Let's take a look at the most important properties of Fructose from this amazing study and literature survey presented in this study:
I will summarize the most important findings from this paper, trying to simplify the language to make it easier to understand.
Fructose is a simple sugar found in honey, fruit, table sugar (sucrose), and high-fructose corn syrup (HFCS).
Fructose intake has quadrupled since the early 1900s, primarily in the past 30 years in part because of the introduction of high fructose corn syrup.
Fructose can induce most features of the metabolic syndrome, including insulin resistance, elevated triglycerides, abdominal obesity, elevated blood pressure, inflammation, oxidative stress, endothelial dysfunction, microvascular disease, hyperuricemia, glomerular hypertension and renal injury, and fatty liver.
These effects are not seen in animals pair-fed glucose or starch, which suggests that the mechanism is not mediated by excessive caloric intake.
The consumption of large amounts of dietary fructose also can rapidly induce insulin resistance, postprandial hypertriglyceridemia, and blood pressure in humans more than starch (or glucose). Moreover, it is a potential risk factor for fatty liver disease (7).
Fructose causes metabolic syndrome because of its unique metabolism that results in intracellular ATP depletion, uric acid generation, endothelial dysfunction, oxidative stress, and lipogenesis.
Fructose uniquely up-regulates its own transporter (Glut5) and metabolism (fructokinase), and, thereby, the more fructose one eats, the more sensitive one becomes to its effects. This is a potential explanation for the fact that obese persons appear to be more sensitive to the lipogenic effects of acute fructose ingestion than are non-obese persons.
Fructose consumption is associated with weight gain, but, as Livesey and Taylor discuss, that association has not been consistently shown in short-term clinical trials. Nevertheless, fructose does not appear to trigger the endocrine signals involved in the long-term control of energy balance to the same extent as does glucose.
Ingestion of glucose stimulates insulin secretion, which also results in the release of leptin by adipocytes and the inhibition of ghrelin secretion from the gastrointestinal tract, and these alterations stimulate centers in the brain that regulate satiety and energy homeostasis.
However, fructose does not acutely stimulate insulin, which would lead to attenuated leptin and ghrelin responses. In one study, subjects fed fructose reported a greater appetite the following day than did glucose-fed controls.
Chronic administration of fructose also may result in leptin resistance. Once leptin resistance is developed, and one switches to high-fat high-energy diet, a greater energy intake and weight gain than starch-fed diet is expected.
Fructose does not acutely raise blood glucose. As such, fructose has a lower glycemic index than do starch-based foods, and it has been used as an energy source in diabetes patients because it may aid glycemic control.
In a small number of studies, HbA1c was lowered in subjects receiving fructose.
Whereas low doses of fructose may improve glucose control in diabetes patients, the effects of fructose in inducing features of metabolic syndrome, stimulating the production of advanced glycation end products, and causing cataracts in diabetic patients make fructose a poor choice for a diabetes patient.
The study proposes that it is the fructose content of sweeteners (sucrose and HFCS, which have a relatively high glycemic index due to the presence of glucose) that is largely responsible for correlation of the glycemic index with cardiovascular disease in persons without diabetes and that a better index for cardiovascular risk may be a fructose index based on the percentage and amount of fructose in various foods.
One of the central issues raised in the article by Livesey and Taylor is whether high doses of fructose (>50 g/d) are safe. They concluded that fructose intake up to 90 g/d may actually be beneficial because of its effects of lowering HbA1c concentrations, despite the potential countering effects of increases in plasma triglycerides. However, it is probably misleading to conclude that this amount of fructose consumption is safe by examining only the effects of fructose on plasma triglycerides, weight, and HbA1c.
There is increasing evidence that high fructose intake can also raise blood pressure, decrease insulin sensitivity, lower glucose tolerance, increase apolipoprotein-B concentrations, and cause microvascular disease, glomerular hypertension, renal injury, fatty liver, systemic inflammation, endothelial dysfunction, oxidative stress, and activation of the renin angiotensin system.