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Fructose Consumption and Leptin Resistance: What Have We Learnt From Animal Studies? pp. 209-230 $100.00
Authors:  Marta Alegret, Núria Roglans, Juan C. Laguna Pharmacology Unit, School of Pharmacy, University of Barcelona, IBUB (Institute of Biomedicine of the University of Barcelona), and CIBERobn (CIBER Obesity and Nutrition)
In recent decades human population has markedly increased consumption of hypercaloric diets enriched in saturated fats and simple sugars, such as fructose. High fructose intake in humans increases body weight, plasma lipids and fat tissue mass. Furthermore, a high intake of energy from fructose-sweetened beverages seems to increase the risk of type 2 diabetes mellitus and cardiovascular diseases. The rat is a good model for the study of fructose metabolism in humans. Several animal species transform a substantial part of ingested fructose into glucose, a situation that does not occur in rats and humans. Solid diets that contain 50-60% of calories as fructose induce hypertriglyceridemia and a marked state of insulin resistance. Diets that incorporate lower fructose concentrations in drinking water (10 % weight/volume) induce hypertriglyceridemia and fatty liver in a short period of time (from days to two weeks), but they take far longer to induce insulin resistance. The administration of fructose in liquid form to rats mimics the human pattern of fructose consumption, with daily fructose intake equivalent to that found in the upper quartile of fructose consumption in human populations. By using this model, we have shown that the appearance of hypertriglyceridemia and liver steatosis is exclusive to rats supplemented with fructose, and is absent in rats supplemented with glucose, even though they consumed exactly the same amount of liquid diet. Fructose, but not glucose, simultaneously induced: an increase in the expression and activity of the transcription factor carbohydrate response element binding protein, which controls the expression of lipogenic enzymes; and a reduction in the hepatic activity of the fatty acid -oxidation system, which is related to reduced expression and transcriptional activity of the peroxisome proliferator activated receptor  (PPAR. Fructose administration to healthy young men increases plasma leptin concentrations. Leptin is an adipocytokine that can activate PPARand increase fatty acid -oxidation activity through activation by phosphorylation of the transcription factor signal transducer and activator of transcription-3 (STAT-3). 

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Fructose Consumption and Leptin Resistance: What Have We Learnt From Animal Studies? pp. 209-230