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Groundbreaking new understanding of stem cells

May 3, 2010 By vani Leave a Comment

London, May 3 (ANI): Researchers from The Scripps Research Institute have detailed some striking differences between the biochemistry of stem cells versus mature cells—a feat that could one day lead to new therapies.

Led by Gary Siuzdak, the researchers used a unique approach to better understand stem cells, which have the ability to change or “differentiate” into adult cell types (such as hair cells, skin cells, nerve cells).

Understanding how stem cells mature opens the door for scientists and physicians to manipulate the process to meet the needs of patients, potentially treating such intractable conditions as Parkinson”s disease and spinal injury.

“In the past, scientists trying to understand stem cell biology focused on genes and proteins. In our study, we looked at stem cell regulation in a different way—on the biochemical level, on a functional level. With metabolomics profiling, we were able to look at naturally occurring small molecules and how they control cell fate on a completely different level,” Nature quoted Ding as saying.

The new paper describes parts of the stem cell “metabolome”— the complete set of substances (“metabolites”) formed in metabolism, including all naturally occurring small molecules, biofluids, and tissues.

The scientists then compared this profile to those of more mature cells, specifically of nerve cells and heart cells.

After tallying the results, the scientists had found about 60 previously unidentified metabolites associated with the progression of stem cells to mature cells, as well as an unexpected pattern in the chemistry that mirrored the cells” increasing biological maturity.

The study of metabolomics is relatively new, having emerged only over the past decade or so.

“One of the most interesting aspects of metabolomics is how little we know. We don”t know what the vast majority of metabolites are, or what they do. It is an area ripe for discovery,” commented Siuzdak.

In the current study, the team used liquid chromatography-mass spectrometry (LCMS), which draws on two more traditional techniques to provide scientists with the ability to chemically analyse virtually any molecular species.

The group then analysed the resulting data using an open-access bioinformatics platform XCMS.

The XCMS software allows researchers to identify and assess metabolite and peptide features that show significant change between sample groups—in this case mouse stem cells versus mature cells.

The most difficult part of untargeted metabolomics studies is analysing the results and characterizing metabolites, said Oscar Yanes, the new paper”s first author.

Still, Yanes shifted though the data on stem cells and identified an unexpected pattern— stem cell metabolites had highly unsaturated structures compared with mature cells, and levels of highly unsaturated molecules decreased as the stem cells matured.

Highly unsaturated molecules, which contain little hydrogen, can easily react and change into many other different types of molecules.

“The study reveals an astounding cellular strategy. The capacity of embryonic stem cells to generate a whole spectrum of cell types characteristic of different tissues (a phenomenon referred to as plasticity) is mirrored at the metabolic level,” said Yanes.

“We were not expecting these results. Although in retrospect it makes sense that stem cells (which can form almost any cell) have metabolites that are chemically flexible,” said Siuzdak.

The study was published in an advance, online edition of the prestigious journal Nature Chemical Biology. (ANI)

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Gene that ties stress to obesity and diabetes identified

April 20, 2010 By vani Leave a Comment

Washington, April 20 (ANI): Scientists have discovered a gene that ties stress to obesity and diabetes.

Dr. Alon Chen of the Weizmann Institute”s Neurobiology Department and his research team have now discovered that changes in the activity of a single gene in the brain not only cause mice to exhibit anxious behavior, but also lead to metabolic changes that cause the mice to develop symptoms associated with type 2 diabetes.

All of the body”s systems are involved in the stress response, which evolved to deal with threats and danger.

Behavioural changes tied to stress include heightened anxiety and concentration, while other changes in the body include heat-generation, changes the metabolism of various substances and even changes in food preferences.

The research team suspected that a protein known as Urocortin-3 (Ucn3) ties all of these things together. This protein is produced in certain brain cells – especially in times of stress – and it”s known to play a role in regulating the body”s stress response.

These nerve cells have extensions that act as ”highways” that speed Ucn3 on to two other sites in the brain: One, in the hypothalamus – the brain”s center for hormonal regulation of basic bodily functions – oversees, among other things, substance exchange and feelings of hunger and satiety; the other is involved in regulating behavior, including levels of anxiety.

Nerve cells in both these areas have special receptors for Ucn3 on their surfaces, and the protein binds to these receptors to initiate the stress response.

The researchers developed a new, finely-tuned method for influencing the activity of a single gene in one area in the brain, using it to increase the amounts of Ucn3 produced in just that location.

They found that heightened levels of the protein produced two different effects: The mice”s anxiety-related behavior increased, and their bodies underwent metabolic changes, as well.

With excess Ucn3, their bodies burned more sugar and fewer fatty acids, and their metabolic rate sped up.

These mice began to show signs of the first stages of type 2 diabetes: A drop in muscle sensitivity to insulin delayed sugar uptake by the cells, resulting in raised sugar levels in the blood. Their pancreas then produced extra insulin to make up for the perceived ”deficit.”

“We showed that the actions of single gene in just one part of the brain can have profound effects on the metabolism of the whole body,” Chen said.

These findings were published online this week in the Proceedings of the National Academy of Sciences (PNAS). (ANI)

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Slow mind means more creativity

March 31, 2010 By vani Leave a Comment

London, March 31 (ANI): A slow brain can nurture more creative ideas, a new American research has suggested.

Rex Jung at the University of New Mexico in Albuquerque and his team discovered that creativity is associated with low levels of the chemical N-acetylaspartate, found in neurons, and seems to promote neural health and metabolism.

But neurons constitute the brain”s grey matter – the tissue long thought to be linked with thinking power, rather than creativity. Consequently, Jung is now focusing his creativity studies on white matter, which largely comprises the fatty myelin sheaths that wrap around neurons. Less myelin signifies the white matter has a lower “integrity” and transmits information more slowly.

Numerous recent studies have suggested that white matter of high integrity in the cortex, which is linked to higher mental function, means increased intelligence.

However, when Jung analysed the connection between white matter and creativity, he came across something very different.

For the study, Jung selected 72 volunteers and used diffusion tensor imaging, which measures the direction in which water diffuses through white matter – an indication of its integrity.

The subjects” capacity for divergent thinking – a factor in creativity that includes coming up with new ideas – had already been tested.

Jung saw that the most creative people had lower white-matter integrity in a region connecting the prefrontal cortex to a deeper structure called the thalamus, compared with their less creative peers.

Jung believes slower communication between some areas may actually make people more creative.

“This might allow for the linkage of more disparate ideas, more novelty, and more creativity,” New Scientist quoted Jung, as saying.

According to Jung, creativity and intelligence can still go hand in hand. Each appears to be controlled by white matter in a different region. Thus, theoretically, there”s no reason why someone might not have high integrity in the cortex, producing intelligence, but low integrity between the cortex and deeper brain regions, leading to creative thinking.

He said: “They appear to function relatively independently.”

The study has appeared in the open access journal PLoS ONE. (ANI)

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How life might evolve with “exotic” biochemistry and solvents

September 19, 2009 By admin Leave a Comment

London, September 18 (ANI): Scientists at a new interdisciplinary research group in Austria are working to uncover how life might evolve with “exotic” biochemistry and solvents, such as sulfuric acid instead of water.

The research group for Alternative Solvents as a Basis for Life Supporting Zones in (Exo-) Planetary Systems was established by the University of Vienna.

Traditionally, planets that might sustain life are looked for in the ‘habitable zone’, the region around a star in which Earth-like planets with carbon dioxide, water vapor and nitrogen atmospheres could maintain liquid water on their surfaces.

Consequently, scientists have been looking for biomarkers produced by extraterrestrial life with metabolisms resembling the terrestrial ones, where water is used as a solvent and the building blocks of life, amino acids, are based on carbon and oxygen.

However, these may not be the only conditions under which life could evolve.

“It is time to make a radical change in our present geocentric mindset for life as we know it on Earth,” said scientist Johannes Leitner.

“Even though this is the only kind of life we know, it cannot be ruled out that life forms have evolved somewhere that neither rely on water nor on a carbon and oxygen based metabolism,” he added.

One requirement for a life-supporting solvent is that it remains liquid over a large temperature range.

Water is liquid between 0 degree Celsius and 100 degrees C, but other solvents exist which are liquid over more than 200 degrees C.

Such a solvent would allow an ocean on a planet closer to the central star.

The reverse scenario is also possible. A liquid ocean of ammonia could exist much further from a star.

Furthermore, sulfuric acid can be found within the cloud layers of Venus and it is now known that lakes of methane/ethane cover parts of the surface of the Saturnian satellite Titan.

Consequently, the discussion on potential life and the best strategies for its detection is ongoing and not only limited to exoplanets and habitable zones.

The newly established research group at the University of Vienna, together with international collaborators, will investigate the properties of a range of solvents other than water, including their abundance in space, thermal and biochemical characteristics as well as their ability to support the origin and evolution of life supporting metabolisms. (ANI)

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Exposure to second-hand tobacco smoke linked to liver disease

September 12, 2009 By admin Leave a Comment

Washington, September 11 (ANI): People can develop liver disease even when they are exposed to second-hand tobacco smoke, according to a study.

Scientists at the University of California, Riverside (UCR) have found that exposure to second-hand tobacco smoke can lead to non-alcoholic fatty liver disease (NAFLD), a common disease and rising cause of chronic liver injury wherein fat accumulates in the liver of people who drink little or no alcohol.

For their study, the researchers exposed some mice to second-hand cigarette smoke for a year in the lab, and observed fat build-up in their liver cells, a sign of NAFLD that eventually leads to liver dysfunction.

The researchers focused on two key regulators of lipid (fat) metabolism that are found in many human cells as well: SREBP (sterol regulatory element-binding protein) that stimulates synthesis of fatty acids in the liver, and AMPK (adenosine monophosphate kinase) that turns SREBP on and off.

They found that second-hand smoke exposure inhibits AMPK activity, which, in turn, causes an increase in activity of SREBP.

More active SREBP results in more fatty acids getting synthesized, they say.

The result is NAFLD induced by second-hand smoke, according to the researchers.

“Our study provides compelling experimental evidence in support of tobacco smoke exposure playing a major role in NAFLD development,” said Manuela Martins-Green, a professor of cell biology, who led the study.

“Our work points to SREBP and AMPK as new molecular targets for drug therapy that can reverse NAFLD development resulting from second-hand smoke. Drugs could now be developed that stimulate AMPK activity, and thereby inhibit SREBP, leading to reduced fatty acid production in the liver,” Martins-Green added.

A research article describing the study has been published in the Journal of Hepatology. (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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‘Master switch’ gene may help control obesity

September 4, 2009 By admin Leave a Comment

Washington, Sept 4 (ANI): Scientists from University of Michigan claim to have discovered a gene, which when switched off, can control obesity in mice and help them remain thin.

According to Alan Saltiel, the Mary Sue Coleman Director of the U-M Life Sciences Institute, deleting the gene, called IKKE, appears to protect mice against conditions that, in humans, lead to Type 2 diabetes, which is associated with obesity.

He said that if follow-up studies confirm IKKE is tied to obesity in humans, the gene and the protein it will be prime targets for the development of drugs to treat obesity and diabetes.

“We’ve studied other genes associated with obesity – we call them ‘obesogenes’ – but this is the first one we’ve found that, when deleted, stops the animal from gaining weight,” said Saltiel, senior author of a paper.

“The fact that you can disrupt all the effects of a high-fat diet by deleting this one gene in mice is pretty interesting and surprising,” Saltiel added.

During the study, the high-fat-diet mice were fed a lard-like substance with 45 percent of its calories from fat. Control mice were fed standard chow with 4.5 percent of its calories from fat.

The gene IKKE produces a protein kinase also known as IKKE. The IKKE protein kinase appears to target proteins, which, in turn, control genes that regulate the mouse metabolism.

When the high-fat diet is fed to a normal mouse, IKKE protein-kinase levels rise, the metabolic rate slows, and the animal gains weight. In that situation, the IKKE protein kinase acts as a brake on the metabolism.

The new study showed that knockout mice placed on the high-fat diet did not gain weight, apparently because deleting the IKKE gene releases the metabolic brake, allowing it to speed up and burn more calories, instead of storing those calories as fat.

The new study is published in the journal Cell. (ANI)

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Climate change mitigation strategies ignore carbon cycling processes of inland waters

September 2, 2009 By admin Leave a Comment

Washington, Sept 2 (ANI): In a new report, scientists have determined that climate change mitigation strategies ignore carbon cycling processes of inland waters.

Scientists from the University of Vienna, Uppsala University in Sweden, University of Antwerp, and the US based Stroud Water Research Center, authored the report, which is published in the September issue of Nature Geoscience.

They argue that current international strategies to mitigate manmade carbon emissions and address climate change have overlooked a critical player – inland waters.

Streams, rivers, lakes, reservoirs, and wetlands play an important role in the carbon cycle that is unaccounted for in conventional carbon cycling models.

According to Dr. Tom J. Battin of the department of Freshwater Ecology at the University of Vienna and lead author of the report, “While inland waters represent only 1 percent of the Earth’s surface, their contribution to the carbon cycle is disproportionately large, underestimated, and not recognized within the models on which the Kyoto protocol was based.”

The team of scientists points out that all current global carbon models consider inland waters static conduits that transfer carbon from the continents to the oceans.

In reality, inland waters are dynamic ecosystems with the potential to alter the fates of terrestrial carbon delivered to them including: burial in sediments leading to long-term storage or sequestration; and metabolism in rivers and subsequent outgassing of respired carbon dioxide to the atmosphere.

“Twenty percent of the continental carbon sequestration actually occurs as burial in inland water sediments,” said Dr. Lars Tranvik, Professor of Limnology at Uppsala University in Sweden.

“River outgassing of respired carbon, contributes carbon to the atmosphere in an amount equivalent to 13 percent of annual fossil fuel burning,” said Dr. Anthony K. Aufdenkampe, a scientist at the Stroud Water Research Center.

Because the amount of atmospheric carbon is well known and conservation of matter requires a balanced global carbon budget, this previously unaccounted for source of carbon to the atmosphere implies the existence of an additional continental carbon sink such as higher rates of biomass accrual in forests.

“A larger accumulation of carbon in forest ecosystems that could offset the outgassing from rivers would be more consistent with current independently-derived estimates of carbon sequestration on the continents,” said Dr. Sebastian Luyssaert of the department of Biology at University of Antwerp in Belgium. (ANI)

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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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Gene breakthrough could banish inherited diseases

August 27, 2009 By admin Leave a Comment

London, Aug 26 (ANI): Researchers at Oregon Health and Science University’s Oregon National Primate Research Center (ONPRC) have developed a new technique that could banish a host of crippling inherited diseases forever.

The landmark research raises the prospect of wiping out diseases passed on from mothers to their children through mutated DNA in cell mitochondria.

“We believe this discovery in nonhuman primates can rapidly be translated into human therapies aimed at preventing inherited disorders passed from mothers to their children through the mitochondrial DNA, such as certain forms of cancer, diabetes, infertility, myopathies and neurodegenerative diseases,” said Shoukhrat Mitalipov, from Oregon Health and Science University (OHSU).

Mitochondria are structures that are found in all cells that provide energy for cell growth and metabolism, which is why they are often called the cell’s “power plant.”

The structures produce energy to power each individual cell. Mitochondria also carry their own genetic material.

When an egg cell is fertilized by a sperm cell during reproduction, the embryo almost exclusively inherits the maternal mitochondria present in the egg. This means that any disease-causing genetic mutations that a mother carries in her mitochondrial DNA can be passed on to her offspring.

OHSU researchers’ method transfers the mother’s chromosomes to a donated egg that has had its chromosomes removed, but which has healthy mitochondria, thereby preventing the disease from being passed on to one’s offspring.

During the research, scientists collected groups of unfertilized eggs from two female rhesus macaque monkeys (monkeys A and B). They then removed the chromosomes, which contain the genes found in the cell nucleus, from the eggs of monkey B, and then transplanted the nuclear genes from the eggs of monkey A into the eggs of monkey B.

Then the eggs from monkey B, which now contained their own mitochondria but monkey A’s nuclear genes, were fertilized. The fertilized eggs developed into embryos that were implanted in surrogate monkeys.

The initial implantation of two embryos resulted in the birth of healthy twin monkeys. These monkeys are the world’s first animals derived by spindle transfer.

Follow-up testing showed that there was little to no trace of cross-animal mitochondrial transfer using this procedure. This shows that the researchers were successful in isolating nuclear genetic material from mitochondrial genetic material during the transfer process.

“In theory, this research has demonstrated that it is possible to use this therapy in mothers carrying mitochondrial DNA diseases so that we can prevent those diseases from being passed on to their offspring,” Mitalipov said.

“We believe that with the proper governmental approvals, our work can rapidly be translated into clinical trials for humans, and, eventually, approved therapies,” Mitalipov added.

The research has been published in the Aug. 26 advance online edition of the journal Nature. (ANI)

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Fatness can lead to ‘brain shrinkage’

August 25, 2009 By admin Leave a Comment

London, Aug 24 (ANI): A new study from University of California in Los Angeles suggests that piling on the pounds can shrink brains of older people, making them more vulnerable to cognitive problems.

According to Paul Thompson, brains of elderly obese people looked 16 years older than the brains of leaner peers.

The research involving 94 people in their 70s showed that people with higher body mass indexes had smaller brains on average, with the frontal and temporal lobes – important for planning and memory, respectively – particularly affected.

While no one knows whether these people are more likely to develop dementia, a smaller brain is indicative of destructive processes that can develop into dementia.

The team also found that the brains of the 51 overweight people were 6 per cent smaller than those of their normal-weight counterparts, on average, and those of the 14 obese people were 8 per cent smaller.

“The brains of overweight people looked eight years older than the brains of those who were lean, and 16 years older in obese people,” New Scientist quoted Thompson as saying.

Thompson suggests that as increased body fat ups the chances of having clogged arteries, which can reduce blood and oxygen flow to brain cells, the resulting reduction in metabolism could cause brain cell death and the shrinking seen.

He said that exercise protects the very brain regions that had shrunk.

“The most strenuous kind of exercise can save about the same amount of brain tissue that is lost in the obese,” he said.

The findings appear in journal Human Brain Mapping. (ANI)

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Why we sleep – ‘science-wise’

August 21, 2009 By admin Leave a Comment

London, Aug 21 (ANI): From animals to humans, everybody requires a good night sleep. However, the function of sleep still remains one of the greatest unsolved mysteries of science, say researchers.

While many theories suggest that sleep helps in brain “maintenance” – including memory consolidation and pruning- reverse damage from oxidative stress suffered while awake and promote longevity, none of them are well established.

Now, researchers from University of California, Los Angeles have come up with a new theory that sleep’s primary function is to increase animals’ efficiency and minimize their risk by regulating the duration and timing of their behaviour.

“Sleep has normally been viewed as something negative for survival because sleeping animals may be vulnerable to predation and they can’t perform the behaviors that ensure survival,” Nature quoted Jerome Siegel, professor of psychiatry and director of the Centre for Sleep Research at the Semel Institute for Neuroscience and Human Behaviour at UCLA as saying,iegel said.

“These behaviours include eating, procreating, caring for family members, monitoring the environment for danger and scouting for prey.

“So it’s been thought that sleep must serve some as-yet unidentified physiological or neural function that can’t be accomplished when animals are awake,” he added.

In the study conducted using platypus, walrus, and echidna – a small, burrowing, egg-laying mammal covered in spines, the researchers showed that sleep itself is highly adaptive, much like the inactive states seen in a wide range of species, starting with plants and simple microorganisms; these species have dormant states – as opposed to sleep – even though in many cases they do not have nervous systems.

That challenges the idea that sleep is for the brain, said Siegel.

“We see sleep as lying on a continuum that ranges from these dormant states like torpor and hibernation, on to periods of continuous activity without any sleep, such as during migration, where birds can fly for days on end without stopping,” he said.

In humans, the most notable thing about sleep is that it reduces body and brain metabolism while still allowing high level of responsiveness to the environment, such as parent arousing at a baby’s whimper but sleeping through a thunderstorm.

“This Darwinian perspective can explain age-related changes in human sleep patterns as well,” said Siegel.

“We sleep more deeply when we are young, because we have a high metabolic rate that is greatly reduced during sleep, but also because there are people to protect us.

“Our sleep patterns change when we are older, though, because that metabolic rate reduces and we are now the ones doing the alerting and protecting from dangers,” the expert added.

The study appears in journal Nature Reviews Neuroscience. (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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How obesity leads to diabetes

July 10, 2009 By admin Leave a Comment

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)

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Eating more and using less energy made dinos gigantic

July 10, 2009 By admin Leave a Comment

Sydney, July 9 (ANI): A US scientist has said that some dinosaurs grew larger than today’s elephants because they ate more and used less energy.

According to a report in ABC Science, the study suggests two factors, energy expenditure and food intake, influence the size of animals.

Using a mathematical model, study author Dr Brian McNab of the University of Florida, determined that animals that expend more energy and have a faster metabolism, which is typically linked to temperature regulation, have a smaller body mass.

Fast metabolism is a characteristic of large warm blooded animals. They use food to generate heat and maintain a constant body temperature, he writes.

Cold blooded animals, like most reptiles, have a slow metabolism and rely on the environment for body warmth.

McNab has proposed that, rather than use all their energy to maintain body temperature the way warm-blooded animals do, large dinosaurs used their energy to grow.

Large present-day mammals, like the African elephant, haven’t reached sizes similar to dinosaurs because they use most of their energy on temperature regulation, he added.

McNab said that due to their size, large dinosaurs were able to maintain a constant body temperature through thermal inertia and a small surface-to-volume ratio.

As a result, McNab concludes that dinosaurs like sauropods were homeothermic – had an intermediate body temperature.

Palaeontologist Dr John Long, of Museum Victoria, said that the idea that dinosaurs had intermediate body temperatures is not unusual.

He said that some large cold blooded animals can maintain a constant body temperature regardless of the environment – much like warm blooded animals.

“If you think of the giant turtles that live in the cold waters of the Atlantic they can have much higher body temperatures than the sea water around them,” said Long.

He said that the bigger an animal is, the less energy it takes to maintain a constant and higher body temperature.

“They can generate heat through their muscle metabolism,” he said. (ANI)

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20 cholesterol-regulating genes identified

July 8, 2009 By admin Leave a Comment

Washington, July 8 (ANI): Scientists at the European Molecular Biology Laboratory (EMBL) and the University of Heidelberg, Germany, have identified 20 genes that play a vital role in maintaining cholesterol balance.

The researchers believe that the newly identified genes may help uncover the mechanisms that regulate cholesterol levels, and lead to new treatments for cholesterol-related diseases.

“This finding may open new avenues for designing targeted therapies, for example by looking for small molecules that could impact these genes,” said Heiko Runz, whose group at the University Clinic Heidelberg carried out the research together with Rainer Pepperkok’s lab at EMBL.

High levels of cholesterol in the bloodstream are a major risk factor for atherosclerosis and coronary heart disease.

During the study, the researchers deprived isolated human cells of cholesterol, and then looked at the whole genome to find the genes that react to changes in cholesterol levels by altering their expression.

With a microscope, they then observed what effect switching off different genes had both on cholesterol uptake and on the total amount of cholesterol inside cells.

Of the 20 genes the scientists identified as involved in regulating cholesterol levels and uptake, 12 were previously unknown.

The scientists are now trying to discover exactly how the novel genes regulate cholesterol levels inside cells, as well as looking at patients to determine whether these genes (or alterations in them) do constitute risk factors, and investigating if and how they could be useful drug targets.

The study appears in journal Cell Metabolism. (ANI)

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Identification of potential drug target gives new hope for Alzheimer’s patients

July 2, 2009 By admin Leave a Comment

London, July 2 (ANI): A collaborative study conducted by researchers from UC Santa Barbara and several other institutions has provided laboratory that a cluster of peptides may be the toxic agent in Alzheimer’s disease.

The researchers believe that the finding made in the laboratory of Michael T. Bowers, a professor of Chemistry and Biochemistry at UCSB, may lead to new drugs for the disease.

In their study report, they have explained the process in which the toxic Amyloid Beta 42 peptides aggregate, and outlined the new technology they use to study these peptides.

“We believe that we have put a face, a structure, on the molecular assembly that is responsible for Alzheimer’s disease,” Nature magazine quoted Bowers as saying.

He and his colleagues used an innovative technology called ion mobility-based mass spectroscopy, a method that allows researchers to investigate the structure, aggregation, and energetics of protein and peptide systems.

The Amyloid Beta (AB) 42 peptide is clipped from a much larger protein, the amyloid precursor protein (APP), and is composed of 42 amino acid residues.

A second peptide, AB40, is 10 times more abundant than AB42 in healthy human brains, and is also clipped from APP. It is identical to AB42 except it is missing the last two amino acids.

Both peptides aggregate, but AB42 more so than AB40.

Bowers points out that AB40 never grows beyond a tetramer-a cluster of four AB40 peptides. As a consequence, it is nontoxic.

By contrast, adds the researcher, AB42 grows to form rings of six units each.

His team say that two of these “six-mer” rings stack to form a dodecamer, or “twelve-mer”, and then the aggregation stops.

These dodecamer clusters are long-lived, but may eventually rearrange to form so-called B-sheet structures, which lead to the large fibrils that form the plaques found in the brains of those with Alzheimer’s disease and other neurodegenerative diseases.

While experimenting on mice, the researchers observed that the animals implanted with the gene that expresses human APP, and hence able to form AB42 in their brains, quickly developed memory deficits-as if they had Alzheimer’s disease.

Since mice have a much faster metabolism than humans, the disease progresses more quickly. Of importance is the fact that the only AB species found in the brains of the transgenic mice correlates with the dodecamer of AB42 characterized in the Bowers lab experiments. These two pieces of data together strongly implicate the dodecamer of AB42 as the toxic agent in Alzheimer’s disease.

“Our group, along with our collaborators, are searching for drug candidates that can prevent AB42 from aggregating to form the toxic dodecamer. While it is early in the search, we are hopeful good candidates can be found. As a consequence, there is a need to find an early marker for Alzheimer’s disease so that we can use these drugs to radically slow down the disease progression,” said Bowers.

Writing about the study in the journal Nature Chemistry, Bowers said that his team’s method was new, but was gaining acceptance in the biological community.

He said that to fully understand the disease, effects of the oligomerization process would have to be observed at the cellular level, however.

“These latest results are a very hopeful thing. I’m more hopeful now than I have ever been that we can make some real progress on this terrible disease,” said Bowers. (ANI)

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‘Super-sleepers’ can store enough energy to fight obesity

June 29, 2009 By admin Leave a Comment

Washington, June 29 (ANI): In a new research, a team of scientists has found that animals that sleep longer store energy for a long duration, a finding that can be useful in the treatment of obesity.

Many species of animals go through a period of torpor to conserve energy when resources are scarce.

But, when it comes to switching to energy-saving mode, the champion by far among vertebrates is the burrowing frog (Cyclorana alboguttata), which can survive for several years buried in the mud in the absence of any food or water.

Now, a team of scientists at the University of Queensland, Australia, have discovered that the metabolism of their cells changes radically during the dormancy period allowing the frogs to maximize the use of their limited energy resources without ever running on empty.

This discovery could prove to have important medical applications in the long term.

“It could potentially be useful in the treatment of energy-related disorders such as obesity,” explained scientist Sara Kayes.

When the operation efficiency of the mitochondria, the tiny “power plants” of the cell, was measured during the dormancy period, it was found to be significantly higher compared to that observed in active animals.

This trick, known as mitochondrial coupling, allows these frogs to be extremely efficient in the use of the limited energy stores they have by increasing the total amount of energy obtained per unit consumed, allowing them to easily outperform other species whose energy production efficiency remains essentially the same even when they happen to be inactive for extended periods. (ANI)

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Sienna Miller fears she’s losing her good looks

June 20, 2009 By admin Leave a Comment

Washington, June 19 (ANI): Hollywood actress Sienna Miller fears that she’s losing her good looks as she heads towards 30.

The 27-year-old actress believes that it’s time for her to start working out a bit.

“I’m lucky I’ve got a good metabolism. I’m very grateful for that. But I’m not toned at all. I think I’ve reached an age at 27 where it’s time for me to start working out a bit. I can’t get away with it any more,” Contactmusic quoted her as saying.

“I used to be quite firm and tiny and, as I hit 25, things started to change. Now I’m 27 I’m noticing more changes – bare legs at the top and back is not a pretty sight. I’m lazy and if I wear clothes, it’s hidden well.

“I don’t feel like a beauty icon. I get pretty insecure and have the same insecurities as everyone else – sometimes more because there is more focus put on me,” she added. (ANI)

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