Nectarines, Plums And Peaches May Fight Obesity And Diabetes

Stone fruits, also known as drupes, such as nectarines, plums and peaches, may contain useful compounds that help fight-off metabolic syndrome, which can lead to diabetes, heart attack and stroke, say researchers from Texas AgriLife Research, a member of Texas A & M University System.
Food scientist, Luis Cisneros-Zevallos and team showed that compounds that exist in stone fruits could be useful in the fight against metabolic syndrome, in which inflammation and obesity eventually lead to serious illnesses and health problems.
The scientists will present their findings at the American Chemical Society in Philadelphia in August, 2012.
Cisneros-Zevallos said:
"In recent years obesity has become a major concern in society due to the health problems associated to it. In the U.S., statistics show that around 30% of the population is overweight or obese, and these cases are increasing every year in alarming numbers."
Everyone now knows that diet, genetics, lack of sleep, and physical inactivity play a major role in the obesity epidemic. The main concern is obesity's association with metabolic syndrome. Metabolic syndrome is a collection of conditions, including high blood sugar levels, hypertension (high blood pressure), too much fat around the waist, and excessively highcholesterol levels - together, they considerably raise the risk of developing diabetes, having astroke, or a heart attack.
Cisneros-Zevallos said:
"Our studies have shown that stone fruits - peaches, plums and nectarines - have bioactive compounds that can potentially fight the syndrome.
Our work indicates that phenolic compounds present in these fruits have anti-obesity, anti-inflammatory and anti-diabetic properties in different cell lines and may also reduce the oxidation of bad cholesterol LDL which is associated to cardiovascular disease."

Stone fruits (drupes) have a mixture of bioactive compounds that work together and attack different components of metabolic syndrome.
Cisneros-Zevallos explained:

"Our work shows that the four major phenolic groups - anthocyanins, clorogenic acids, quercetin derivatives and catechins - work on different cells - fat cells, macrophages and vascular endothelial cells. They modulate different expressions of genes and proteins depending on the type of compound.
However, at the same time, all of them are working simultaneously in different fronts against the components of the disease, including obesity, inflammation, diabetes and cardiovascular disease."

The researchers say that this is the first time bioactive compounds from a fruit have been demonstrated to have the potential to attack a disease from several different fronts.
Zevallos said "Each of these stone fruits contain similar phenolic groups but in differing proportions so all of them are a good source of health promoting compounds and may complement each other."
The scientists now plan to determine what the role each type of compound has, at a molecular level. They also wish to confirm their animal studies.
Written by Christian Nordqvist

Virus Hitches Ride On Blood Cells To Kill Cancer

Scientists have discovered when a cancer-killing virus is injected in the bloodstream it hitches a ride on blood cells and evades attack from the immune system, allowing it to reach cancer tumors, and start destroying cancer cells. They suggest this means it may be possible to use promising "viral therapy" during routine outpatient sessions, like chemotherapy, to treat a wide range ofcancers.
Certain viruses, like the reovirus, that causes colds and mild stomach upsets, prefer to attack cancer cells. They also stimulate the immune system to attack tumors.
Using these "oncolytic" viruses to kill cancer is a fairly new approach that is currently being tested. Trials are currently under way to test "viral therapy" as an approach to treat cancer in human patients.
But the challenge is how to get the viruses into tumors without alerting the immune system to destroy them. One way is to inject them into the tumors, but this is technically difficult and particularly so for tumors that are deep inside the body, such as in the lungs, stomach, liver and pancreas.
Another way could be to inject the virus into the bloodstream; however, scientists have assumed this would not be feasible because the virus would likely be spotted and destroyed by the immune system before it could reach the tumor.
But when a group of scientists decided to test this by injecting the virus into the bloodstream of patients with advanced colorectal cancer, they found the virus was able to evade the immune system by "going under cover" and hitching a ride on red blood cells.
The study, led by researchers from the University of Leeds and The Institute of Cancer Research (ICR) in the UK, reveals how the "hitch-hiking" virus is shielded from antibodies in the bloodstream that might otherwise neutralize its anti-cancer properties.
The team writes about its work in a paper published online in Science Translational Medicineon 13 June.
The study participants were 10 patients with advanced colorectal cancer that had spread to the liver and who were scheduled to undergo surgery on the secondary tumors in their livers.
In the weeks leading up to their surgery, all patients received up to five doses of the reovirus as outpatients.
From blood samples taken shortly after treatment, the researchers found that the active virus associated with blood cells. Later samples showed the virus was no longer in the blood cells and had quickly cleared from the system.
When the researchers examined samples of liver tissue removed during surgery up to four weeks later, they found "viral factories" and active virus in the tumor samples but not in normal tissue samples. This confirmed the virus had travelled specifically to the tumor after being injected into the bloodstream.
Professor Alan Melcher of the University of Leeds, and Dr Kevin Harrington from The Institute of Cancer Research and The Royal Marsden NHS Foundation Trust, jointly led the study.
Melcher told the press:
"It seems that reovirus is even cleverer than we had thought. By piggybacking on blood cells, the virus is managing to hide from the body's natural immune response and reach its target intact. This could be hugely significant for the uptake of viral therapies like this in clinical practice."
Harrington commented that:
"Viral treatments like reovirus are showing real promise in patient trials. This study gives us the very good news that it should be possible to deliver these treatments with a simple injection into the bloodstream," he added.
He said if these treatments could only be delivered by injecting into the tumor, they would have limited use, but discovering that the virus "can hitch a ride on blood cells will potentially make them relevant to a broad range of cancers".
"We also confirmed that reovirus was specifically targeting cancer cells and leaving normal cells alone, which we hope should mean fewer side-effects for patients," said Harrington.
Funds from Cancer Research UK, Leeds Experimental Cancer Medicine Centre, University of Leeds, The Institute of Cancer Research, Leeds Cancer Vaccine Appeal, and the Rays of Hope Appeal, paid for the study.
Written by Catharine Paddock PhD

From Infection To Inflammation To Cancer: Scientists Offer New Clues

Article Date: 14 Jun 2012 - 0:00 PDT

Chronic inflammation of the liver, stomach or colon, often as a result of infection by viruses and bacteria, is one of the biggest risk factors for cancer of these organs. Scientists at the Massachusetts Institute of Technology (MIT) in the US have been researching this for over three decades, and now in a new paper published online this week they offer the most comprehensive clues so far about the potential underlying molecular mechanisms.
A bacterium called Helicobacter pyloricauses stomach ulcers and cancer in humans. Helicobacter hepaticus has a similar effect in mice, so the researchers used it as a model to study how such a bacterial infection alters genes and chemicals in the liver and colon.
They write about their findings in a paper that appeared online in the 11 June issue of theProceedings of the National Academy of Sciences, PNAS.
One of the four senior authors of the paper is Peter Dedon, a professor of biological engineering at MIT. Biological engineering is where molecular life scientists work with engineers to discover how biological systems function; the resulting knowledge can be used to develop new medical technologies.
Dedon and his co-authors hope their findings will help other researchers develop ways to predict the health problems caused by chronic inflammation and design drugs to stop it.
"If you understand the mechanism, then you can design interventions," he said in a statement. "For example, what if we develop ways to block or interrupt the toxic effects of the chronic inflammation?"
Inflammation is a natural body reaction to an infection or wound, but if the inflammation persists too long, it can damage healthy tissue.
A study published recently in The Lancet found that inflammation caused by infections account for around 16% of new cancer cases worldwide.
Inflammation begins when the immune system detects cell damage or pathogens: both of these are potential threats to health. This triggers a surge of immune cells called macrophages and neutrophils that come along to clean up and remove the threat. They engulf the invading organisms, dead cells, debris and materials released by dead or damaged cells, such as proteins, nucleic acids and other molecules.
As well as removing these materials, the immune cells produce highly reactive chemicals to break down the bacteria. And it appears that it is this part of the process that is linked to cancer risk, because, as Dedon explained, "in engulfing the bacteria and dumping these reactive chemicals on them, the chemicals also diffuse out into the tissue".
If the inflammation persists, the tissue is constantly bathed in the reactive chemicals.
For the new study, which was funded by the National Cancer Institute, Dedon and colleagues studied mice infected with H. hepaticus for 20 weeks. After 10 weeks, the mice developed severe colitis and hepatitis, and at 20 weeks, some had also developed colon cancer.
Over the 20 weeks they examined the tissue damage in the mice, and assessed damage to DNA, RNA and proteins. They also identified which genes were switched on and off.
They found that levels of one of the damaged products in DNA and RNA, chlorocytosine, correlated well with the severity of the inflammation. This could serve as a marker to predict the risk chronic inflammation in patients with infections in the colon, liver or stomach, said the researchers.
But Dedon said this does not necessarily mean you could use such a marker to predict the risk for cancer from these damaged molecules.
The researchers also noticed that the liver responded differently to the colon.
When DNA of healthy tissue comes under attack, it triggers a mechanism that attempts to repair the DNA. The researchers found that DNA repair was more active in the liver than in the colon, even though both experienced DNA damage.
Another difference was that in the colon, but not the liver, neutrophils released hypochlorous acid (a constituent of household bleach). This acid causes significant damage to molecules like DNA, RNA and proteins by attaching a chlorine atom. It is an effective way to kill bacteria, but if the acid leaks into surrounding tissue, it can cause similar damage to the epithelial cells in the lining of the colon.
Dedon said:
"It's possible that we have kind of a double whammy [in the colon]. You have this bacterium that suppresses DNA repair, at the same time that you have all this DNA damage happening in the tissue as a result of the immune response to the bacterium."
The team also identified two other unknown types of DNA damage, the molecules spiroiminodihydantoin and guanidinohydanotoin, which result from oxidation of guanine, a building block of DNA.
They now plan to look at the mechanisms more closely, for instance to find out why some types of DNA damage are more frequent than others.
Written by Catharine Paddock PhD