New role for zebrafish in human studies

Washington, May 20 (ANI): Zebrafish – an important animal model in disease and environmental studies – could eventually help scientists in revealing the function of a mysterious enzyme linked to the steroid cortisol, and found in the human brain, found a researcher at the University of California, San Diego School of Medicine.

In people and other vertebrates, steroids like cortisol perform a variety of diverse duties, including regulating immune response, bone formation and brain activity.

However, too much cortisol is unhealthy. High levels of the steroid have been linked to type 2 diabetes and may impair the brain”s ability to store memories.

The human body regulates cortisol by employing an enzyme called 11 beta-hydroxysteroid dehydrogenase-type 1 or 11beta-HSD1, which catalyzes the synthesis of cortisol in liver and fat cells.

A related enzyme known as 11 beta-HSD-type3 or 11 beta-HSD3 is expressed in the brain, though its utility remains unknown.

In new findings, Dr. Michael E. Baker has reported that 11 beta-HSD3 (but not 11 beta-HSD1) is present in zebrafish, where it appears to serve an important role in fish endocrine physiology.

This makes the fish a potentially useful analog for cortisol studies, including discovering the purpose and function of 11 beta-HSD3 in human brains, which may be an evolutionary precursor to 11 beta-HSD1.

Interestingly, Baker found that the genomes of mice and rats do not contain 11 beta-HSD3.

This means that inserting the appropriate gene for the enzyme in these animal models could provide additional avenues of investigation.

The study will be published in the latest issue of FEBS Letters. (ANI)

Why men store fat in their bellies, women in their hips

Washington, May 15 (ANI): Researchers claim to have answered the age-old question of why men store fat in their bellies and women store it in their hips – the fat tissue is almost completely different, genetically speaking that is.

“We found that out of about 40,000 mouse genes, only 138 are commonly found in both male and female fat cells,” said Dr. Deborah Clegg, assistant professor of internal medicine at UT Southwestern Medical Center and senior author of the study appearing in the International Journal of Obesity. “This was completely unexpected. We expected the exact opposite – that 138 would be different and the rest would be the same between the sexes.”

The study involved mice, which distribute their fat in a sexually dimorphic pattern similar to humans.

“Given the difference in gene expression profiles, a female fat tissue won”t behave anything like a male fat tissue and vice versa,” Dr. Clegg said. “The notion that fat cells between males and females are alike is inconsistent with our findings.”

In humans, men are more likely to carry extra weight around their guts while pre-menopausal women store it in their butts, thighs and hips.

The bad news for men is that belly, or visceral, fat has been associated with numerous obesity-related diseases including diabetes and heart disease. Women, on the other hand, are generally protected from these obesity-related disorders until menopause, when their ovarian hormone levels drop and fat storage tends to shift from their rear ends to their waists.

“Although our new findings don”t explain why women begin storing fat in their bellies after menopause, the results do bring us a step closer to understanding the mechanisms behind the unwanted shift,” Dr. Clegg said.

For the study, researchers used a microarray analysis to determine whether male fat cells and female fat cells were different between the waist and hips and if they were different based on gender at a genetic level.

Because the fat distribution patterns of male and female mice are similar to those of humans, the researchers used the animals to compare genes from the belly and hip fat pads of male mice, female mice and female mice whose ovaries had been removed – a condition that closely mimics human menopause. Waist and hip fat (subcutaneous fat) generally accumulates outside the muscle wall, whereas belly fat (visceral fat), a major health concern in men and postmenopausal women, develops around the internal organs.

In addition to the genetic differences among fat tissues, the researchers found that male mice that consumed a high-fat diet for 12 weeks gained more weight than female mice on the same diet. The males” fat tissue, particularly their belly fat, became highly inflamed, while the females had lower levels of genes associated with inflammation. The female mice whose ovaries had been removed, however, gained weight on the high-fat diet more like the males and deposited this fat in their bellies, also like the males.

“The fat of the female mice whose ovaries had been removed was inflamed and was starting to look like the unhealthy male fat,” Dr. Clegg said. “However, estrogen replacement therapy in the mice reduced the inflammation and returned their fat distribution to that of mice with their ovaries intact.”

Dr. Clegg said the results suggest that hormones made by the ovaries may be critical in determining where fat is deposited. (ANI)

Proper calcium supplement early in life key to lifelong bone health

Washington, May 14 (ANI): A new study has revealed that not only is calcium required for strong and healthy bones, it could also play a vital role in determining bone health for life.

The new research from North Carolina State University conducted an 18-day trial involving 24 newborn pigs, half of which were fed a calcium deficient diet, and the other half, calcium rich diet.

They found that the bone densities in the pigs that were fed the calcium-deficient diet were lower as compared to that of the other half. Moreover, certain stem cells in bone marrow, in the calcium-deficient piglets appeared to have already been programmed to become fat cells instead of bone-forming cells.

However, blood tests didn”t indicate any difference in levels of the hormonal form of vitamin D, which regulates the amount of calcium circulating in the blood of older children and adults. Dr. Chad Stahl, an associate professor of animal science who led the study, said this suggests that calcium regulation in newborns isn”t dependent on vitamin D.

Because these programmed mesenchymal stem cells replicate to provide all the bone-forming cells for an animal”s entire life, very early calcium deficiency may have predisposed the piglets to have bones that contain more fat and less mineral. That could make those pigs more prone to osteoporosis and obesity in later life, said Stahl.

The researchers plan to extend this study to see if the calcium deficiency in early life in the piglets also has an impact on sexual maturity.

The researchers are using pigs as a model for human health because pigs and humans are similar when it comes to bone growth and nutrition. Pigs are one of the few animals known to experience bone breaks related to osteoporosis, Stahl said.

“For me,” Stahl said, “the biggest message is that calcium nutrition, or mineral nutrition as a whole, needs to be a priority from day one. Early life nutrition is setting children up physiologically for the rest of their lives.” (ANI)

Spare tyres ”a major health hazard”

London, April 20 (ANI): Experts have said that people carrying excess weight around their waists, are oblivious to the health risk they are putting themselves in.

Three leading UK charities are launching a new Active Fat campaign to raise awareness of the dangers, after it was seen that most people do not realise that their spare tyre puts them at increased risk of cancer, diabetes and heart disease.

The poll on 2,085 people showed that in all, 97 percent of people were unaware of a link despite 71 percent of those surveyed saying they had an expanding waistline.

Excess weight around the middle generates oestrogen and excess chemicals in the stomach, which put people at higher risk of killer diseases.

Women are at risk of Type 2 diabetes and heart disease if their waist measures more than 80cm (31.5 inches) while men are at risk at more than 94cm (37 inches).

“That ”harmless” spare tyre around your waist is actually a major health hazard,” the BBC quoted Dr Mike Knapton, of the British Heart Foundation charity which is working alongside Cancer Research UK and Diabetes UK, as saying.

“While you might be relaxing at home, your fat cells are working overtime to pump out excess hormones and other chemicals that can cause disease.

“Wrapping a tape measure around your middle takes just a few seconds, but it could be your vital first step towards a healthier future,” he said.

Waist size is likely to increase throughout life, but many are in denial about their spare tyre, say the charities.

In the poll, women were less likely than men to worry about the health consequences of their muffin top and instead were more concerned with how they looked and whether they could fit into their clothes.

Less than half of men and women (44 percent) had tried to do more exercise as a way to avoid going up in belt size, while some 27 percent of people bought bigger sized clothes.

As part of the campaign, the charities are calling for standard labelling on foods, highlighting the “traffic lights” system for nutrition. (ANI)

New stem cell therapy to help women regrow breasts after cancer surgery

Melbourne, Apr 17 (ANI): A new stem cell therapy developed by Melbourne scientists could help women regrow their breasts after cancer surgery.

Doctors at the Bernard O”Brien Institute of Microsurgery will start the trial for new technique called Neopec in coming months.

The new method uses a woman”s own regenerative capacity to grow new fat tissue in her breasts.

The world-first trial will involve five women who have had tissue removed during surgery to remove cancer, and the first results could be reported by the end of the year.

Neopec involves implanting a breast-shaped biodegradable chamber into the chest before surgeons redirect blood vessels into the chamber with the patient”s own fat cells.

A gel is inserted to help the cells multiply over four to six months, and the chamber dissolves when the new breast is fully formed.

According to lead researcher Wayne Morrison, after successfully trialling the procedure on pigs, he was about 50 per cent sure it would work in humans.

””If it works it will be great, but we can”t be sure that it will yet,” the Age quoted Professor Morrison as saying.

The new chief executive of the operation, Dr Peter Mountford, said if the trial was successful, by 2013 he would offer the procedure to women in Australia, Europe and south-east Asia who had had a partial mastectomy, defects of previous reconstructions or congenital deformities.

And the cosmetic market would come next.

””By 2015, Neopec will be able to provide full breast reconstruction and by 2020, in conjunction with a global partner, it will provide a natural alternative to women within the burgeoning breast augmentation market,”” said Mountford.

He said the procedure would be marketed at a premium price to implants currently on the market because it would be safer and more natural than the insertion of foreign materials.

Once perfected, it would also involve only one procedure and a shorter hospital stay than existing implantation methods. (ANI)

New strategy to treat type 2 diabetes

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)

Body fat could act as a natural scaffold for tissue growth

Washington, Mar 26 (ANI): When Deepak Nagrath, the Indian-origin researcher at Rice University, threw away the sticky substance secreted by the cells while finding ways to grow cells in a scaffold, little did he know that it was the very thing he was looking for— body fat.

The substance, derived from adipose cells—body fat—turned out to be a natural extracellular matrix.

“I thought it was contamination, so I threw the plates away,” said Nagrath.

And since then, Nagrath and his colleagues have built a biological scaffold that allows cells to grow and mature.

He hopes the new material, when suffused with stem cells, will someday be injected into the human body, where it can repair tissues of many types without fear of rejection.

And the basic idea is simple—prompt fat cells to secrete what bioengineers call “basement membrane.”

The membrane mimics the architecture tissues naturally use in cell growth, literally a framework to which cells attach while they form a network.

When the cells have matured into the desired tissue, they secrete another substance that breaks down and destroys the scaffold.

Structures that support the growth of living cells into tissues are highly valuable to pharmaceutical companies for testing drugs in vitro. Companies commonly use Matrigel, a protein mixture secreted by mouse cancer cells, but for that reason it can”t be injected into patients.

“Fat is one thing that is in excess in the body. We can always lose it,” said Nagrath.

The substance derived from the secretions, called Adipogel, has proven effective for growing hepatocytes, the primary liver cells often used for pharmaceutical testing.

“My approach is to force the cells to secrete a natural matrix,” he said.

The matrix is a honey-like gel that retains the natural growth factors, cytokines and hormones in the original tissue.

Nagrath is convinced that his strategy is ultimately the most practical for rebuilding tissue in vivo, and not only because it may cost significantly less than Matrigel.

“The short-term goal is to use this as a feeder layer for human embryonic stem cells. It”s very hard to maintain them in the pluripotent state, where they keep dividing and are self-renewing,” he said.

Once that goal is achieved, Adipogel may be just the ticket for transplanting cells to repair organs.

“You can use this matrix as an adipogenic scaffold for stem cells and transplant it into the body where an organ is damaged. Then, we hope, these cells and the Adipogel can take over and improve their functionality,” said Nagrath.

The research appeared last week in the Federation of American Societies for Experimental Biology (FASEB) Journal. (ANI)

Leptin therapy shows promise for diabetes

Washington, March 24 (ANI): UT Southwestern Medical Center researchers have found that using leptin alone in place of standard insulin therapy could abate symptoms of type 1 diabetes.

Using mouse models, the researchers found that leptin administered instead of insulin showed better management of blood-sugar variability and lipogenesis, the conversion of simple sugars into fatty acids.

Leptin is a hormone produced by fat cells and involved in the regulation of body weight.

Dr. Roger Unger, professor of internal medicine at UT Southwestern, led the study.

Insulin treatment has been the gold standard for type 1 diabetes (insulin-dependent diabetes) in humans since its discovery in 1922. Dr. Unger’s laboratory found that insulin’s benefit resulted from its suppression of glucagon, a hormone produced by the pancreas that raises blood sugar levels in healthy individuals.

“Insulin cells are destroyed in people with type 1 diabetes, however, and matching the high insulin levels needed to reach glucagon cells with insulin injections is possible only with amounts that are excessive for other tissues,” said Unger, senior author of the latest study.

“Peripherally injected insulin cannot accurately duplicate the normal process by which the body produces and distributes insulin,” Unger added.

People on insulin therapy tend to experience large swings in blood-sugar levels, said Dr. Unger. Other studies have shown that frequent blood-sugar variation complicates the symptoms of type 1 diabetes, which affects about 1 million people in the U.S.

Benefits of letpin’s glucose-lowering action appear to involve the suppression of glucagon. Normally, glucagon is released when the glucose level in the blood is low, thanks to supervision by insulin release from neighboring cells.

In insulin deficiency situations, however, glucagon levels are inappropriately high and cause the liver to release excessive amounts of glucose into the bloodstream.

This action is opposed by insulin, which tells the body’s cells to remove sugar from the bloodstream.

“Leptin treatment in the non-obese type 1 diabetic mouse profoundly reduced food intake, which in turn reduced body fat. And like insulin, leptin suppresses glucagon in the body and helps increase lean body mass,” Unger said.

The findings are available online and in a future issue of the Proceedings of the National Academy of Sciences. (ANI)

‘Two for one’ breast boosting technique not as viable as it seems

London, Sep 16 (ANI): A technology that was claimed as the ultimate solution to give a boost to women’s breasts by using fat removed from thighs is not viable as it seems, say experts.

Mel Graham, chairman of the Harley Medical Group, recently claimed that the “two for one” procedure could extract excess fat from where it was not wanted – the belly, hips or thighs – and relocate it to the bust.

However, rival cosmetic surgeons criticised the “hype” surrounding the new operation, insisting that it was “premature”.

“(This) is setting consumers up for disappointment and there are many reasons for vigilance,” the Independent quoted Dai Davies, of Plastic Surgery Partners in Harley Street, as saying.

He said that doctors have long been experimenting with innumerable aids to give women larger busts, including using body fat as a procedure.

The technique of removing fat by liposuction, and then injecting it into the chest has been tried for almost 20 years but with limited success, said Davies.

“Where you are injecting small amounts of fat into the face, which has a good blood supply, there is good evidence that it works. Most plastic surgeons would agree there is a place for it. But this involves injecting a large blob of fat into the breast area. Fat consists of living cells and living cells must have a blood supply, otherwise they die,” he explained.

In a Japanese study last year, 230 women underwent fat transfer, and it was found that, on average, half the fat injected was lost and all the women needed a second procedure after a year.

There are also fears that dying fat cells could cause micro-calcification in the breast leading to difficulties in breast screening and an increase in biopsies – an invasive procedure to remove tissue to check for cancer.

“I don’t think we should be a testing ground for all these techniques. You are feeding on a susceptible group of people. There should be controls but, sadly, the Government has decided it won’t implement regulation,” said Davies.

Professor David Sharpe, a plastic surgeon in Yorkshire and the founding chairman of the breast special interest group of BAAPS, said: “This sounds like another example of creative marketing. Breast implants are a well-tried and tested method. At the moment, I would stick with that.”

Mel Braham, chairman of the Harley Medical Group, said results of a US trial to be presented next month would demonstrate the success of the operation.

“The results will be assessed by our medical board and, if approved, the operation will be introduced next year. I don’t take risks with patients. I am confident this is a safe procedure,” he said. (ANI)

Exercise the best bet to fight weight regain

Washington, Sept 3 (ANI): Exercise can help control weight regain after dieting by reducing appetite and burning fat before burning carbohydrates, according to a new study.

According to researchers from the University of Colorado Denver, burning fat first and storing carbohydrates for use later in the day slows weight regain and may minimize overeating by inducing a feeling of fullness to the brain.

They insist that exercise prevents the increase in the number of fat cells that occurs during weight regain.

This discovery also challenges the conventional wisdom that the number of fat cells is set and cannot be altered by dietary or lifestyle changes.

These coordinated physiological changes in the brain and the body lower the ‘defended’ weight, that is, the weight that our physiology drives us to achieve, and suggest that the effects of exercise on these physiological processes may make it easier to stay on a diet.

During the study, the researchers used obesity-prone rats. For the first 16 weeks, the rats ate a high-fat diet, as much as they wanted, and remained sedentary.

They were then placed on a diet. For the following two weeks, the animals ate a low-fat and low-calorie diet, losing about 14pct of their body weight.

The rats maintained the weight loss by dieting for eight more weeks. Half the rats exercised regularly on a treadmill during this period while the other half remained sedentary.

The findings revealed that exercising rates regained less weight and burned more fat early in the day, and more carbohydrates later in the day.

It reduced drive to overeat and enhanced the ability to balance energy intake with energy expended.

The team will do further research to demonstrate that exercise is, indeed, preventing the formation of new fat cells early in relapse and not simply altering the size of pre-existing fat cells.

The study appears in American Journal of Physiology. (ANI)

Genetic discovery could pave way for obesity, diabetes treatments

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)

Signalling pathway operational in intra-abdominal fat identified

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)

How obesity leads to diabetes

Washington, July 9 (ANI): Monash University researchers have found how obesity leads to type 2 diabetes – a finding that could lead to the design of a drug to prevent the disease.

Though obesity is associated as a leading cause of diabetes, no one has understood the exact mechanism of how obesity inhibits the body’s ability to use insulin leading to type 2 diabetes until now.

Now, the research team, led by Associate Professor Matthew Watt, discovered that fat cells release a novel protein called PEDF (pigment epithelium-derived factor), which triggers a chain of events and interactions that lead to development of Type 2 diabetes.

“When PEDF is released into the bloodstream, it causes the muscle and liver to become desensitised to insulin. The pancreas then produces more insulin to counteract these negative effects, ” Watt said.

“This insulin release causes the pancreas to become overworked, eventually slowing or stopping insulin release from the pancreas, leading to Type 2 diabetes.

“It appears that the more fat tissue a person has the less sensitive they become to insulin. Therefore a greater amount of insulin is required to maintain the body’s regulation of blood-glucose.

“Our research was able to show that increasing PEDF not only causes Type 2 diabetes like complications but that blocking PEDF reverses these effects. The body again returned to being insulin-sensitive and therefore did not need excess insulin to remain regulated,” Watt added.

The findings were published today in respected journal Cell Metabolism. (ANI)

Scientists exploring possibility of using Asian herbs to fight diabetes, obesity

Washington, July 8 (ANI): A team of researchers from the University of Massachusetts Amherst and Chungbuk Oriental Medicine Center in South Korea are exploring the possibility of using Asian medicinal herbs to manage the global epidemic of Type II diabetes and obesity.

Young-Cheul Kim, a UMass Amherst assistant professor of nutrition and an expert in how fat cells develop in the body, will study molecular-level biological function of certain medicinal herbs such as the vetch, Astragalus, also known as milk vetch or huang chi.

His lab will use a well characterized fat cell differentiation model to test a number of plant-based compounds or phytochemicals for potential anti-obesity and anti-diabetes properties, first in vitro cell culture, then in whole animals and finally in humans.

He says: “Overall, we are trying to understand the cellular and molecular mechanisms underlying the development of fat cells in the body, especially by bioactive food components, with the goal to find therapeutic strategies for not only preventing chronic diseases such as obesity, cancer and heart disease, but promoting overall health.

These chronic disorders are all related to our diet, illustrating the importance of nutrition.”

Despite its use for hundreds of years in Asia to prevent or treat certain diseases, evidence for health claims of the herb Astragalus is “limited” at present, according to the U.S. National Center for Complementary and Alternative Medicine. This is partly because one herb may contain so many different active components.

Kim notes the time has come to investigate, with rigorous scientific methods, what compounds are present and how they work.

Therefore, he says: “One of the goals of our collaboration with this prestigious center of Asian medicine in Chungbuk will be to identify any biologically active ingredients.”

Kim’s lab has already shown some preliminary evidence from experiments on mouse cells that an extract of the hardy high-altitude shrub, Rhodiola, also known as “golden root”, inhibits the generation of new fat cells from precursor cells called pre-adipocytes.

It acts by interfering with the genes that determine the progression of adipogenesis, or the formation of fat, the researcher says.

His team will extend their future studies to more compounds, and explore effects in primary cultures of human cells. If replicated, studies can move on to test effectiveness in whole body systems.

Though some may be surprised by the Korean medical center’s interest in research on obesity and diabetes, Kim says these conditions have emerged as public health problems in Asia over the past two decades with the availability of fast foods and a tendency toward decreased physical activity.

“We know from immigrant epidemiologic studies that a balanced diet and exercise play a critical role in maintaining health, preventing chronic diseases and reducing the incidence of metabolic syndromes such as diabetes and obesity. Unfortunately we can now see obese children throughout Asia, and many more people with diabetes,” says Kim, who grew up in Korea.

“So the major research centers and food industry are now very interested to investigate the possible functional and beneficial roles of plants and herbs, as well as their nutritional value,” he adds. (ANI)

Scientists identify new glucose-regulating protein linked with diabetes

Washington, May 29 (ANI): Scientists have found that a specialized protein in human muscles is linked with the process that clears glucose out of the bloodstream.

The finding by researchers at the University of California, San Francisco, and collaborators at Harvard Medical School, could shed light on what goes wrong in type 2 diabetes on a cellular level.

If the function of this protein (apparently absent in mice) is established, it could pave the way for future study and possible therapies for diabetes.

“Much has been learned from mouse models about glucose metabolism that is relevant to human diabetes, but what happens on a cellular level is now found to be different between the two species. This research shows one significant species-specific difference that will influence our understanding of mechanisms of type 2 diabetes,” said Dr. Frances Brodsky, senior author on the paper.

The researchers said that in humans, muscles play a key role in clearing glucose from the bloodstream-a process normally controlled by insulin, which stimulates the muscle cells to import glucose by means of a system known as the GLUT4 glucose transporter.

Usually GLUT4 is stored inside both human and mouse muscles in a special compartment that releases it upon insulin stimulation. Fat cells also form a GLUT4 compartment and take up glucose in response to insulin.

But, in type 2 diabetes, the muscle and fat cells fail to respond appropriately to the insulin and the GLUT4 compartment is abnormal-a function thought to be identical across mammal species.

The current research identified a protein in both human muscle and fat cells-called CHC22-that appears to control the formation of the GLUT4 storage compartments.

The team determined that this protein is a specialized form of an omnipresent housekeeping protein called clathrin, which is known to be instrumental in moving proteins between cellular compartments.

The researchers observed that CHC22 was associated with the abnormal GLUT4 compartments in muscles from diabetic patients, which, for an unknown reason, do not mobilize to the muscle cell surface when stimulated by insulin.

She particularly said that while mice have an insulin-responsive GLUT4 compartment, they lack the CHC22 protein.

Thus, this work has implications for developing better models for the study of type 2 diabetes.

The study has been published in the journal ‘Science’. (ANI)

Big waistline could surprisingly be a lifeline for heart disease sufferers

Washington, May 19 (ANI): Despite being a leading contributor to heart disease, obesity appears to play a protective role in a range of cardiovascular problems, says a new study.

Researchers found that obese heart patients respond better to strokes and heart attacks compared to normal or underweight patients.

Although obesity is a leading cause of heart disease, paradoxically scientists say fat and even high cholesterol may have protective benefits.
However, researchers say, losing weight is still best because obesity triggers more heart attacks and strokes.

The study has been published in the May 26, 2009, issue of the Journal of the American College of Cardiology.

“Obese patients with heart disease respond well to treatment and have paradoxically better outcomes and survival than thinner patients,” said Carl Lavie, M.D., F.A.C.C., medical director of Cardiac Rehabilitation and Prevention, Ochsner Medical Center, New Orleans, LA and lead author of the article.

“Although these patients have a more favorable short- and long-term prognosis, we don’t yet understand the mechanisms for why this might be the case,” the expert added.

The obesity paradox in patients with cardiovascular disease (CVD), which was first noticed earlier this decade, is complex. It is likely due to a combination of obesity’s impact on fat cells and other metabolic processes (e.g., insulin resistance, glucose metabolism, metabolic syndrome), as well as other consequences of being obese.

Dr. Lavie speculates that excess weight may be somewhat protective because these patients have more reserves to fight disease than thinner patients. Another explanation might be that obese patients present with problems earlier due to physical deconditioning (being out of shape) and other non-cardiovascular symptoms and, therefore, have the opportunity to be diagnosed with milder disease.

Although obese patients appear to experience fewer cardiovascular events and have better survival rates, Dr. Lavie is quick to caution that patients with heart disease shouldn’t incorrectly assume that gaining weight is the answer.

“Obesity is often what’s causing high blood pressure, blockages in arteries, and increased risk of sudden death in the first place. Such excess weight has adverse effects on all of the major cardiovascular risk factors and has increased the prevalence of heart disease,” he said.

“Taken together, most studies are supportive of purposeful weight loss for preventing and treating cardiovascular disease,” he added.

Health-promoting behaviors to stay active and lose weight can also confer benefits beyond initial heart disease. (ANI)

Anti-cellulite ‘wonder pants’ flying off shelves of renowned Brit store

London, May 11 (ANI): Fat-busting knickers from John Lewis disappeared in half an hour after the British store’s online shop was plagued by enthusiastic customers.

And the in-store stocks of the new anti-cellulite ‘wonder pants’ were further taken home by shoppers within hours of going on sale.

The Scala Bio-Fir underwear allegedly expels cellulite by using bio-crystals to heat the skin on contact, which in effect melts fat cells and smoothes the dimpled skin.

Sales of the 25-pound went sky rocketing after independent tests revealed that 82 per cent of women, who had tried the product for six hours every day, could see a “significant” reduction in cellulite over 30 days.

The store has now come up with a waiting list after thousands placed several pre-orders for the pants, claimed to be a firm favourite of celebrities such as Sienna Miller.

“Although we have always had confidence in this product, the unprecedented customer response has taken us a little bit by surprise. However more stock will be through in time,” the Mirror quoted the chain’s lingerie buyer Helen Spencer as saying. (ANI)

White tea may combat obesity epidemic

Washington, May 1 (ANI): A daily cup of white tea may help beat the bulge, say researchers.

Possible anti-obesity effects of white tea have been demonstrated in a series of experiments on human fat cells (adipocytes).
esearchers writing in BioMed Central’s open access journal Nutrition and Metabolism have shown that an extract of the herbal brew effectively inhibits the generation of new adipocytes and stimulates fat mobilization from mature fat cells.

Marc Winnefeld led a team of researchers from Beiersdorf AG, Germany, who studied the biological effects of an extract of white tea – the least processed version of the tea plant Camellia sinensis.

He said, “In the industrialized countries, the rising incidence of obesity-associated disorders including cardiovascular diseases and diabetes constitutes a growing problem. We’ve shown that white tea may be an ideal natural source of slimming substances”.

After treating lab-cultured human pre-adipocytes with the tea extract, the authors found that fat incorporation during the genesis of new adipocytes was reduced.

According to Winnefeld, “The extract solution induced a decrease in the expression of genes associated with the growth of new fat cells, while also prompting existing adipocytes to break down the fat they contain”.

White tea is made from the buds and first leaves of the plant used to make green tea and the black tea most commonly drunk in Western countries. It is less processed than the other teas and contains more of the ingredients thought to be active on human cells, such as methylxanthines (like caffeine) and epigallocatechin-3-gallate (EGCG) – which the authors believe to be responsible for many of the anti-adipogenic effects demonstrated in their study. (ANI)

Energy-burning brown fat’s presence in adults offers new obesity treatment strategy

Washington, April 17 (ANI): Swedish researchers have found that adults use brown fat to convert energy into heat, a finding that may lead to novel treatments for overweight and obesity.

Sven Enerback, Professor at the Institute of Biomedicine at the Sahlgrenska Academy, University of Gothenburg, points out that the brown fat found in infants is traditionally believed to disappear as a person grows up.

However, the researcher insists, the new study has shown the presence of brown fat cells in the lower part of the neck in adults, just above their collarbones.

During the study, the researchers tested the region of brown fat cells in the neck by placing five volunteers, in thin clothing, in a chilly room for a couple of hours.

Using PET scanning, the researchers studied this region, and found that metabolism there was on average 15 times higher than in the neighbouring white fat tissue.

Prof. Enerback says that the result suggests that the brown fat may play a significant role in metabolism.

The expert believes that this finding may pave the way for new and better ways of treating obesity.

Prof. Enerback reckons that any such novel treatments would be based on an exciting strategy that focuses on increasing the amount of fat burnt by the body, instead of focusing solely on reducing the intake of energy.

A report on this study has been published in The New England Journal of Medicine. (ANI)

Choose exercise over creams in fight against cellulite

Munich – Cellulite is a terrible part of aging for some women. They stare into the mirror appalled when they discover the ugly dips and dents on their bottoms and thighs.

But young, slim women also develop the undesirable feature, which makes the skin look a bit like an orange peel. Women who get it are at the mercy of the connective tissue under their skin. There is a range of products that promise help, but experts say a healthy diet and exercise are better to counteract cellulite.

“Every woman has a predisposition for developing cellulite,” said dermatologist Christoph Liebich of Munich. It’s one of nature’s injustices: Men generally don’t get it. The reason for that lies in the structure of the female connective tissue. A woman’s skin is more pliable and has more fat cells stored below it.

Aside from those differences, the collagen fibres of the female connective tissue are laid out parallel to each other and upright. In a man, they are woven in a network and slanted. Fat cells can squeeze into the collagen, creating the ugly dents on the surface. If the connective tissue gets weak while fat cells grow at the same time, cellulite is the result. There are ways to fight it.

“Lots of exercise, a proper diet that includes a lot of fruits and vegetables, carbohydrates that metabolize quickly, little fat and sufficient fluids are the most effective measures against cellulite,” said dermatologist Anne Hundgeburth of Cologne, a member of Germany’s professional association for dermatologists. Three goals are reached by taking these steps: Increased circulation in the connective tissue, fewer waste deposits and shrinkage of the fat cells.

“Doing sports helps to tighten the muscles underlying the tissue,” Liebich said. “When everything isn’t hanging down limp and untoned, the bottom and legs look a lot better.”

Because basic instincts lurk in everyone and can corrupt a training programme and iron discipline when eating, the cosmetic industry tries to steer customers toward a large selection of creams and gels that are supposed to inhibit cellulite.

The palette is multifaceted: One product has caffeine and sea algae to support the microcirculation of the skin and at the same time make it firm and elastic. Another with birch bark among its ingredients is meant to counter congestion in the tissue. Other products promise to improve circulation or stop fat cells from multiplying. Some of them say they can tighten one’s silhouette while sleeping.

The products are aimed generally at the same thing that is at the centre of any cellulite therapy. But experts doubt their effectiveness.

“Thus far no test has found a cream to be effective,” said Hanne Vedder of Germany’s consumer centre in Stuttgart. “People who believe they are getting rid of their cellulite because they are using a cream are mistaken.”

Doctors point to the fact that creams, gels and oils do not penetrate deeply enough into the skin to work where cellulite is.

“If anything at all, an increase in circulation in the upper layer of skin is induced,” said Hundgeburth. The active ingredients in the creams, gels and oils as a rule don’t reach the fat cells below the skin.

More important than the creams themselves is the massage effect of rubbing them into the skin, said Liebich.

“A proper massage stimulates circulation and lymphatic drainage,” he added. It helps carry waste products away, lowers the amount of water stored in the tissue and promotes circulation. “That’s important at least to contain cellulite.”

It doesn’t hurt to sufficiently moisturize the skin and to use products that have active ingredients such as fruit acids or vitamin A – also called retinol, said Vedder. But this can be done without an expensive cellulite cream.

The old recommendations remain the best: drink enough liquids, massage the area, ride a bike, take the stairs, Vedder added. This doesn’t completely prevent cellulite, but there is at least a chance that this will delay the development of the bothersome orange peel skin. (dpa)