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Carbohydrates
Published in Geoffrey P. Webb, Nutrition, 2019
Fructose from fruits, vegetables, sucrose and high-fructose corn syrups may provide as much as 10% of the calories in some Western diets. Most of the dietary fructose is metabolised in the liver where it is converted to fructose-1-phosphate and then this is split by a specific aldolase into two three-carbon sugars which can enter the glycolytic pathway as glyceraldehyde-3-phosphate. Unlike glucose, fructose does not stimulate insulin release and is absorbed more slowly than glucose from the small intestine. Dietary galactose is converted to glucose-1-phosphate by a four-reaction pathway and then enters the glycolytic sequence.
Carbohydrate and glycosylation disorders
Published in Steve Hannigan, Inherited Metabolic Diseases: A Guide to 100 Conditions, 2018
Hereditary fructose intolerance is an inherited disorder that is characterised by the inability to digest fructose (a natural fruit sugar used in foods, including many baby foods) or sucrose (cane sugar or brown sugar). This intolerance is due to a deiciency of an enzyme known as fructose-1-phosphate aldolase, which results in a build-up of fructose-1-phosphate in the kidney, liver and small intestine. The gene responsible for this disorder is located on the long arm of chromosome 9.
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).
Glucokinase as an emerging anti-diabetes target and recent progress in the development of its agonists
Published in Journal of Enzyme Inhibition and Medicinal Chemistry, 2022
Yixin Ren, Li Li, Li Wan, Yan Huang, Shuang Cao
GK, located in liver cells, mainly plays a role in regulating the glycogen content in the liver. Insulin and glucagon can trigger the transport of GK by glucose transporters, altering the amount of GK in the cytoplasm of hepatocytes and controlling the intracellular glucose content (Figure 5)11. In the liver, GK controls blood sugar by converting glucose to liver sugar; hence, the activity of GK directly determines the glucose conversion rate. GK regulatory protein (GKRP) is a polypeptide (molecular weight: 68 kDa) that only exists in mammalian liver. It can competitively bind GK with glucose, prevent GK from catalysing the process of glucose phosphorylation to glucose 6-phosphate, and regulate GK activity in liver cells12. Under hypoglycaemic conditions, GK forms a complex with GKRP (GK–GKRP complex) that aggregates in the nucleus. Following an increase in glucose levels, GKRP is replaced by glucose, the GK–GKRP complex is dissociated, and the levels of GK in the cytoplasm are markedly increased, thereby leading to an increase in GK activity13. In mammals, the content of the GK–GKRP complex is affected by the levels of glucose, activated by fructose 6-phosphate, and inhibited by fructose 1-phosphate14–16.
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.