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e transported from the mitochondria into the cytosol of hepatocytes, converted to acetyl CoA<br />
by citrate lyase and directed toward fatty acid synthesis. Additionally, DHAP can be converted to<br />
glycerol 3-phosphate as previously mentioned, providing the glycerol backbone for the triglyceride<br />
molecule. Triglycerides are incorporated into very low density lipoproteins (VLDL), which are<br />
released from the liver destined toward peripheral tissues for storage in both fat and muscle cells.<br />
Metabolic syndromes<br />
Excess processed fructose consumption has been hypothesized to be a cause of insulin resistance,<br />
obesity, elevated LDL cholesterol and triglycerides, leading to metabolic syndrome. <strong>Fructose</strong><br />
consumption has been shown to be correlated with obesity, especially central obesity which is<br />
thought to be the most dangerous kind of obesity. A study in mice showed that a high fructose<br />
intake increases adiposity.<br />
Although all simple sugars have nearly identical chemical formulae, each has distinct chemical<br />
properties. This can be illustrated with pure fructose. A journal article reports that, "...fructose<br />
given alone increased the blood glucose almost as much as a similar amount of glucose (78% of<br />
the glucose-alone area)".<br />
One study concluded that processed high fructose corn syrup "produced significantly higher fasting<br />
plasma triacylglycerol values than did the glucose diet in men" and "...if plasma triacylglycerols are<br />
a risk factor for cardiovascular disease, then diets high in processed fructose may be undesirable".<br />
Bantle et al. "noted the same effects in a study of 14 healthy volunteers who sequentially ate a<br />
high-fructose diet and one almost devoid of the sugar."<br />
<strong>Fructose</strong> is a reducing sugar, as are all monosaccharides. The spontaneous chemical reaction of<br />
simple sugar molecules to proteins, known as glycation, is thought to be a significant cause of<br />
damage in diabetics. <strong>Fructose</strong> appears to be equivalent to glucose in this regard and so does not<br />
seem to be a better answer for diabetes for this reason alone, save for the smaller quantities<br />
required to achieve equivalent sweetness in some foods. This may be an important contribution<br />
to senescence and many age-related chronic diseases.<br />
Health effects<br />
Figure 7: Metabolic conversion of fructose to triglyceride in the liver.<br />
Digestive problems<br />
<strong>Fructose</strong> absorption occurs via the GLUT-5 (fructose only) transporter, and the GLUT2 transporter,<br />
for which it competes with glucose and galactose. A deficiency of GLUT 5 may result in excess<br />
fructose carried into the lower intestine.[citation needed] There, it can provide nutrients for the<br />
existing gut flora, which produce gas. It may also cause water retention in the intestine. These<br />
effects may lead to bloating, excessive flatulence, loose stools, and even diarrhea depending on<br />
the amounts eaten and other factors. For many people, fructose malabsorption is a major health<br />
concern.<br />
Compared to sucrose<br />
Studies that have compared high-fructose corn syrup (an ingredient in nearly all soft drinks sold<br />
in the US) to sucrose (common table sugar) find that most measured physiological effects are<br />
equivalent. For instance, Melanson et al. (2006), studied the effects of HFCS and sucrose sweetened<br />
drinks on blood glucose, insulin, leptin, and ghrelin levels. They found no significant differences in<br />
any of these parameters. This is not surprising, since sucrose is a disaccharide that digests to 50%<br />
fructose and 50% glucose, whereas the high-fructose corn syrup most commonly used on soft<br />
drinks is 55% fructose and 45% glucose. The difference between the two lies in the fact that HFCS<br />
contains little sucrose, the fructose and glucose being independent moieties.<br />
<strong>Fructose</strong> is often recommended for diabetics because it does not trigger the production of insulin<br />
by pancreatic ß cells, probably because ß cells have low levels of GLUT5. <strong>Fructose</strong> has a very low<br />
glycemic index of 19 ± 2, compared with 100 for glucose and 68 ± 5 for sucrose. <strong>Fructose</strong> is also<br />
seventy-three percent sweeter than sucrose (see 2.1 Relative Sweetness) at room temperature, so<br />
diabetics can use less of it. Studies show that fructose consumed before a meal may even lessen<br />
the glycemic response of the meal. Its sweetness changes at higher temperatures, so its effects in<br />
recipes are not equivalent to those of sucrose (i.e., table sugar).[citation needed]<br />
Liver disease<br />
"The medical profession thinks fructose is better for diabetics than sugar," says Meira Field, Ph.D.,<br />
a research chemist at United States Department of Agriculture, "but every cell in the body can<br />
metabolize glucose. However, all fructose must be metabolized in the liver. The livers of the rats<br />
on the high fructose diet looked like the livers of alcoholics, plugged with fat and cirrhotic." While<br />
a few other tissues (e.g., sperm cells and some intestinal cells) do use fructose directly, fructose is<br />
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