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(NaturalNews) A chemical naturally found in grapefruit may help prevent the physiological changes that produce the condition known as metabolic syndrome, a major risk factor for cardiovascular disease and Type 2 diabetes, a new study has found.
Metabolic syndrome refers to a cluster of symptoms including high blood pressure, central obesity high triglycerides, low HDL ("good") cholesterol, and high levels of blood sugar between meals.
A handful of prior studies have previously suggested that some component or mix of components in grapefruit might be helpful to the body in regulating blood fats and sugars. One study, published in the Journal of Agricultural and Food Chemistry, found that people who ate one red grapefruit each day might reduce their cholesterol levels by 15 percent and their triglycerides by 17 percent. Both lab studies and experiments in humans suggested that the grapefruit might also act through other channels in the body to reduce the risk of heart disease.
Another study, conducted by researchers from the University of Western Ontario found that the flavonoid naringenin, which occurs naturally in grapefruit, might perform a role similar to the sugar-regulating hormone insulin. The laboratory experiment found that naringenin appeared to stop the liver from secreting very low-density lipoproteins, thereby lowering the levels of certain triglycerides in the blood. In theory, this means that naringenin might be able to compensate for the effects of insulin resistance, a characteristic of both metabolic syndrome and Type 2 diabetes.
In the newest study, published in the journal Diabetes, the same team of researchers conducted a follow-up to the naringenin study using live mice instead of laboratory cultures. First, the researchers specifically bred mice to have a deficiency in low-density lipoprotein (LDL) receptors in their livers. Because LDLs carry cholesterol, a receptor deficiency causes blood levels of cholesterol to stay high. When such mice are fed a high-fat diet (with 42 percent of its calories from fat), they quickly develop obesity and other symptoms characteristic of human metabolic syndrome.
At eight to 12 weeks of age, the modified mice were separated into four groups: one fed a normal diet, one fed a high-fat diet, one fed a high-fat diet plus 1 percent naringenin, and the last fed a high-fat diet plus 3 percent naringenin. After four weeks, the mice fed the high-fat diet alone developed obesity, insulin resistance, reduced glucose tolerance and increased levels of liver lipids, all characteristic of metabolic syndrome. Those fed a high-fat diet plus naringenin, however, maintained a normal weight, had normal levels of cholesterol, triglycerides and insulin sensitivity, and retained normal glucose metabolism.
"The marked obesity that develops in [mice fed a high fat diet] was completely prevented by naringenin," lead researcher Murray Huff said.
The researchers then repeated the experiment in unmodified mice. After 30 weeks, normal mice also developed obesity and symptoms of metabolic syndrome, except when their diet was supplemented with 3 percent naringenin.
Naringenin did not appear to act by suppressing appetite, as mice in all the high-fat groups at the same amount of food. Instead, it caused the liver to burn excess fat rather than store it, decreased the ability of liver cells to make cholesterol and reduced levels of insulin.
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