Metabolism of sugars: A window to the regulation of glucose and lipid homeostasis by splanchnic organs.
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- doi: 10.1016/j.clnu.2020.12.022
- issn: 0261-5614
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info:eu-repo/semantics/altIdentifier/urn/urn:nbn:ch:serval-BIB_F024B328D29D7
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L. Tappy, « Metabolism of sugars: A window to the regulation of glucose and lipid homeostasis by splanchnic organs. », Serveur académique Lausannois, ID : 10.1016/j.clnu.2020.12.022
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Dietary sugars are absorbed in the hepatic portal circulation as glucose, fructose, or galactose. The gut and liver are required to process fructose and galactose into glucose, lactate, and fatty acids. A high sugar intake may favor the development of cardio-metabolic diseases by inducing Insulin resistance and increased concentrations of triglyceride-rich lipoproteins. A narrative review of the literature regarding the metabolic effects of fructose-containing sugars. Sugars' metabolic effects differ from those of starch mainly due to the fructose component of sucrose. Fructose is metabolized in a set of fructolytic cells, which comprise small bowel enterocytes, hepatocytes, and kidney proximal tubule cells. Compared to glucose, fructose is readily metabolized in an insulin-independent way, even in subjects with diabetes mellitus, and produces minor increases in glycemia. It can be efficiently used for energy production, including during exercise. Unlike commonly thought, fructose when ingested in small amounts is mainly metabolized to glucose and organic acids in the gut, and this organ may thus shield the liver from potentially deleterious effects. The metabolic functions of splanchnic organs must be performed with homeostatic constraints to avoid exaggerated blood glucose and lipid concentrations, and thus to prevent cellular damages leading to non-communicable diseases. Excess fructose intake can impair insulin-induced suppression of glucose production, stimulate de novo lipogenesis, and increase intrahepatic and blood triglyceride concentrations. With chronically high fructose intake, enterocyte can switch to lipid synthesis and accumulation of triglyceride, possibly causing an enterocyte dysfunction.