Abstract
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.
Highlights
Background &aims: Dietary sugars are absorbed in the hepatic portal circulation as glucose, fructose, or galactose
Fructose when ingested in small amounts is mainly metabolized to glucose and organic acids in the gut, and this organ may shield the liver from potentially deleterious effects
With chronically high fructose intake, enterocyte can switch to lipid synthesis and accumulation of triglyceride, possibly causing an enterocyte dysfunction
Summary
Several small scales clinical trials, reviewed in an elegant metaanalysis, confirmed that replacing sucrose by fructose in the diet of healthy subjects and of patients with type 2 diabetes decreased average 24-h blood glucose concentration [29]. Other conventional tracer methods showed that the extrahepatic clearance of secreted VLDL-TG was lower after ingestion of a fructose than a glucose meal [26], further enhancing postprandial hypertriglyceridemia Another consequence of carbohydrate-induced de novo lipogenesis relates to non-alcoholic fatty liver disease. It became rapidly apparent that non-alcoholic fatty liver diseases, which start with a deposition of intrahepatic fat within hepatocytes, and proceeds to hepatic steatosis, non-alcoholic steatohepatitis, cirrhosis, and eventually hepatocarcinoma, were highly prevalent in the population [42] It was observed, using magnetic resonance spectroscopy to noninvasively assess intrahepatic fat concentrations, that consumption of a high fructose diet was associated within a few days to significant increases in intrahepatic fat content in healthy subjects [32]. This effect was subsequently shown not to be restricted to fructose, since it was observed with fructose and glucose when energy intake exceeded actual energy needs [43]
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