A new study by researchers at St. Michael's Hospital suggests that fructose may not be as bad for us as previously thought and that it may even provide some benefit.
"Over the last decade, there have been connections made between fructose intake and rates of obesity," said Dr. John Sievenpiper, a senior author of the study. "However, this research suggests that the problem is likely one of overconsumption, not fructose."
The study reviewed 18 trials with 209 participants who had Type 1 and 2 diabetes and found fructose significantly improved their blood sugar control. The improvement was equivalent to what can be achieved with an oral anti-diabetic drug.
Even more promising, Dr. Sievenpiper said, is that the researchers saw benefit even without adverse effects on body weight, blood pressure, uric acid (gout) or cholesterol.
Fructose, which is naturally found in fruit, vegetables and honey, is a simple sugar that together with glucose forms sucrose, the basis of table sugar. It is also found in high-fructose corn syrup, the most common sweetener in commercially prepared foods.
In all the trials they reviewed, participants were fed diets where fructose was incorporated or sprinkled on to test foods such as cereals or coffee. The diets with fructose had the same amount of calories as the ones without.
"Attention needs to go back where it belongs, which is on the concept of moderation," said Adrian Cozma, the lead author of the paper and a research assistant with Dr. Sievenpiper.
"We're seeing that there may be benefit if fructose wasn't being consumed in such large amounts," Cozma said. "All negative attention on fructose-related harm draws further away from the issue of eating too many calories."
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Fructose In Moderation Could Be Beneficial For Diabetics
Maxonidine, A Second-Generation Drug Used For Hypertension Aids Heart Function Independent Of Blood Pressure
Heart failure is the most common cause of death throughout the world, typically the result of chronic high blood pressure, also known as hypertension. As a result, research efforts have focused on an array of approaches aimed at preventing and treating high blood pressure. Recently, Japanese researchers examined the utility of an anti-hypertensive drug, moxonidine, which acts on the imidazoline receptors in the cardiovascular center of the brainstem. They found, using an animal model, that the drug can improve heart function and survival independent of its effect on blood pressure. They also found the drug had a favorable effect on oxidative stress, which is related to insulin resistance, the underlying abnormality in diabetes, which is common in people with heart failure.
An abstract presentation about the findings was offered at the meeting Experimental Biology 2012, being held April 21-25 at the San Diego Convention Center. The study was conducted by Yoshitaka Hirooka, Nobuhiro Honda, Ryuichi Matsukawa, Koji Itou and Kenji Sunagawa, all of the Department of Cardiovascular Medicine, Kyushu University Graduate School of Medical Sciences in Fukuoka, Japan. It is entitled, "Central sympathoinibition improves left ventricular function during the transition from hypertrophy to heart failure in Dahl salt-sensitive rats." The abstract is sponsored by the American Society for Investigative Pathology (ASIP), one of six scientific societies sponsoring the conference which last year attracted some 14,000 attendees.
Heart failure is a chronic disease that takes many forms and a variety of medications are used to treat it. Drugs such as ACE inhibitors and beta blockers target the causes of systolic heart failure. Clonidine, a first-generation central sympathoinhibitory drug, targets brain receptors that reduce cardiac output and lower blood pressure. Moxonidine, a second-generation drug, targets diastolic heart failure and function by reducing the effect of the central nervous system (CNS) receptors to decrease sympathetic activation and thus reduce blood pressure. In the study, salt-sensitive, hypertensive rats either received Moxonidine or were assigned to the control group. Researchers later found that the animals who received the drug had a marked inhibition of the sympathetic activity (an area of the brain) compared to those that did not. The findings suggest that inhibition of the central sympathetic outflow is important in the mechanism of hypertension. According to Dr. Hirooka, "The findings are important because they suggest that moxonidine may be useful in targeting the central receptors in the brain that are known to occur in patients with hypertension."
Next Steps
The study is the latest in a series conducted by the research team whose focus is on neural control of circulation in hypertension and heart failure. Looking ahead, they will work to identify the precise mechanisms involved in the beneficial effect of moxonidine, Dr. Hirooka said. They will also study other ways to see if the compound is a possible therapeutic tool for hypertensiveheart disease to prevent heart failure. As the drug had beneficial effects on insulin resistance, they would like to further investigate the issue, he added.
Maxonidine is available in select countries in Europe and Asia. It is not currently available in the United States.
Common Blood Pressure Drugs Help Prevent Diabetes Drugs promote the survival of pancreatic beta cells
A common class of oral high blood pressure drugs is associated with improved survival of insulin-producing pancreatic β-cells and improved glucose homeostasis, according to a study published in the April issue ofDiabetes.
Noting that their previous studies showed high levels of thioredoxin-interacting protein (TXNIP) led to β-cell death, and that TXNIP levels could be reduced in the heart by calcium channel blockers, Guanlan Xu, Ph.D., and colleagues from the University of Alabama at Birmingham, examined whether these drugs could reduce TXNIP levels in islets and in mouse models of diabetes.
The researchers found that verapamil significantly reduced the expression of TXNIP in human islets. Mice treated with verapamil had reduced TXNIP expression in islets, less β-cell death, greater endogenous insulin levels, and were protected against chemically-induced diabetes. Verapamil treatment of an obese, diabetes-prone mouse strain also resulted in greater β-cell survival, improved glucose homeostasis, and improved insulin sensitivity.
"Thus, for the first time, we have identified an oral medication that can inhibit proapoptotic β-cell TXNIP expression, enhance β-cell survival and function, and prevent and even improve overt diabetes," Xu and colleagues conclude.