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Nonalcoholic Fatty Liver Disease
Published in Nicole M. Farmer, Andres Victor Ardisson Korat, Cooking for Health and Disease Prevention, 2022
In addition to fructokinase, a second mechanism by which fructose may contribute to NAFLD is that fructose metabolism may raise uric acid levels (Lanaspa et al. 2012). Foods high in fructose can increase uric acid levels in the liver, increasing oxidative stress, which may lead to gout, kidney disease, and metabolic disease. Uric acid levels are a predictor of NAFLD. Reducing the amount of fructose has shown to reduce uric acid levels and the impact on the body (Jensen et al. 2018).
Effects and Mechanisms of Fructose-Containing Sugars in the Pathophysiology of Metabolic Syndrome
Published in Nathalie Bergeron, Patty W. Siri-Tarino, George A. Bray, Ronald M. Krauss, Nutrition and Cardiometabolic Health, 2017
Kimber L. Stanhope, Peter J. Havel, Nathalie Bergeron, Patty W. Siri-Tarino, George A. Bray, Ronald M. Krauss
Hepatic glucose metabolism is regulated by insulin and hepatic energy needs, and this allows most of the ingested glucose, from starch or a glucose-sweetened beverage, arriving via the portal vein to bypass the liver and reach the systemic circulation. In contrast, the initial phosphorylation of dietary fructose is largely catalyzed by fructokinase, which is not regulated by hepatic energy status (Mayes 1993, Havel 2005). This results in unregulated fructose uptake by the liver, with most of the ingested fructose being metabolized in the liver and very little reaching the systemic circulation (Teff et al. 2009). The excess substrate generated from the unregulated metabolism of fructose in the liver leads to increased DNL (Stanhope et al. 2009). Recent evidence from the research group of Schwarz and colleagues demonstrates that fructose consumption can increase DNL more than isocaloric complex carbohydrates even in subjects consuming energy-balanced, weight-maintaining diets (Schwarz et al. 2015).
Fatty Liver Disease
Published in David Heber, Zhaoping Li, Primary Care Nutrition, 2017
Continuous fructose ingestion may impose a metabolic burden on the liver through the induction of fructokinase and fatty acid synthase. In the liver, fructose is metabolized to fructose-1-phosphate by fructokinase, which consumes ATP (Lim et al. 2010; Lustig 2010). As a consequence, a massive incorporation of fructose into liver metabolism can lead to high levels of metabolic stress via ATP depletion. In an experimental study in the rat (Koo et al. 2008), it was shown that fructose-induced fructokinase hyperexpression in the liver can be reduced (by 0.6-fold) by the hydroxymethyl-glutaryl-coenzyme A reductase inhibitor atorvastatin. Of note, clinical studies have shown that atorvastatin can improve liver injury in NAFLD patients with hyperlipidemia (Teff et al. 2004; Lê and Tappy 2006). Fatty acid synthase catalyzes the last step in the fatty acid biosynthetic pathway and is a key determinant of the maximal capacity of the liver to synthesize fatty acids by de novo lipogenesis (D’Angelo et al. 2005). In a clinical study, increased fructose consumption in patients with NAFLD was associated with hyperexpression of hepatic mRNA for fatty acid synthase, suggesting that this molecular derangement could play a crucial role in fructose-induced fatty liver infiltration (Ackerman et al. 2005).
Camel milk protein hydrosylate alleviates hepatic steatosis and hypertension in high fructose-fed rats
Published in Pharmaceutical Biology, 2022
Mohammad A. Alshuniaber, Ghedeir M. Alshammari, Samy M. Eleawa, Abu ElGasim A. Yagoub, Abdullrahman S. Al-Khalifah, Maha H. Alhussain, Laila Naif Al-Harbi, Mohammed Abdo Yahya
The salient findings of this study showed that short-term administration of CMH attenuates HF-rich diet-induced hyperglycaemia, hyperlipidaemia, IR, and hepatic steatosis in rats, an effect that is greater than that afforded by ICM. According, several mechanisms of protection are reported, including 1) hypoglycaemic and insulin-sensitizing effects, 2) suppressing the hepatic fructokinase C and the subsequent production of uric acid, 3) upregulating hepatic antioxidants, and 4) activating AMPK and subsequent downregulation of the sterol regulatory element-binding proteins 1 and 2 (SREBP1/2 and upregulation of the transcription factor the peroxisome proliferator-activated receptor α (PPARα), and 5) inhibiting ANG II synthesis and ACE activation. To the best of our knowledge, these data are the first to mechanistically explain such protective effects afforded by CMH in metabolically impaired animals. A summary of these effects is shown in the graphical abstract (Figure 6).
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
Although fructose has the same molecular formula and mass as glucose, it is processed physiologically differently. Insulin is not required for the entry of fructose into the cell. Phosphorylation of fructose to fructose-1-phosphate occurs under the action of fructokinase, leading to the formation of two pentoses, dihydroxyacetone, and glyceraldehyde. This enzyme is not regulatory and therefore can stimulate lipogenesis (Ramos et al.2017). In this study, the live weight of the rats that received fructose for 57 days was significantly higher than the control group. This weight gain in fructose groups was compatible with other studies (Barros et al.2007, Ramos et al.2017, Bellamkonda et al.2018). The increase in body weight of the fructose + EPO group compared to the control group may be a result of combined fructose and oil. While the food consumption of fructose groups was significantly lower than the control group, the consumption of fructose-containing water was significantly higher than the control group. These findings are consistent with the study of Ramos et al. (2017).
Detrimental effects of fructose on mitochondria in mouse motor neurons and on C. elegans healthspan
Published in Nutritional Neuroscience, 2022
Divya Lodha, Sudarshana Rajasekaran, Tamilselvan Jayavelu, Jamuna R. Subramaniam
Fructose is metabolized with the help of fructokinase largely in hepatocytes and converted to fructose-1-phosphate. This is then utilized to produce lactate and converted to uric acid or pyruvate which is used by the citric acid cycle to produce energy26. It is also utilized for gluconeogenesis and stored as glycogen in the liver to be used as glucose when necessary. Unlike glucose metabolism or glycolysis, which is tightly regulated by the rate-limiting enzyme phosphofructokinase and depends on the concentration of glucose for metabolism, Fructolysis is regulated loosely by fructokinase and continues till fructose is fully consumed27. This leads to mitochondrial stress (ROS production) which usually precedes dysfunction eventually leading to cell death28. But how fructose affects neurons and its severity of mitochondrial impairment and healthspan of an organism is not understood.