Active Ingredient in Chinese Herb Used to Reduce High Blood Pressure

Some 50 million Americans have hypertension, that is, blood pressure measuring above the normal range (less than 120/80 mmHg). If untreated, it can lead to heart attacks, strokes, or kidney disease. Lifestyle changes are the first-stage treatment for the disease, but if they fail, medications are prescribed.

Many patients with high blood pressure have sought relief from complementary and alternative medicine (CAM). In so doing, many have consumed danshen, a Chinese herb used in Oriental medicine that promotes blood flow and treats cardiovascular disease.

Tanshinone IIA is an active ingredient of danshen. Since tanshinone IIA is widely available, a team of researchers has used it to investigate if this active ingredient can reduce blood pressure. In a soon-to-be-released study, using an animal model, the scientists have found that tanshinone IIA does reduce blood pressure.

Summary of Methodology

To assess the effect of tanshinone IIA, the protocol consisted of several parts. The researchers applied the 2-kidney-1-clip protocol to induce renal hypertension in male golden Syrian hamsters. The animals were anesthetized and a retroperitoneal approach was used to place a silver clip to constrict the right renal artery. Sham-operated hamsters and mice underwent the same procedure, except for the placement of a clip.

Both sets of hamsters received 50 ¦Ìg of tanshinone IIA/100g of body weight once a day for two weeks. After the two-week treatment period, mean arterial blood pressure was measured in the right carotid artery. To examine the microvascular actions of tanshinone IIA researchers applied it topically to the hamsters¡¯ cheek pouch or mice cremaster muscles to achieve the final concentration of one ¦Ìg/ml or five ¦Ìg/ml. After the application of tanshinone IIA, the experiment was continued for an additional 60-minute period in order to measure arteriolar diameter and peri-arteriolar nitric oxide concentration.

Results

Tanshinone IIA was found to have significantly reduced blood pressure in the hamsters. The experimental constriction of the renal artery increased mean arterial pressure to 161.2¡À6.9 mmHg relative to 114.3¡À9.2 mmHg in age-matched hamsters. Treatment with 50 ¦Ìg tanshinone IIA/100g body for two weeks reduced the mean arterial pressure from 161.2¡À6.9 to 130.0¡À7.8 mmHg.

The research team also discovered that tanshinone IIA caused widening of the arterioles in the hamster cheek pouch microcirculation via enhanced expression of endothelial nitric oxide synthase. The topical application of tanshinone IIA at one ¦Ìg/ml and five ¦Ìg/ml caused significant dose-related vasodilation, indicated by the increased agent/control ratio of arteriolar diameters from 1.0 to 1.25¡À0.08 and 1.57¡À0.11, respectively, in the hamster cheek pouch. The increase in arteriolar diameter ratio was significant relative to the vehicle for each concentration as well as for comparison between the two concentrations of tanshinone IIA.

Conclusions

As a result of the findings the researchers concluded that tanshinone IIA: (1) significantly reduced blood pressure in hamsters, (2) enhanced the expression of endothelial nitric oxide synthase, (3) increased the production of nitric oxide and (4) induced blood pressure changes through vasodilation in hamster blood microvessels. While the mechanisms of how tanshinone IIA or danshen work in hypertension are not yet fully understood, these results contribute to the effort to bring complementary and alternative medicine and allopathic care closer together in the treatment of hypertensive patients.

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Article adapted by MD Only from original press release.
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Contact: Donna Krupa
American Physiological Society

Their study will soon be published in the American Journal of Physiology ¨C Heart and Circulatory Physiology (December 15, 2006), doi:10.1152/ajpheart.01027.2006, and is entitled Endothelial Nitric Oxide Synthase is a Molecular Vascular Target for the Chinese Herb Danshen in Hypertension. It was conducted by the team of David D. Kim, PhD, OMD; Fabiola A. S¨¢nchez, PhD; Ricardo G. Dur¨¢n, BS; Takehito Kanetaka, MD; and Walter N. Dur¨¢n, PhD, all of the Program in Vascular Biology, Department of Pharmacology and Physiology and Department of Surgery, UMDNJ-New Jersey Medical School, Newark, NJ.

JOURNAL PUBLICATION INFORMATION: American Journal of Physiology ¨C Heart and Circulatory Physiology Articles in Press, doi: 10.1152/ajpheart.01027.2006.

Physiology is the study of how molecules, cells, tissues and organs function to create health or disease. The American Physiological Society (APS) has been an integral part of this scientific discovery process since it was established in 1887.

A brisk walk daily is the easiest way to trim waistline

Research from Duke University Medical Center shows that even a modest amount of brisk walking weekly is enough to trim waistlines and cut the risk of metabolic syndrome (MetS), an increasingly frequent condition linked to obesity and a sedentary lifestyle.

It’s estimated that about a quarter of all U.S. adults have MetS, a cluster of risk factors associated with greater likelihood of developing heart disease, diabetes and stroke: large waist circumference, high blood pressure, high levels of triglycerides, low amounts of HDL, or “good” cholesterol, and high blood sugar. To be diagnosed with MetS, patients must have at least three of these five risk factors, and according to many studies, a growing number of people do.

But Johanna Johnson, a clinical researcher at Duke Medical Center and the lead author of a new study examining the impact of exercise on MetS, said a person can lower risk of MetS by walking just 30 minutes a day, six days per week. “That’s about 11 miles per week. And our study shows that you’ll benefit even if you don’t make any dietary changes.”

“The results of our study underscore what we have known for a long time,” said Duke cardiologist William Kraus. “Some exercise is better than none; more exercise is generally better than less, and no exercise can be disastrous.”

The study appears in the December 15 issue of the American Journal of Cardiology.

The results come from a multi-year, federally funded study called STRRIDE (Studies of a Targeted Risk Reduction Intervention through Defined Exercise) that examined the effects of varying amounts and intensity of exercise on 171 middle-aged, overweight men and women.

Before exercising regularly, 41 percent of the participants met the criteria for MetS. At the end of the 8-month exercise program, only 27 percent did.

“That’s a significant decline in prevalence,” said Johnson. “It’s also encouraging news for sedentary, middle-aged adults who want to improve their health. It means they don’t have to go out running four or five days a week; they can get significant health benefits by simply walking around the neighborhood after dinner every night.”

Still, some exercise regimens were better than others. Those who exercised the least, walking about 11 miles per week, gained significant benefit, while those who exercised the most, jogging about 17 miles per week, gained slightly more benefit in terms of lowered MetS scores.

One group puzzled the researchers, however. Those who did a short period of very vigorous exercise didn’t improve their MetS scores as much as those who performed less intense exercise a longer period.

Kraus said there may be more value in doing moderate intensity exercise every day rather than more intense activity just a few days a week.

In all three of the study’s exercise groups, waistlines got smaller over the 8-month period. In general, men who exercised saw greater improvement in their MetS risk factors than women. But Johnson points out that at baseline, the men generally had worse scores than women, “so they had more room to improve,” she said.

Over the course of the STRRIDE study, the inactive control group – those who didn’t change their diet or activity level at all – gained an average of about one pound and a half-inch around the waist. “That may not sound like much, but that’s just six months,” Kraus said. “Over a decade, that’s an additional 20 pounds and 10 inches at the beltline.”

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Article adapted by MD Only Weblog from original press release.
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Contact: Michelle Gailiun
Duke University Medical Center

The study was funded by the National Institutes of Health.

Colleagues at Duke who contributed to the study include Cris Slentz, Gregory Samsa, Lori Bateman and Brian Duscha. Collaborating authors from East Carolina University include Joseph Houmard, Jennifer McCartney and Charles Tanner.

Overeating disrupts body clock causes weight gain

Our body’s 24-hour internal clock, or circadian clock, regulates the time we go to sleep, wake up and become hungry as well as the daily rhythms of many metabolic functions. The clock — an ancient molecular machine found in organisms large and small, simple and complex — properly aligns one’s physiology with one’s environment.Now, for the first time, a Northwestern University and Evanston Northwestern Healthcare (ENH) study has shown that overeating alters the core mechanism of the body clock, throwing off the timing of internal signals, including appetite control, critical for good health. Animals on a high-fat diet gained weight and suddenly exhibited a disruption in their circadian clocks, eating extra calories during the time they should have been asleep or at rest.

The study, which will be published in the Nov. 7 issue of the journal Cell Metabolism, also shows that changes in metabolic state associated with obesity and diabetes not only affects the circadian rhythms of behavior but also of physiology. Probing beyond the behavioral level, the researchers observed actual changes in genes that encode the clock in the brain and in peripheral tissues (such as fat), resulting in diminished expression of those genes.

These findings close an important loop in studies led by Joe Bass, M.D., assistant professor of medicine and neurobiology and physiology at Northwestern and head of the division of endocrinology and metabolism at ENH, of the relationship between the body clock and metabolism. Two years ago Bass and his colleagues reported in the journal Science that a faulty or misaligned body clock can wreak havoc on the body and its metabolism, increasing the propensity for obesity and diabetes.

Since then, knowing that genetic mutations rarely are the reason for a malfunctioning body clock, Bass has been wondering what could upset the operation of this internal timing device. What are the environmental factors or common influences that might affect the clock and in turn disrupt the sleep/wake cycle”

“Our study was simple — to determine if food itself can alter the clock,” said Bass, senior author of the paper. “The answer is yes, alterations in feeding affect timing. We found that as an animal on a high-fat diet gains weight it eats at the inappropriate time for its sleep/wake cycle — all of the excess calories are consumed when the animal should be resting. For a human, that would be like raiding the refrigerator in the middle of the night and binging on junk food.”

The clock-metabolism cycles feed on each other, creating a vicious loop, says Bass. Once weight gain starts, the clock is disrupted, and a disrupted clock exacerbates the original problem, affecting metabolism negatively and increasing the propensity for obesity and diabetes.

“Timing and metabolism evolved together and are almost a conjoined system,” said Bass. “If we perturb the delicate balance between the two, we see deleterious effects.”

The biological clock is central to behavior and tissue physiology. Clocks function in the brain as well as lung, liver, heart and skeletal muscles. They operate on a 24-hour, circadian (Latin for “about a day”) cycle that governs functions like sleeping and waking, rest and activity, fluid balance, body temperature, cardiac output, oxygen consumption and endocrine gland secretion.

In their study, Bass and his team studied mice with the same genetic backgrounds. After feeding them a regular diet for two weeks, they were split into two groups for the remaining six weeks, one kept on a regular diet and the other fed a high-fat diet. After two weeks, those on the high-fat diet showed a spontaneous shift in their normal pattern of activity/eating and resting/sleeping. They began to eat during their typical rest or sleep period (daylight for a mouse). The animals on a regular diet did not exhibit this behavior.

“It’s not just that the animals are eating more at regular meals,” said Bass. “What’s happened is that they actually shift their eating habits so that all excess food intake occurs during their normal rest period.”

In the study’s high-calorie, high-fat diet, 45 percent of calories was contributed by fat. For humans, a diet with no more than 30 percent of calories from fat is recommended.

The entire study was conducted in darkness so that the behavior of the animals simply reflected their internal clock; a normal animal has a very fixed daily period of just less than 24 hours. For animals on a high-fat diet, after two weeks on that diet the animals’ behavior changed: their daily period of sleep/wake was lengthened by a significant amount. This suggests, says Bass, that the central mechanism in the brain that controls the timing of the cycle of activity and rest is affected by a high-fat diet.

“Our findings have implications for human disease,” said Bass. “These basic advances in science can be applied to the studies of common disorders like obesity and diabetes. It is important to understand what happens when diet changes.”

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Article adapted by MD Only Weblog from original press release.
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Contact: Wendy Leopold
Northwestern University

In addition to Bass, other authors of the paper, titled “High-Fat Diet Disrupts Behavioral and Molecular Circadian Rhythms in Mice,” are Akira Kohsaka, of Northwestern (lead author); Aaron Laposky, research assistant professor at Northwestern’s Center for Sleep and Circadian Biology; Kathryn Moynihan Ramsey, Carmela Estrada and Corrine Joshu, of Northwestern; Yumiko Kobayashi, of Evanston Northwestern Healthcare; and Fred W. Turek, professor of neurobiology and physiology at Northwestern and director of the Center for Sleep and Circadian Biology.

Adding Vitamins C and E to diet improves effectiveness of insulin

Adding antioxidants to therapy improves drug’s ability to reduce blood sugar

Boosting insulin with vitamins C and E may improve the drug’s effectiveness for treating diabetes.

A UC Irvine College of Medicine study has found that the popular antioxidant supplements not only enhance insulin’s ability to reduce blood sugar, but also lower the risks of organ damage that can occur despite insulin treatments. The study appears in the January issue of Kidney International.

Dr. Nick Vaziri, professor of medicine, and his team found that untreated diabetes raised blood pressure and increased the production of damaging oxidizing agents called free radicals. The free radicals converted sugars and proteins into harmful chemicals, increasing the risks of tissue damage often seen in untreated diabetes.

Treating the rats with insulin alone improved high blood pressure somewhat and partially spared the sugars and proteins from the free radicals’ assault. But it also added a new problem, as the free radicals turned their attack on nitric oxide, a ubiquitous molecule that usually protects the body from free radicals. This new attack results in yet more toxic chemicals, with the potential to inflict damage to tissues.

Adding vitamins C and E to insulin, however, spared the sugars, proteins and nitric oxide from attack.

“Blood pressure was lowered to normal, and free radicals were not in sufficient numbers to degrade the sugars, proteins and nitric oxide,” Vaziri said. “We think this shows that a diet rich in antioxidants may help diabetics prevent the devastating cardiovascular, kidney, neurological and other damage that are common complications of diabetes.”

Diabetes affects nearly 17 million Americans. Insulin is the predominant treatment, but patients eventually develop complications, like various forms of heart disease and nerve, liver and kidney damage. Studies would still have to be tested in humans, but Vaziri believes that adding vitamins C and E to an insulin-dependent diabetic’s diet should help treat the disease and perhaps prevent future organ damage.

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Article adapted by MD Only Weblog from original press release.
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Contact: Andrew Porterfield
University of California – Irvine

Does High Meat Intake Lead to Obesity?

Meat consumption appears to be a factor for obesity in women, according to a new study presented at the 54th Annual Meeting of the American College of Sports Medicine (ACSM) in New Orleans. Although the reasons are still unclear, high meat intake was associated with obesity in a preliminary study sample of more than 280 women.

More than half of the women classified as having high meat intake were obese, according to body fat percentage. Conversely, only 18.6 percent of women classified as having low meat intake were obese.

The study divided participants into groups classified by low, moderate, and high meat intake per 1,000 calories consumed a day. The low intake group consumed less than 1.9 three-ounce servings of meat per day, as opposed to more than 3.18 servings for the high intake group. Participants were nonsmoking, premenopausal women whose diet was monitored during a seven-day period.

Lead study author Garrett Hoyt says he can only speculate on the physiological causes behind his findings, but several factors may be to blame.

“It’s possible that eating more meat causes people to weigh more, or that people who weigh more eat more meat,” Hoyt said. “That sounds odd, but it’s possible that diets with lots of meat consumption, like the Atkins diet, have attracted people with higher body fat percentages.”

Hoyt points out that vegetarians and semi-vegetarians have been shown to be consistently leaner than meat-eaters. This may be because meat consumption increases insulin levels, which may lead to a hormonal response that leads to body growth.

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Article adapted by MD Only Weblog from original press release.
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The conclusions outlined in this news release are those of the researchers only, and should not be construed as an official statement of the American College of Sports Medicine.

Contact: Communications and Public Information
American College of Sports Medicine 

The American College of Sports Medicine is the largest sports medicine and exercise science organization in the world. More than 20,000 international, national, and regional members are dedicated to advancing and integrating scientific research to provide educational and practical applications of exercise science and sports medicine.

Brain hormone wires people to be obese or thin

Some brains may be wired to encourage fidgeting and other restless behaviors that consume calories and help control weight, according to new research published by The American Physiological Society.

The study found that the brains of rats bred to be lean are more sensitive to a chemical produced in the brain, orexin A, which stimulates appetite and spontaneous physical activity such as fidgeting and other unconscious movements. Compared to rats bred to be obese, the lean rats had a far greater expression of orexin receptors in the hypothalamus.

“The greater expression of orexin receptors suggests the lean rats’ brains were more sensitive to the orexin the brain produces,” said Catherine M. Kotz, the study’s senior researcher. “The results point to a biological basis for being a couch potato.”

This line of research suggests that frequent minor unconscious movements such as fidgeting and other behaviors associated with restlessness burn calories and help control weight, Kotz said. Further, it suggests a strategy to reduce weight gain and could lead to the development of a drug to stimulate minor activity.

The study “Elevated hypothalamic orexin signaling, sensitivity to orexin A and spontaneous physical activity in obesity resistant rats,” appears in the online edition of the American Journal of Physiology-Regulatory, Integrative and Comparative Physiology published by The American Physiological Society. The study was done by Jennifer A. Teske and Allen S. Levine of the University of Minnesota and the Minnesota Obesity Center, St. Paul; Michael Kuskowski, VA Medical Center, Minneapolis; James A. Levine, Mayo Clinic, Rochester, Minnesota; and Catherine M. Kotz, the VA Medical Center, University of Minnesota, and the Minnesota Obesity Center.

Study looks at obese versus lean rats

“Many people focus on diet, but it may be more feasible for some people to stand or move more throughout the day” as a way to control their weight, Kotz said. Contrary to common belief, metabolism rates don’t vary greatly from person to person and weight gain usually results from eating too much, burning too few calories, or both, she said.

The researchers drew their conclusions after performing a series of experiments with obesity-prone and obesity-resistant rats. The obesity-prone strain was developed for obesity research by breeding obese rats with other obese rats. The obesity-resistant rats were developed by breeding lean rats with lean rats, Kotz noted. The study also employed a control group of normal laboratory rats.

Each rat consumed the same number of calories each day. The researchers took baseline measurements of each rat’s activity using sensors to measure even minor movements, such as grooming and standing.

They found that the lean group moved significantly more during this baseline period than the obese group, Kotz said. This was true even though the rats were young and both groups weighed the same — eliminating the obesity itself as the cause of the decreased movement. After the baseline data gathering, the researchers moved to the experimental part of the study.

Lean rats have elevated expression of orexin receptors

“We knew from previous studies that orexin stimulated physical activity, and so we wanted to find out whether it enhances activity more in lean rats than in obese rats, Kotz explained. The researchers injected orexin into the lateral hypothalamus area of the brains of both groups and found that the lean rats became even more active, while the obese rats didn’t respond much at all. “Not only do the lean rats have a higher base activity rate but they respond more to orexin,” she said.

Orexin must bind to receptors in the brain to produce increased activity, so the researchers reasoned that the lean rats must have more orexin receptors. When they did a blind analysis of the brains of obese and lean rats of various ages, they found that the lean rats had double the gene expression level of orexin receptors compared to the obese rats, Kotz explained.

The greater gene expression of orexin receptors does not conclusively prove that there are more orexin receptors, but it is highly suggestive of that finding. Kotz and her fellow researchers are now looking to see if the lean rats have a greater number of orexin receptors in their brains.

Activity level important to weight control

Because the rats in this study ate the same amount of food, the researchers concluded that the weight gain of the obese rats comes more from expending too few calories than from consuming too many. Other studies have shown that disabling the orexin system of lean rats causes them to eat less and move less, which leads them to become obese, Kotz said. When the orexin system is working optimally, the increase in eating which orexin causes is believed to be offset by increased physical activity, she said.

It would be impossible to do a similar study of the brain in humans. But one of the researchers, James Levine, found in a previous study with humans that lean individuals move about two hours per day more than obese individuals. What does this mean for those who are overweight?

“If we can get obese individuals to a slightly higher level of activity, that would be very beneficial,” Kotz concluded.

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Article adapted by MD Only Weblog from original press release.
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Contact: Christine Guilfoy
American Physiological Society

The link between lack of sleep and obesity traced to brain cells

A possible link between lack of sleep (insomnia) and obesity has been traced to hypocretin/orexin cells in the hypothalamus region of the brain that are easily excited and sensitive to stress, Yale School of Medicine researchers report in the April 2005 issue of Cell Metabolism.

“If these neurons are over-activated by environmental or mental stress in daily situations, they may support sustained arousal, triggering sleeplessness, leading to overeating,” said lead author Tamas Horvath, associate professor in the Departments of Obstetrics, Gynecology & Reproductive Sciences (Ob/Gyn) and Neurobiology at Yale School of Medicine. “The more stress you have, the lower the threshold becomes for exciting these hypocretin neurons.”

Horvath and co-author Xiao-Bing Gao, assistant professor in Ob/Gyn, studied hypocretin/orexin neurons in mice using electrophysiology and electron microscopy. They found a unique, previously un-described organization of inputs on hypocretin neurons in which excitatory nerve junctions outnumber inhibitory contacts by almost 10 fold. Stressors such as fasting further excite these neurons.

“This unique wiring and acute stress-induced plasticity of the hypocretin neurons correlates well with its involvement in the control of arousal and alertness, which are vital to survival,” said Horvath. “But it may also be an underlying cause of insomnia and associated metabolic disturbances, including obesity. In addition, insomnia is characteristic of perimenopause (early onset of menopause), which may lead to increased prevalence of obesity in postmenopausal women.”

Previous studies demonstrated the association between lack of sleep and obesity and suggested a good night’s sleep to help obesity. Horvath found that the neurological basis of the link between obesity and insomnia make them both independent and related products of the overactivated hypocretin system. Therefore, he said, “people with weight and sleep problems could benefit from cutting back on stressful aspects of their lives, rather than trying to specifically medicate either insomnia or obesity.”

Obesity and metabolic disorders are a major cause of death and illness in the United States, with one of the highest financial burdens on the health care system.

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Article adapted by MD Only Weblog from original press release.
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Contact: Karen N. Peart
Yale University

Citation: Cell Metabolism Vol. 1, Issue 4 (April 2005).

Hormone links sleep, hunger and metabloism

While investigating how the hormone orexin might control sleep and hunger, researchers at UT Southwestern Medical Center have discovered, to their surprise, that it activates a protein, HIF-1, long known to stimulate cancerous tumor growth. 

The study, appearing today in the online version of the journal Genes and Development, is among the first to show how HIF-1 operates in healthy tissues rather than in tumors, said Dr. Thomas Kodadek, chief of translational research at UT Southwestern and senior author of the study. 

“HIF-1 is very big in the cancer community,” Dr. Kodadek said. “So we were intrigued to find this important and very basic mechanism that is unrelated to cancer.” 

Orexin was already known for its role in sleep and hunger. Researchers, including Dr. Masashi Yanagisawa, professor of molecular genetics at UT Southwestern, had found that lack of orexin causes the sleep disorder narcolepsy.  

“It’s really the most straightforward system relevant to the biology of sleep you can look at,” Dr. Kodadek said. “You lack orexin? You’ve got narcolepsy. End of story.” 

Dr. Kodadek’s project is part of an initiative funded by the National Heart, Lung and Blood Institute to develop technologies to understand and treat sleep disorders.  In the current study, the researchers used a massive gene-screening technique to identify genes that orexin either turned on or inhibited. 

Surprisingly, the activity of a component of HIF called HIF1-alpha was among the most highly activated of any gene in the study. And when orexin stimulated HIF1-alpha, it in turn increased the expression of a variety of genes dedicated to burning sugar to provide energy for the body. Studies in brain slices of mice with and without orexin receptors support their results. 

The findings help explain orexin’s link to the metabolic system, the researchers said. The body is known to step up its production of orexin when blood sugar gets low. The researchers hypothesized that when a body has low blood sugar and gets hungry, the increase in orexin activates HIF-1 production, revving up metabolism so the body gets the most energy out of the sugar on hand.  

This action of HIF-1 when stimulated by orexin is different than how it acts in tumors, Dr. Kodadek said. In tumors, HIF-1 changes cells’ metabolism so they can burn sugar for energy without oxygen. This method is inefficient, but allows cells to stay alive.  

Orexin, on the other hand, forces HIF-1 to switch cells to burn sugar using oxygen, which burns sugar faster but more efficiently. This strategy makes sense, they said, in terms of evolution.  

“You need to be active and energetic, especially when you’re hungry, so you can search for a meal,” said Dr. Devanjan Sikder, instructor of internal medicine and lead author of the study. 

“This orexin pathway we found is basically an overdrive function. Even though blood sugar levels are low, you’re not only awake, but you’re also energetic because of the action of HIF-1,” said Dr. Kodadek. “In retrospect, our findings make a lot of sense, but they were surprising at the time.”  

Not only was this orexin-HIF link unexpected, but it showed an entirely new way HIF-1 operates, Dr. Kodadek said. There have been a few recent studies on its function in healthy tissues, but none involving mechanisms related to sleep, he said. 

The study also illustrates a potential complication of anti-cancer therapies that target HIF-1, Dr. Kodadek said. These results reveal that anti-HIF-1 chemotherapy could interfere with this essential function.  

“If anything, our findings may be a cautionary tale about whether HIF-related mechanisms are going to be appropriate targets for chemotherapy,” Dr. Kodadek said.  

The researchers next plan to genetically engineer mice that lack HIF-1 in the brain in order to determine the effects on wakefulness and activity levels of the animals. They also plan to further study how orexin and oxygen levels interact to control energy metabolism in cells.

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Article adapted by MD Only Weblog from original press release.
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Contact: Aline McKenzie
UT Southwestern Medical Center

CLA reduces weight, blood sugar and leptin levels

Supplementing the diet with a certain fatty acid may lead to better weight control and disease management in diabetics, a new study suggests.Diabetics who added an essential fatty acid called conjugated linoleic acid (CLA) to their diets had lower body mass as well as lower blood sugar levels by the end of the eight-week study. Hyperglycemia, or high blood sugar, is a hallmark of diabetes.

Researchers also found that higher levels of this fatty acid in the bloodstream meant lower levels of leptin, a hormone thought to regulate fat levels. Scientists think that high leptin levels may play a role in obesity, one of the biggest risk factors for adult-onset diabetes.

“In previous work, we found that CLA delayed the onset of diabetes in rats,” said Martha Belury, the senior author of the study and an associate professor of human nutrition at Ohio State University. “In this study, we found that it also helped improve the management of adult-onset diabetes in humans.”

CLA is made up of various fatty acid isomers – compounds that share the same chemical formula but differ in chemical structure. Related isomers can have very different effects.

In the current study, the researchers found that one particular CLA isomer, t10c12-CLA, helped control both body weight and leptin levels. Nutritionists sometimes call this isomer the 10-12, isomer.

The research appears in the January issue of the Journal of Nutrition. Belury conducted the study while with the department of foods and nutrition at Purdue University. She is continuing the research at Ohio State.

The researchers asked 21 people with adult-onset diabetes to take either a supplement containing a mix of rumenic acid and 10-12 isomer or a safflower oil supplement as a control. The group was divided roughly in half. Rumenic acid is the predominant isomer in foods that contain CLA, while the 10-12 isomer is less abundant.

Participants were instructed to take their respective supplements every day for eight weeks.

“The amount of CLA, how long it’s taken and the type taken all impact the fatty acid’s ability to affect obesity in humans, and therefore help manage diabetes.”

While CLA supplements are available to consumers, Belury encourages diabetics to get their CLA from food sources – primarily beef, lamb and dairy products.

“Not only does it taste better, it’s also safer and more beneficial to get the nutrients from food,” she said. “Besides, we don’t yet know the long-term effects of taking CLA in supplement form.”

At the end of the trial, the researchers took blood samples from each participant to check CLA levels. By then, fasting blood glucose levels had decreased in nine of the 11 people taking the CLA supplement, but only in two of the 10 taking safflower supplements, meaning that CLA was helping to control certain symptoms of diabetes.

Fasting blood glucose levels decreased nearly five-fold in patients taking CLA, compared to patients taking the safflower oil.

The researchers also studied the impact each isomer had on changes in body weight and levels of the hormone leptin.

It was the 10-12 isomer, and not rumenic acid, that was linked to a reduction in body weight and leptin levels. While the average weight loss among patients taking CLA supplements was small (about 3.5 pounds), they had been asked to not change their normal caloric intake during the study. The group taking safflower supplements neither lost nor gained weight. Leptin levels decreased in the CLA group, and rose slightly in the safflower group.

“The effect of the 10-12 isomer on reducing body mass and leptin levels was key,” Belury said, adding that other researchers have shown the 10-12 isomer to be helpful in reducing body mass in animals.

“The amount of CLA, how long it’s taken and the type taken all impact the fatty acid’s ability to affect obesity in humans, and therefore help manage diabetes,” Belury said.

A 2002 study conducted by the Diabetes Prevention Program Research Group found that a modest reduction in body weight resulted in a 58 percent reduction in the incidence of diabetes in a group of people at high risk for developing the disease.

Belury conducted the study with Annie Mahon of the department of foods and nutrition at Purdue University and Sebastiano Banni of the department of experimental biology at the University of Cagliari, Italy.

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Article adapted by MD Only Weblog from original press release.
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Contact: Martha A. Belury
Ohio State University

Reduce the risk of hypertension by 50 percent drinking skim milk

The American Journal of Clinical Nutrition is the peer-reviewed journal of international reference in the field of nutrition. In its latest issue, of November, it published an article which demonstrated that non-fat milk products can reduce the risk of hypertension by 50%, while nevertheless there is no appreciable connection between that disease and the consumption of whole milk.

The research was carried out by a team of researchers from the University of Navarra and Álvaro Alonso, currently a researcher in the School of Public Health at Harvard University who is the lead author of the article.

Research population of 6,000 persons.

This was a study which evaluated the relationship between the consumption of milk products and the risk of developing arterial hypertension.

They performed a research project that followed 6,000 people over the course of two years.

Those persons with an elevated consumption of skimmed milk and milk products showed a reduction of 50% in their risk of developing hypertension, compared with those with a low consumption or who did not consume these products. Nevertheless, no relationship was encountered between the consumption of whole milk products and the risk of hypertension.

These results can contribute to a clearer definition of dietary guidelines for the prevention of arterial hypertension. In particular, although data from prior studies indicated a possible preventative role of lactose products in the development of arterial hypertension, these results have been the first to demonstrate that this association exists in adults.

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Article adapted by MD Only Weblog from original press release.
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Contact: Garazi Andonegi
Elhuyar Fundazioa