Advances in technology in the 1960s made possible the production of inexpensive high-fructose syrups from corn starch.
When ingested by humans, fructose is absorbed by an active transport system but at a slower rate than is glucose. Coingestion of glucose increases intestinal absorptive capacity for fructose.
The metabolism of dietary fructose to yield energy is known as fructolysis. The process of fructolysis utilizes most of the same enzymes and metabolic intermediates as the glycolysis pathway.
Fructose utilization in humans and animals occurs mainly in the liver, kidney, and small intestine. Unlike glucose, fructose can enter muscle cells and adipocytes in the absence of insulin by using facilitative glucose transport proteins (GLUT).
Fructose metabolizes predominantly in the liver. It directs toward the replenishment of liver glycogen and the synthesis of triglycerides. A high flux of fructose to the liver, the main organ capable of metabolizing this simple carbohydrate, perturbs glucose metabolism and glucose uptake pathways, and leads to a significantly enhanced rate of de novo lipogenesis and triglyceride synthesis.
A high intake of fructose also will increase the body fat. Excess fructose consumption increasingly influences the global epidemics of diabetes mellitus, obesity, and the associated cardiometabolic risks.
Fructose metabolism in human body
