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Carbohydrate supplementation
Published in Jay R Hoffman, Dietary Supplementation in Sport and Exercise, 2019
Parker N Hyde, Richard A LaFountain, Carl M Maresh
As mentioned previously, glucose consumption and oxidation rates are limited by uptake in the small intestine by the SGLT1 transporters. In order to facilitate greater rates of oxidation for exogenous carbohydrate supplements, a heterogenous form is now, by in large, the preferred method. The concept of MTC largely championed by Asker Jeukendrup and colleagues involves the addition of fructose to the carbohydrate containing supplement. Fructose uses the GLUT5 transporter and is able to help overcome rate limiting transport. When using a glucose + fructose carbohydrate oxidation rates can reach ~1.3–1.5 g/min (9, 37, 38).
The Physiology of Digestion, Absorption, and Metabolism in the Human Intestine
Published in Victor R. Preedy, Ronald R. Watson, Alcohol and the Gastrointestinal Tract, 2017
Glucose transport occurs via a Na+-linked transporter SGLT1, a tetrameric protein with 73,000 Da subunits which is unrelated to the GLUT family of glucose transporters.103 It is very closely related to the glucose transporter in the renal tubular brush-border membrane104 and their kinetic and biochemical properties are reviewed elsewhere.105 Expression of this transporter can be upregulated by luminal glucose concentrations, which is the nutrient load.106 In contrast, uptake of fructose occurs by a distinct transporter, GLUT5 (Table 6.2), which provides a carrier-mediated system which is not inhibited by phloridzin or metabolic inhibitors.107 A second component is electrogenic and can be inhibited by phloridzin, a specific inhibitor of the Na+-glucose cotransporter,108
Fatty Liver Disease
Published in David Heber, Zhaoping Li, Primary Care Nutrition, 2017
Fructose is an isomer of glucose (Stanhope and Havel 2010) but is metabolized very differently from glucose. Recent decades have witnessed an enormous rise in fructose consumption. Studies on ancient diets have shown that at the dawn of agriculture 8500 years ago, the intake of fructose per capita was around 2 kg/year from fruits and vegetables. The industrialization of sugar production from plantations in the seventeenth century converted a rare spice from the Orient into an expensive staple item used in baked goods and candies. Significant increases in consumption occurred following the abolition of sugar taxes in the 1870s. By 1950, annual consumption had increased to 45 kg/person/year, and by 1997, nearly 20 years after the introduction of high-fructose corn syrup into the food supply, consumption had risen to 69 kg/year (Lim et al. 2010; Lustig 2010). Fructose is used in a wide variety of food products due to its sweeter taste and its lack of inhibition of satiety compared with other sugars (Lustig 2010). From a metabolic standpoint, fructose is absorbed by the small intestine and is transported across the epithelial barrier into cells and the bloodstream by the fructose-specific GLUT5 transporter (Tappy et al. 2010). Entry of fructose into cells is not insulin dependent and does not promote insulin secretion, unlike glucose. Absorbed fructose is transported in plasma via the hepatic portal vein to the liver, where fructose is predominantly metabolized via its phosphorylation; only a small amount of fructose is metabolized by hexokinase in muscle and adipose tissue (Lim et al. 2010; Lustig 2010).
Lactobacillus plantarum improves lipogenesis and IRS-1/AKT/eNOS signalling pathway in the liver of high-fructose-fed rats
Published in Archives of Physiology and Biochemistry, 2022
Esra Sumlu, Aykut Bostancı, Gökhan Sadi, Mehmet Eray Alçığır, Fatma Akar
It is widely accepted that fructose is absorbed in the small intestine via GLUT5 and GLUT2 transporters and delivered to peripheral organs including the liver. Previously, it was reported that high intake of fructose increased the expressions of GLUT5 and GLUT2 in the jejunum of rats, thus supplying excess intestinal absorption of the monosaccharide (Kishi et al.1999). In previous studies, hepatic expression of GLUT2 and GLUT5 was also found to be increased in high consumption of fructose in rats (Alwahsh 2014, Narasimhan et al.2015). Fructose enters into the liver cells via mainly GLUT2 transporter and induces lipogenic genes to produce triglyceride synthesis (Sakar et al.2009). Further supporting above data, we found that GLUT5 and GLUT2 were expressed at high levels in the liver of high-fructose-fed rats implying excess fructose uptake by liver. Overall, hepatic insulin resistance may lead to a compensatory increase in fructose transporters thus supplying substrate abundance for overproduction of triglyceride by the hepatic tissue.
Antioxidant and Anti-Diabetic Functions of a Polyphenol-Rich Sugarcane Extract
Published in Journal of the American College of Nutrition, 2019
Jin Ji, Xin Yang, Matthew Flavel, Zenaida P.-I. Shields, Barry Kitchen
Overall, fructose uptake study results shown in Figure 2 indicate that PRSE induced moderate inhibition of fructose uptake (IC50 of 4.468 mg/mL). Fructose uptake mainly takes place through GLUT2 and GLUT5, two facilitative glucose transporters. Previous studies indicated that GLUT5 is responsible for most of luminal fructose uptake, while GLUT2 is particularly important postprandially when a high amount of fructose is ingested (7). The two facilitative fructose transporters, GLUT2 and GLUT5, have been studied actively as therapeutic targets for polyphenols (24). To explore the pathway(s) where PRSE interferes with fructose uptake, we further studied the impact of PRSE on the expression of GLUT2 and GLUT5. Results indicate that PRSE inhibited cellular production of GLUT2, a major fructose transporter, while at the same time, increased the expression of GLUT5, another transporter that is unique to fructose transport and uptake. In the meantime, treatment of Caco-2 cells with quercetin, a plant polyphenol, inhibited both GLUT2 and GLUT5 expression in a concentration-dependent manner.
Cow milk protein allergy and other common food allergies and intolerances
Published in Paediatrics and International Child Health, 2019
Wiparat Manuyakorn, Pornthep Tanpowpong
Fructose is a monosaccharide found in fruits and often added as high-fructose corn syrup in food processing worldwide [58]. It can be absorbed without further enzymatic breakdown. Two main small intestinal transporters are GLUT2 and GLUT5. GLUT2 is responsible for absorption via the glucose-dependent co-transporter, while GLUT5 uses facilitated diffusion [59]. Excess intraluminal fructose in the small bowel causes effects and symptoms similar to those of lactose, but when fructose is given as sucrose (i.e. a disaccharide with glucose and fructose), the absorptive capacity is greatly improved [60]. The prevalence of fructose intolerance in the general population remains unknown. A breath test can also be used to define fructose maldigestion/intolerance.