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Nanotech breath sensor can tell if someone has diabetes or not

May 21, 2010 By vani Leave a Comment

Washington, May 21 (ANI): A nanotechnology-based sensor could soon tell whether someone has Type I diabetes – just by analysing their breath.

The sensor, which has been successfully tested by researchers in Switzerland, could also be used by emergency room doctors to determine whether a patient has developed diabetic ketoacidosis, a potentially serious complication that happens when diabetics do not take enough insulin.

Even diabetics could use the technology someday in their own homes, to determine whether they need more insulin.

Professor Sotiris E. Pratsinis and colleagues at ETH Zurich in Switzerland explain that everyone has a little bit of acetone in their breath.

But people with Type I diabetes release unusually high levels of the chemical when they exhale.

If they have diabetic ketoacidosis, a dangerous buildup of acetone in the blood, they exhale even-larger amounts of acetone.

The researchers built an extremely sensitive acetone detector by directly depositing from a flame plume a thin film of semiconducting, mixed ceramic nanoparticles between a set of gold electrodes.

The device acts like an electrical resistor. When it gets hit with a puff of acetone-filled air, its resistance drops, allowing more electricity to pass between the electrodes.

If a diabetic were to breathe on the sensor, its resistance would suddenly drop.

When a healthy person exhales onto the nanoparticles, their resistance will not change very much.

The scientists found this new sensor can detect acetone in extremely moist air, an attribute that is critical for any breath test.

It is sensitive enough to detect acetone at 20 parts per billion, a concentration that is 90 times lower than the level at which it can be found in the breath of diabetic patients.

The study has been published in ACS” Analytical Chemistry, a semi-monthly journal. (ANI)

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Popular diabetes drug may help treat cancer

May 5, 2010 By vani Leave a Comment

Washington, May 5 (ANI): Researchers have learned that the popular diabetes medication metformin doesn”t work the way they thought.

And the discovery could open the door to using metformin to treat cancer, tuberous sclerosis complex and other diseases.

The results of this study, led by George Thomas, PhD, scientific director of UC”s Metabolic Diseases Institute, are published in the May 5 edition of Cell Metabolism.

Metformin is widely prescribed to people with type 2 diabetes and may be extended to the treatment of certain cancers.

The drug blocks the production of glucose (sugar) and increases sensitivity to insulin—a hormone that converts sugar and other foods into energy within the body.

Researchers have thought that metformin, an energy-deprivation agent, disables the mTOR (mammalian target of rapamycin) complex by first activating the tuberous sclerosis complex (TSC) proteins through the enzyme AMPK.

Thomas” team determined that mTOR could actually be disabled without AMPK, and even without TSC. The team was able to determine that metformin works to knock out mTOR through another enzyme, RAG GTPase.

“We”ve poked a hole in dogma,” says Thomas, a professor in the cancer and cell biology department. “Scientists can and should go back and ask about things they had crossed off their list.”

The importance of this finding, says Thomas, is the possibility it holds for broader use of metformin.

“Metformin is already prescribed to 100 million people worldwide, and our study raises the question, ”Could this drug be used even more widely?”” (ANI)

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Specific Vitamin E dose can benefit nonalcoholic steatohepatitis patients

April 29, 2010 By vani Leave a Comment

London, Apr 29 (ANI): A daily dose of a specific form of vitamin E could improve the liver disease, nonalcoholic steatohepatitis (NASH), reveals a new study.

In addition, Actos (pioglitazone), a drug used to treat diabetes, also improved many features of NASH but was associated with weight gain.

NASH is a chronic liver disease that is linked to weight gain and obesity and can lead to cirrhosis, or scarring, liver cancer and death. It resembles alcoholic liver disease but occurs in patients who drink little or no alcohol. NASH can occur in children, the elderly, normal-weight, and non-diabetic persons.

The disease is apparently caused by abnormal metabolism of fats, which increases levels of oxidants, compounds that transfer oxygen in the liver.

In the Pioglitazone or Vitamin E for NASH Study (PIVENS), investigators from the NASH Clinical Research Network (CRN) compared the two different treatments to placebo.

Vitamin E functions as an anti-oxidant while Actos improves the sensitivity of cells to insulin, a hormone that controls sugar and fat metabolism.

PIVENS is the largest placebo-controlled, randomized clinical trial of therapies ever conducted for NASH.

“This is an important landmark in the search for effective treatments for NASH,” said Dr. Pat Robuck, the NASH CRN project scientist.

The PIVENS trial randomly assigned 247 adults with NASH and without diabetes into three groups.

Researchers reported that vitamin E and Actos helped certain patients with NASH.

After 96 weeks of treatment, vitamin E improved all features of NASH except the degree of cirrhosis in the liver.

Forty-three percent of participants treated with vitamin E met the primary endpoint of the trial compared to only 19 percent of those who received a placebo.

The primary endpoint was a composite of the scores for several features of NASH—retention of lipids, liver inflammation, and liver degeneration. The scores were used to assess disease activity.

While Actos improved liver inflammation and retention of lipids in 34 percent of individuals who received it, suggesting a benefit, the improvement fell short of being statistically significant.

Actos also led to an undesirable weight gain of 10 pounds over the 96-week trial. There was an early improvement in liver enzyme tests among participants receiving either Actos or vitamin E.

However, upon stopping the medications, the liver enzymes worsened again suggesting the need for long-term treatment.

“This study was conducted in people who had NASH but did not have diabetes. The benefits of either treatment in NASH patients who have diabetes remain unknown. Also, the study lasted only two years and the potential long-term benefits and risks of taking vitamin E or Actos in these doses are still uncertain,” said Dr. Arun Sanyal, NASH CRN co-chair.

The results were published online in the New England Journal of Medicine. (ANI)

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New strategy to treat type 2 diabetes

March 29, 2010 By vani Leave a Comment

London, Mar 29 (ANI): A cellular pathway that fails when people become obese has been identified, and scientists believe that it could act as a new strategy for treating type 2 diabetes.

By activating this pathway artificially, researchers at Children”s Hospital Boston could normalize blood glucose levels in severely obese and diabetic mice.

Epidemiologists have long known that obesity contributes to type 2 diabetes.

In previous work, Dr. Umut Ozcan showed that the brain, liver and fat cells of obese mice have increased stress in the endoplasmic reticulum (ER)— a structure in the cell where proteins are assembled, folded into their proper shapes, and dispatched to do jobs for the cell.

In the presence of obesity, the ER is overwhelmed and its operations break down.

This so-called “ER stress” activates a cascade of events that suppress the body”s response to insulin, and is a key link between obesity and type 2 diabetes.

However, until now, researchers haven”t known precisely why obesity causes ER stress to develop.

The researchers have now shown that a transcription factor that normally helps relieve ER stress, called X-box binding protein 1 (XBP-1), is unable to function in obese mice.

Instead of travelling to the cell nucleus and turning on genes called chaperones, necessary for proper ER function, XBP-1 becomes stranded.

And on further probing, the researchers found the reason— XBP-1 fails to interact with a protein fragment called p85, part of an important protein that mediates insulin”s effect of lowering blood glucose levels (phosphotidyl inositol 3 kinase or PI3K).

Ozcan”s group identified a new complex of p85 proteins in the cell, and showed that normally, when stimulated by insulin, p85 breaks off and binds to XBP-1, helping it get to the nucleus.

“What we found is, in conditions of obesity, XBP1 cannot go to the nucleus and there is a severe defect in the up-regulation of chaperones. But when we increase levels of free p85 in the liver of obese, severely diabetic mice, we see a significant increase in XBP1 activity and chaperone response and, consequently, improved glucose tolerance and reduced blood glucose levels,” Nature quoted Ozcan as saying.

When people are obese, the insulin signalling that normally increases free p85 is impaired, leading to more ER stress and more insulin resistance, ultimately leading to type 2 diabetes.

However, Ozcan thinks this vicious cycle can be circumvented through strategies that increase levels of free p85.

The findings have been published in Nature Medicine. (ANI)

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Genes controlling insulin ‘alter’ body clock

September 19, 2009 By admin Leave a Comment

Washington, Sept 18 (ANI): Scientists at University of California, San Diego have identified certain insulin-regulating genes that can also alter the timing of the body clock.

They said that the findings can lead to new approaches to treating disorders such as metabolic syndrome that can result, at least in part, from chronic disruption of the sleep-wake cycle.

“People knew that the clock regulates many different processes, but what they didn’t realize what that when you tweak those processes, it feeds back and alters the clock,” said Steve Kay, Dean of the Division of Biological Sciences at the University of California, San Diego, who led the study along with John Hogenesch of the University of Pennsylvania.

A molecular clock controls daily physiological rhythms in many types of cells, even cells grown in culture.

By engineering cultured cells to glow yellow when a particular clock gene switched on, the team made the cycle visible. They then interfered with every human gene to see which would shift the clock. They found that hundreds altered the timing.

“We just suddenly discovered 350 new genes that affect the clock that weren’t known before,” Kay said.

However, subsequent screening to confirm the genes’ effect on a second clock gene narrowed the list to 200.

Seven genes involved in insulin control also influenced the rhythms of the clock.

“What came out very strongly was this close relationship between circadian regulation and insulin signalling. There’s a reciprocal relationship between circadian dysfunction and metabolic dysfunction,” said Kay.

The researchers suggest that genetically altered mice with malfunctioning clocks become obese and develop diet-induced diabetes.Understanding this close relationship between circadian regulation and metabolic homeostasis should provide novel ways of identifying new therapies for metabolic disease,” Kay added.

The study appears in journal Cell. (ANI)

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Popular diabetes drug may help fight breast cancer

September 15, 2009 By admin Leave a Comment

Washington, Sept 15 (ANI): A popular diabetes drug called metformin has been found to be effective in fighting breast cancer.

The findings of the study from Harvard Medical School showed that metformin, along with conventional chemotherapy, shows promise for treating and delaying recurrence of breast cancer.

“We have found a compound selective for cancer stem cells,” said senior author Kevin Struhl, the David Wesley Gaiser professor of biological chemistry and molecular pharmacology at HMS.

“What’s different is that ours is a first-line diabetes drug,” he added.

The drug seemed to work independently of its ability to improve insulin sensitivity and lower blood sugar and insulin levels, all of which are also associated with better breast cancer outcomes.

“There is a big desire to find drugs specific to cancer stem cells,” said Struhl.

“The cancer stem cell hypothesis says you cannot cure cancer unless you also get rid of the cancer stem cells. From a purely practical point of view, this could be tested in humans. It’s already used as a first-line diabetes drug,” he added.

Lead researchers Heather Hirsch and Dimitrios Iliopoulos found that the combination of metformin and the cancer drug doxorubicin killed human cancer stem cells and non-stem cancer cells in culture.

In mice, pre-treatment with the diabetes drug prevented the otherwise dramatic ability of human breast cancer stem cells to form tumours.

In cases where tumours were allowed to take hold for 10 days, the dual therapy also reduced tumour mass more quickly and prevented relapse for longer than doxorubicin alone.

“This is an exciting study,” said Jennifer Ligibel, a medical oncologist at Dana-Farber Cancer Institute and an HMS instructor in medicine, who was not involved in the study.

“There is a lot of interest in studying metformin in breast cancer, but so far we do not have direct evidence that metformin will improve outcomes in patients,” Ligibel said. “That’s what this trial is for.”

The findings appear online in the journal Cancer Research. (ANI)

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How people lose muscles as they get older

September 12, 2009 By admin Leave a Comment

Washington, Sep 12 (ANI): Even the most well-built people tend to loose their muscles and develop thinner arms and legs as they get older, and researchers in Nottingham have now explained why this happens.

As age catches up, it becomes harder to keep our muscles healthy-they get smaller, which decreases strength and increases the likelihood of falls and fractures.

The researchers have already shown that when older people eat, they cannot make muscle as fast as the young, and now they have found that the suppression of muscle breakdown, which also happens during feeding, is blunted with age.

Led by Michael Rennie, the scientists and doctors at The University of Nottingham Schools of Graduate Entry Medicine and Biomedical Sciences, believe that a ‘double whammy’ affects people aged over 65.

But the team think that weight training may “rejuvenate” muscle blood flow, and help retain muscle for older people.

The study’s results may explain the ongoing loss of muscle in older people- when they eat they do not build enough muscle with the protein in food and also, the insulin (a hormone released during a meal) fails to shut down the muscle breakdown that rises between meals and overnight.

Normally, in young people, insulin acts to slow muscle breakdown.

These problems could be a result of a failure to deliver nutrients and hormones to muscle because of a poorer blood supply.

In the study, the researchers compared one group of people in their late 60s to a group of 25-year-olds, with equal numbers of men and women.

Professor Rennie said: “The results were clear. The younger people’s muscles were able to use insulin we gave to stop the muscle breakdown, which had increased during the night. The muscles in the older people could not.”

“In the course of our tests, we also noticed that the blood flow in the leg was greater in the younger people than the older ones. This set us thinking: maybe the rate of supply of nutrients and hormones is lower in the older people? This could explain the wasting we see,” he added.

Later, Beth Phillips, a PhD student working with Rennie, confirmed the blunting effect of age on leg blood flow after feeding, with and without exercise.

The team predicted that weight training would reduce this blunting.

“Indeed, she found that three sessions a week over 20 weeks ‘rejuvenated’ the leg blood flow responses of the older people. They became identical to those in the young,” said Rennie.

The study has been published in The American Journal of Clinical Nutrition. (ANI)

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Weight gain in adulthood linked to prostate cancer risk

September 12, 2009 By admin Leave a Comment

Washington, Sep 12 (ANI): Body size and weight gain in younger and older adulthood may help weigh a man’s proneness to prostate cancer, according to a study by researchers at the University of Hawaii at Manoa’s Cancer Research Center of Hawaii.

Led by Dr. Brenda Hernandez, the researchers said that the risk varies among different ethnic groups

For the study, the researchers studied the relationship in a multiethnic population consisting of blacks, Japanese, Hispanics, Native Hawaiians and whites, and compared differences among age groups using the Multiethnic Cohort, a longitudinal study of men 45-75 years of age established in Hawaii and California from 1993-1996.

Of the 83,879 men who participated in the study, 5,554 developed prostate cancer.

Overall, men who were overweight or obese by age 21 had a decreased risk of localized and low-grade prostate cancer, according to Hernandez.

Their results suggested that being overweight in older adulthood was associated with increased prostate cancer risk among white and Native Hawaiian men, but a decreased risk among Japanese men.

While excessive weight gain between younger and older adulthood was observed to increase the risk of advanced and high-grade prostate cancers in white men and increase the risk of localized and low-grade disease in black men, it appeared to decrease the risk of localized prostate cancer in Japanese men.

“The relationship of certain characteristics, such as body size, with cancer risk may vary across ethnic groups due to the combined influence of both genes and lifestyle,” said Hernandez.

However, the relationship between body size and prostate cancer risk is not entirely understood.

Excess fat is associated with a number of conditions that contribute to cancer development including low-grade chronic inflammation, insulin resistance, metabolic abnormalities, and hormone imbalances.

These conditions may in turn contribute to more aggressive prostate malignancies.

Ethnic differences in cancer risk may be explained by differences in the distribution of stored body fat that could have a differential effect on the development of prostate cancer.

And the distribution of body fat may influence the specific way that excess fat influences cancer risk.

The study has been published in Cancer Epidemiology, Biomarkers and Prevention, a journal of the American Association for Cancer Research. (ANI)

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Fat-rich junk food may alter genes linked with type II diabetes

September 8, 2009 By admin Leave a Comment

London, September 8 (ANI): A team of scientists in Sweden have warned that gorging too much on fat-rich junk food may cause drastic changes to a gene that helps muscle cells burn fat.

Juleen Zierath, of the Karolinska Institute in Stockholm, says that her team’s findings may help improve the scientific understanding of how type II diabetes develops in adulthood.

“Somehow, the environment plays on the genes we have,” says the lead researcher, adding that her study provides new clues to how this happens.

She says that it may be possible that the altered cells become so engorged with unburnt fat that they become “diabetic”, and stop accepting signals from the hormone insulin, which normally triggers the absorption of glucose from the bloodstream.

However, proving that components in the diet can permanently alter genes is itself a breakthrough, as it provides the first evidence that the food people eat may change the function of their DNA, a process scientifically known as “epigenetics”.

During the study, the researchers observed that the DNA itself remained unchanged, except for a masking process called methylation that can permanently mothball a gene by capping individual chemical units or bases.

Before the researchers undertook this research, they had already found in a previous study that muscle cells from people with type II diabetes showed such telltale epigenetic alterations to their DNA, particularly in the PGC-1 gene, which orchestrates metabolic programmes critical to the burning of fat in mitochondria, the chambers in cells that generate energy.

In the current study, the researchers achieved the most significant result when they exposed the healthy muscle cells to the edible fatty acid, palmitic acid.

The team found that the PGC-1 gene became methylated, just as it is in people with diabetes.

“The palmitic acid essentially switches off the gene,” New Scientist magazine quoted Zierath as saying.

She says that the fact that fat produces such an effect is highly significant, as it means that over-consumption of junk food may cause the same response.

“It suggests that if you eat a fat-rich diet, something in that – either the fat itself or the build up of metabolites – triggers the methylation of genes. The net effect is that it switches off the gene,” says Zierath.

The team’s analyses also reveal that the shutdown of PGC-1 led to inactivation of other genes vital for burning or transporting fat.

Zierath says that her team’s next step will be to find out how different diets affect the methylation status of PGC-1 and other genes vital for burning energy, hoping that their efforts will lead to the discovery of a potential mechanism by which type II diabetes develops.

A research article on her study has been published in the journal Cell Metabolism. (ANI)

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Kudzu extract shows promise as dietary supplement for metabolic syndrome

September 4, 2009 By admin Leave a Comment

Washington, Sep 4 (ANI): Kudzu, the nuisance vine that has overgrown almost 10 million acres in the southeastern United States, can be used as a dietary supplement for metabolic syndrome.

Scientists in Alabama and Iowa have found that root extracts from kudzu show promise as a dietary supplement for metabolic syndrome that increases the risk of obesity, high blood pressure, high blood cholesterol, and problems with their body”s ability to use insulin.

Those disorders mean a high risk for heart attacks, strokes, and other diseases.

Lead researcher J. Michael Wyss showed that kudzu root extract contains healthful substances called isoflavones.

People in China and Japan have long been using kudzu supplements as a health food.

The study found that a kudzu root extract had beneficial effects on lab rats with metabolic syndrome.

After two months of taking the extract, the rats had lower cholesterol, blood pressure, blood sugar, and insulin levels that a control group not given the extract.

Kudzu root “may provide a dietary supplement that significantly decreases the risk and severity of stroke and cardiovascular disease in at-risk individuals,” the article notes.

The study appears in Journal of Agricultural and Food Chemistry. (ANI)

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Bariatric surgery can eliminate diabetes symptoms

August 28, 2009 By admin Leave a Comment

London, Aug 28 (ANI): Weight-loss surgery can help eliminate the symptoms of type 2 diabetes in nearly 80 percent patients, an international study has found.

The research team led by Professor Henry Buchwald of the Department of Surgery at the University of Minnesota, Minneapolis, observed almost 135,000 patients for the study.

The findings concluded that 78 per cent patients had a “complete resolution” of diabetes for up to two years post-surgery, while 87 either saw resolution or noted an improvement in their condition, reports Timesonline.

Type 2 diabetes is common to obese people and occurs when the body stops producing or using insulin, the hormone that maintains the sugar level in blood.

Losing weight can help the body to efficiently use available insulin, and thus prevent kidney failure, nerve damage and eye problems.

The weight-loss surgery, medically known as the bariatric surgery, or the gastric-band operation, fits a band around the upper part of the stomach, restricting the amount people can eat before feeling full. Though the operation can benefit diabetes patients, it is advised only for the very obese, who’ve failed to lose weight otherwise.

But charity Diabetes UK is a little sceptical about the findings of the research.

Zoë Harrison, care adviser for the charity, said: “Although the data shows good results from bariatric surgery, it must be remembered that any surgery carries serious risks.

“Bariatric surgery should be considered only as a last resort. It can lead to dramatic weight loss, which in turn may result in a reduction in people taking their type 2 diabetes medication, and even in some people needing no medication at all. This does not mean type 2 diabetes has been cured.

“These people will still need to eat a healthy, balanced diet and be physically active to manage their diabetes.” (ANI)

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Bariatric surgery can eliminate diabetes symptoms

August 28, 2009 By admin Leave a Comment

London, Aug 28 (ANI): Weight-loss surgery can help eliminate the symptoms of type 2 diabetes in nearly 80 percent patients, an international study has found.

The research team led by Professor Henry Buchwald of the Department of Surgery at the University of Minnesota, Minneapolis, observed almost 135,000 patients for the study.

Type 2 diabetes is common to obese people and occurs when the body stops producing or using insulin, the hormone that maintains the sugar level in blood.

Losing weight can help the body to efficiently use available insulin, and thus prevent kidney failure, nerve damage and eye problems.

But charity Diabetes UK is a little sceptical about the findings of the research.

Zoë Harrison, care adviser for the charity, said: “Although the data shows good results from bariatric surgery, it must be remembered that any surgery carries serious risks.

“These people will still need to eat a healthy, balanced diet and be physically active to manage their diabetes.” (ANI)

Molecule having anti-fat, anti-cancer abilities found to be a turnoff for fat genes

August 28, 2009 By admin Leave a Comment

Washington, Aug 28 (ANI): Researchers at Baylor College of Medicine have found that a small molecule, earlier found to have anti-fat and anti-cancer abilities, has the potential to put off fat-making genes.

Such action in mice genetically prone to obesity causes the animals to become leaner, they say.

The researchers have also found the molecule to lowers the amount of fat in the mice’s livers, along with their blood sugar and cholesterol levels.

“We are frankly very excited about it. It goes to the origin of [fat synthesis] – all the way back to gene expression,” said Salih Wakil at Baylor.

Unlike cholesterol-lowering statins in use today, which block a single enzyme in the pathway, the chemical the researchers call fatostatin, “hits fat from the very beginning,” said Motonari Uesugi.

As a result, fatostatin influences many of the genes involved in fat production and in various aspects of metabolic syndrome – a collection of risk factors including obesity, high cholesterol and insulin resistance – in one go.

Studies in cell culture showed that fatostatin, previously known only as 125B11, significantly lowers the activity of 63 genes, including 34 directly associated with fatty acid or cholesterol synthesis.

Many of these genes were known to be under the control of SREBP – a transcription factor which act as a well-known master controller of fat synthesis.

After more detailed analysis, the researchers found that the drug candidate blocked SREBP by preventing it from becoming active and entering the nucleus, where it would otherwise switch on the fat-making program.

According to them, it operates by binding another protein (called SCAP), which serves as SREBP’s escort into the nucleus.

It was found that obese mice injected with fatostatin show noticeable reductions in their weight despite little difference in their eating habits, the researchers report.

After four weeks of treatment, the animals weighed 12 percent less and had 70 percent lower blood sugar levels.

Their cholesterol levels (both LDL and HDL) were down too. The concentration of fatty acids in their blood was actually higher- a sign of their greater demand for fat to burn.

While the livers of the obese mice were heavy and pale with fat, treated animals’ livers were more than 30 percent lighter and were a healthy-looking red.

Although less obvious, the SREBP-blocking ability might also explain the molecule’s earlier reported effects against prostate cancer cells in culture as well.

They explained that cells need fatty acids and cholesterol to build their cell membranes and continue growing.

Researchers are optimistic that fatostatin could prove to be clinically useful in the context of obesity, and perhaps cardiovascular disease and diabetes as well.

“Hopefully down the road, fatostatin or a derivative of fatostatin may be helpful. It could have a broad impact on the key diseases we all suffer from,” said Wakil.

Uesugi said that fatostatin or its analogs may also serve a tool for gaining further insights into the regulation of SREBP and fat metabolism.

The study has been published in the journal Chemistry and Biology. (ANI)

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Genetic discovery could pave way for obesity, diabetes treatments

August 27, 2009 By admin Leave a Comment

Washington, Aug 27 (ANI): Researchers at University of Central Florida have identified a new genetic mechanism that controls the body’s fat-building process, paving way for treatments for obesity and type 2 diabetes.

The discovery has the potential to help hundreds of millions of people and dramatically cut health care costs.

Led by Pappachan Kolattukudy, director of UCF’s Burnett School of Biomedical Sciences in the College of Medicine, found that a gene called MCPIP (Monocyte Chemotactic Protein-1 Induced Protein) controls the development of fat cells.

Until now, a different protein, known as peroxisome proliferator-activated receptor gamma (PPAR gamma), has been universally accepted as the master controller of fat cell formation, known as adipogenesis.

But the new findings has opened new doors for scientists looking forward to develop drugs that could benefit the more than 300 million people worldwide who are clinically obese, and who have much higher risks of suffering from chronic disease and disability.

Besides, it is projected that more than 300 million people will be diabetic by the year 2025.

Kolattukudy said MCPIP is potentially an ideal target for drugs that would prevent the body from becoming resistant to insulin and prone to type 2 diabetes.

“Our research has shown that MCPIP is a regulator of fat cell formation and blood vessel formation that feeds the growing fat tissue. Therefore, a drug that can shut down its function can prevent obesity and the major inflammatory diseases resulting from obesity, including diabetes and cardiovascular diseases,” the expert said.

For the study, the researchers introduced MCPIP to living cells from mice that had been stripped of the PPAR gamma gene and found that the cells still completed the developmental process necessary to build fat.

Now, the researchers are planning to explore chemical combinations to discover drugs that are effective at shutting down the novel gene.

The development of new drugs that can block or slow down the formation of MCPIP likely would take several years.

The findings will be published in the October issue of the Journal of Biological Chemistry. (ANI)

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Kids ‘more likely to develop diabetes in winters’

August 25, 2009 By admin Leave a Comment

London, Aug 24 (ANI): Kids under the age of 15 are at a higher risk of developing type 1 diabetes in winters, finds a new study.

Researchers from National Institute for Health and Welfare have found that this winter trend was more prevalent in boys as well as in both sexes from the older age groups 5 to 14 years old.

Unlike Type 2 diabetes, which develops in middle age, the Type 1 form typically arises in childhood and requires lifelong supplements of insulin.

The condition develops when the insulin-producing cells in the pancreas have been destroyed.

It is not known for sure why these cells have been damaged but the most likely cause is an abnormal reaction of the body to the cells. This may be triggered by a viral or other infection.

“Numerous reasons have been suggested for the apparent seasonality of the onset of Type 1 diabetes,” Times Online quoted Elena Moltchanova, who led the study, as saying.

“These include a seasonal variation in people’s levels of blood glucose and insulin, seasonal viral infections, the fact that young people tend to eat more and do less physical activity during winter months and, similarly, that summer holidays provide a rest from school stress and more opportunity to play outdoors,” Moltchanova added.

Contrary to the previous study results, Victoria King, research manager at the charity Diabetes UK said, “this larger study shows a stronger correlation which is interesting, especially as we still don’t know exactly why Type 1 diabetes develops.

“Investigating why we might be seeing this pattern could tell us more about what may be triggering the development of Type 1 diabetes.”(ANI)

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High insulin levels may increase prostate cancer risk

August 22, 2009 By admin Leave a Comment

Washington, Aug 22 (ANI): Researchers have found that high insulin levels might increase the risk of developing prostate cancer.

Lead researcher Dr Demetrius Albanes, of the Nutritional Epidemiology Branch, Division of Cancer Epidemiology and Genetics at the National Cancer Institute in Bethesda, Md., examined the relationship of the level of serum insulin and glucose, as well as surrogate indices of insulin resistance, to the development of prostate cancer.

The study showed that elevated insulin levels in the normal range appear to be associated with an increased risk of prostate cancer.

When subjects in the second through fourth quartiles of serum insulin concentration were compared with those in the first or lowest quartile, higher insulin levels within the normal range were associated with statistically significantly increased risk of prostate cancer.

The findings appear in the Journal of the National Cancer Institute. (ANI)

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It’s official: weight loss improves depressed people’s mood

July 29, 2009 By admin Leave a Comment

Washington, July 28 (ANI): In a new study, researchers have shown that a weight loss program not only counteracts depressed mood but also reduces risk factors for heart disease and stroke in obese patients.

They found that after a 6-month behavioral weight loss program, depressed patients not only lost 8 percent of their initial weight but also reported significant improvements in their symptoms of depression, as well as reductions in triglycerides, which are a risk factor for heart disease and stroke.

“This research is novel because clinically depressed individuals are not usually included in weight loss trials due to concerns that weight loss could worsen their depression,” said Dr. Lucy Faulconbridge, lead author of the study.

“These concerns, however, are not based on empirical evidence, and the practice of excluding depressed individuals from clinical weight loss trials means that we are learning nothing about this high-risk population,” Faulconbridge added.

The new findings suggest that depressed, obese individuals can indeed lose clinically significant amounts of weight, and that weight loss can actually reduce symptoms of depression.

Faulconbridge and colleagues recruited 51 depressed and non-depressed subjects into the study to follow a supervised weight loss program that included lifestyle modification and meal replacements.

Both depressed and non-depressed subjects lost significant amounts of weight, with depressed individuals losing 8 percent of their initial body weight, compared with 11 percent loss by non-depressed individuals.

After 6 months on the weight loss program, depressed subjects also showed significant improvement of their depressive symptoms, based on a questionnaire.

Additional significant improvements in glucose, insulin and high-density lipoprotein (HDL) cholesterol were observed in both depressed and non-depressed subjects, and depressed individuals showed reduced levels of triglycerides in the blood, which have been linked to risk of heart disease and stroke.

“Depression and obesity are independently associated with increased risk of heart disease and stroke, and so reductions in both body weight and symptoms of depression are likely to improve long-term health outcomes,” said Faulconbridge.

The study is to be presented at the Annual Meeting of the Society for the Study of Ingestive Behavior (SSIB). (ANI)

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Signalling pathway operational in intra-abdominal fat identified

July 15, 2009 By admin Leave a Comment

Washington, July 15 (ANI): Ben-Gurion University of the Negev (BGU) researchers and Germany-based University of Leipzig experts have announced the identification of a signalling pathway that is operational in intra-abdominal fat, the fat depot that is most strongly tied to obesity-related morbidity.

“Fat tissue in obesity is dysfunctional, yet, the processes that cause fat tissue to malfunction are poorly understood-specifically, it is unknown how fat cells ‘translate’ stresses in obesity into dysfunction,” said Dr. Assaf Rudich, senior lecturer from the Department of Clinical Biochemistry at Ben-Gurion University.

Fat tissue is no longer considered simply a storage place for excess calories, but in fact is an active tissue that secretes multiple compounds, thereby communicating with other tissues, including the liver, muscles, pancreas and the brain.

Normal communication is needed for optimal metabolism and weight regulation, but in obesity, fat (adipose) tissue becomes dysfunctional, and mis-communicates with the other tissues.

According to the researchers, this places fat tissue at a central junction in mechanisms leading to common diseases attributed to obesity, like type 2 diabetes and cardiovascular diseases.

The researchers highlight the fact that fat tissue dysfunction is believed to be caused by obesity-induced fat tissue stress: Cells over-grow as they store increasing amounts of fat. They say that this excessive cell growth may cause decreased oxygen delivery into the tissue; individual cells may die (at least in mouse models), and fat tissue inflammation ensues.

Excess nutrients, they add, may also lead to increased metabolic demands, and cause cellular stress.

The BGU and Leipzig teams collected fat tissue samples from people undergoing abdominal surgery, and identified a signalling pathway that is operational in intra-abdominal fat, the fat depot that is most strongly tied to obesity-related morbidity.

They say that the degree of activation of a signalling pathway from these individuals was compared with those of leaner people, those with obesity predominantly characterized by accumulation of “peripheral” fat, and those with obesity with predominant accumulation of fat within the abdominal cavity.

They found that the signalling pathway was more active depending on the amount of fat accumulation in the abdomen, and that it correlated with multiple biochemical markers for increased cardio-metabolic risk.

In their study report, they have revealed that the expression of one of the upstream signaling components, a protein called ASK1, predicts whole-body insulin resistance (an endocrine abnormality that is strongly tied to diabetes and cardiovascular disease), independent of other traditional risk factors.

The researchers have also shown that although non-fat cells within adipose tissue express most of this protein in lean persons, the adipocytes themselves increase its expression by more than four-fold in abdominally-obese persons.

“The importance of this study is not only in contributing to the understanding of adipose tissue dysfunction in obesity, but as a consequence, may provide important leads for novel ways to prevent the dangerous consequences, such as type 2 diabetes, of intra-abdominal fat accumulation,” states Dr. Iris Shai, a BGU researcher at the S. Daniel Abraham International Center for Health and Nutrition and Soroka University Medical Center in Beer-Sheva, Israel.

The study has been published in the Endocrine Society’s the Journal of Clinical Endocrinology and Metabolism. (ANI)

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Grapefruit derivative ‘prevents obesity’

July 14, 2009 By admin Leave a Comment

Washington, July 14 (ANI): A new study on mice, conducted by University of Western Ontario researchers, has shown that grapefruit contains a substance that’s a natural fat fighter.

Derived from citrus fruit, particularly grapefruit, the substance has shown it can reduce weight gain and fatty particles in the body, Murray Huff of UWO’s Robarts Research Institute said.

The substance, a flavonoid – a bioactive molecule – called naringenin, shows promise as an inhibitor of conditions associated with type 2 diabetes and cardiovascular disease, he said.

In the study, one group of mice was fed a high-fat diet to induce the symptoms of metabolic syndrome. A second group was fed the exact same diet and treated with naringenin.

Naringenin corrected the elevations in triglyceride and cholesterol, prevented the development of insulin resistance and completely normalized glucose metabolism.

The researchers found it worked by genetically reprogramming the liver to burn up excess fat, rather than store it.

“Furthermore, the marked obesity that develops in these mice was completely prevented by naringenin,” said Huff.

“What was unique about the study was that the effects were independent of caloric intake, meaning the mice ate exactly the same amount of food and the same amount of fat. There was no suppression of appetite or decreased food intake, which are often the basis of strategies to reduce weight gain and its metabolic consequences,” Huff added.

This study investigated naringenin’s preventative properties, but Huff is also investigating whether it can treat obesity and other existing metabolic problems.

The findings are published online in the journal Diabetes. (ANI)

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Walking or biking to work boosts fitness

July 14, 2009 By admin Leave a Comment

Washington, July 14 (ANI): Walking or biking to work can boost fitness, and reduce the risk of cardiovascular disease, say researchers.

“Active commuting was positively associated with fitness in men and women and inversely associated with body mass index, obesity, triglyceride levels, blood pressure and insulin level in men,” say Dr Penny Gordon-Larsen and colleagues at the School of Public Health, University of North Carolina at Chapel Hill.

During the study, the researchers looked at 2,364 adults in the Coronary Artery Risk Development in Young Adults (CARDIA) study who worked outside the home.

The participants reported the length of their commute in minutes and miles, including details on the percentage of the trip taken by car, public transportation, walking or bicycling.

The researchers further assessed participants’ height, weight and other health variables, including blood pressure and fitness levels as assessed by a treadmill test.

A total of 16.7 percent of the participants used any means of active commuting to reach their workplace.

The study showed active commuters were less likely to be overweight or obese and have healthier triglyceride levels, blood pressure and insulin levels.

The results add to existing evidence that walking or biking to work is beneficial.

“Furthermore, increasing active commuting will have the dual benefits of increasing population health and in reduction of greenhouse gas emissions. Environmental supports for commuting, such as physical environment and sociocultural factors, have been shown to promote active forms of commuting,” said the authors.

The study has been published in the Archives of Internal Medicine. (ANI)

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