose oil (Oenothera biennis) on the level of adiponectin and some biochemical parameters in rats with fructose induced metabolic syndrome
Published in Archives of Physiology and Biochemistry, 2022
Handan Mert, Kıvanç İrak, Salih Çibuk, Serkan Yıldırım, Nihat Mert
Liver in metabolic syndrome caused by a fructose diet; it is the organ that is most affected and damaged by the metabolic changes that occur due to its function in fructose metabolism and its function in carbohydrate and lipid metabolism (Grattagliano et al.2008, Bagul et al.2012). Fructose is highly lipogenic, stimulates triglyceride synthesis, and increases fat storage in the liver through increased diacylglycerol and fatty acyl-coenzyme A (Arslan and Şanlıer 2016). It has been shown that fructose-induced lipogenesis, dyslipidemia, and hepatosteatosis are linked to the fructose metabolism in the liver by ketohexokinase (Marek et al. 2015). Fructose consumption causes the accumulation of visceral fat (Jürgens et al.2005). Although hepatosteatosis contributes to the development of insulin resistance, the molecular mechanism underlying other stress mechanisms is low-grade inflammation in visceral adipose tissue and imbalance in the production of beneficial adipokines with proinflammatory cytokines (Marek et al.2015). In this study, the liver weight of the fructose group was found to be heavier than the control and fructose + EPO group at the end of the trial (Table 1) and Al-Rasheed et al. (2016) consistent with the findings of. Our histopathological data also supports these findings (Figure 1(C)).
Emerging therapeutic targets for NASH: key innovations at the preclinical level
Published in Expert Opinion on Therapeutic Targets, 2020
Sugars are the primary substrate source for DNL, and increased fructose consumption in particular has been linked to the development of the metabolic syndrome and progression to NASH [29–31]. Ketohexokinase is the first and rate-limiting enzyme in the glycolytic breakdown of fructose into Acetyl-CoA [18] and mice deficient in ketohexokinase are protected from metabolic syndrome and also show reduced liver weight compared to wild-type animals [32,33]. Fructose is not only fueling DNL [34] but also negatively regulates fatty acid oxidation by inhibition of carnitine-palmitoyl-transferase 1 (CPT1) activity, suppression of mitochondrial function and post-translational modification of mitochondrial proteins [33] – all changes which are abolished upon knockout of ketohexokinase. As the deficiency of ketohexokinase in humans causes essential fructosuria, a harmless and asymptomatic disease [35], the pharmacologic inhibition of ketohexokinase might be a safe approach in treating NAFLD and NASH. Although no data are publically available on liver inflammation, fibrosis or hepatocarcinogenesis in pre-clincal models of NASH upon targeting of ketohexokinase, one ketohexokinase inhibitor, PF-06835919, has already entered early clinical testing for NASH (NCT03969719) and preliminary results recently suggested decreased liver fat and a trend for improved metabolic function [36].
Bioactive constituents of Salvia przewalskii and the molecular mechanism of its antihypoxia effects determined using quantitative proteomics
Published in Pharmaceutical Biology, 2020
Yafeng Wang, Delong Duo, Yingjun Yan, Rongyue He, Shengbiao Wang, Aixia Wang, Xinan Wu
Differential proteomic results showed the downregulation of Khk and Aldob, proteins related to fructose metabolism. Fructose is a natural monosaccharide broadly used in modern society. Fructose is absorbed via two major facilitative glucose transporters: GLUT5 and GLUT2 (Pan and Kong 2018). Fructose metabolism requires the coordinated action of 2 enzymes, ketohexokinase (Khk), which phosphorylates fructose to form fructose 1-phosphate (Fru1-P), and aldolase B, which splits Fru1-P into dihydroxyacetone phosphate and glyceraldehydes (Lanaspa et al. 2018), thereby producing substrates for fatty acid synthesis. Fructose bypasses glycolysis, and fructose is utilised much faster than glucose in de novo lipogenesis (Samuel 2011); thus, the excessive intake of fructose is closely associated with metabolic diseases such as diabetes and obesity (Walker and Goran 2015). Therefore, the repression of fructose-induced fatty liver is a key strategy for the prevention of these metabolic diseases. In this report, through the use of comparative proteomics, we demonstrate that SPM inhibited fructose metabolism via the downregulation of Khk and Aldob protein expression to prevent the lung injury associated with hypobaric hypoxia.