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Tuesday, January 1, 2013

Understanding Pancreas Weight May Help Unlock Cause Of Type 1 Diabetes

Main Category: Diabetes
Article Date: 15 Dec 2012 - 0:00 PST Current ratings for:
Understanding Pancreas Weight May Help Unlock Cause Of Type 1 Diabetes
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People at risk for Type 1 diabetes may have fewer insulin-producing "beta" cells than people not at risk, a finding that could help researchers shed light on what causes the disease, a new University of Florida study shows.

The study, which will be published Wednesday (Dec. 12) in the Journal of the American Medical Association, revealed that people at risk for Type 1 diabetes had smaller pancreases than people who were not at risk.

"This is the first time this has been noted," said Martha Campbell-Thompson, D.V.M., Ph.D., a professor in the UF College of Medicine department of pathology, immunology and laboratory medicine. "We still don't know what causes Type 1 diabetes, but if people have fewer beta cells to begin with, other confounding factors such as a virus or genetics could help push them over into having clinical diabetes. There are a lot of possibilities."

Type 1 diabetes occurs when the body's immune system begins attacking its own beta cells in the pancreas, which are responsible for producing insulin the body needs to convert sugar into energy. The beta cells stop producing insulin, often beginning in childhood. Because of this, patients must take insulin for the rest of their lives. This differs from the more common Type 2 diabetes, which often can be prevented and treated through lifestyle changes, such as improved diet and increased exercise.

Although genetics plays a big role, researchers still don't know what triggers this autoimmune attack, and after it begins, there is no going back, said Campbell-Thompson, director of the pathology core for the Network for Pancreatic Organ Donors with Diabetes, or nPOD, a human pancreas biorepository housed within the UF Diabetes Center of Excellence.

In the current study, Campbell-Thompson and colleagues at the City of Hope National Medical Center examined 164 pancreases from adult organ donors, including those with auto-antibodies linked to an increased risk for Type 1 diabetes. After examining the organs and comparing them with control samples, the researchers discovered that the people at risk for Type 1 diabetes had pancreases roughly three-fourths the weight of those of patients not at risk for the disease. In addition, patients already diagnosed with Type 1 diabetes had pancreases about half the weight of control samples, Campbell-Thompson said.

"Had they not become organ donors, these people might have eventually developed Type 1 diabetes, so we were trying to carefully characterize their pancreases and their insulin-producing cells to see what was going on. A simple part of that was just weighing the pancreas when we got it," she said. "As we got more and more of these donors, a trend started showing up that these pancreases weighed less. They weighed lower than normal controls."

The ultimate goal of the research, and nPOD, which provides pancreas samples to researchers across the country, is to first understand how the pancreas works and then uncover new and better ways to not only treat Type 1 diabetes, but also to prevent it.

"Thanks to nPOD's valuable and rapidly growing collection of pancreas samples and other tissues, its team of researchers was able to examine, for the first time, the pancreas weight of those at risk for developing Type 1 diabetes," said Teodora Staeva, Ph.D., program director for immune therapies at JDRF, the leading foundation focused on advancing Type 1 diabetes research, which funded the study. "The findings raise significant questions about the development and progression of Type 1 diabetes."

Obtaining and analyzing human pancreas samples has proved crucial for researchers because mouse models used to uncover new treatments for Type 1 diabetes are no longer considered good examples of the disease in humans.

"There are major differences between human Type 1 diabetes and the animal models," Campbell-Thompson said. "It's really changing some of our ideas about when this autoimmune attack might occur, and we still don't know all the players."

The researchers now hope to take the study a step further by using noninvasive methods such as magnetic resonance imaging, or MRI, to gauge pancreas size in live patients.

"This could really change some of the ideas we have about Type 1 diabetes," Campbell-Thompson said. "By understanding how it develops we can think of new ways to treat it."

Article adapted by Medical News Today from original press release. Click 'references' tab above for source.
Visit our diabetes section for the latest news on this subject. Source: UF&Shands, The University of Florida Academic Health Center Please use one of the following formats to cite this article in your essay, paper or report:

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posted by Ali on 21 Dec 2012 at 2:32 pm

I am worried about my son because he got diabetic 4years ago. he is 12 years old. please help to us family because we are at desperation.

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posted by Dr Mohammed ali on 20 Dec 2012 at 9:40 am

sir is it not possible to cure diabetes with stemcell therapy

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'Understanding Pancreas Weight May Help Unlock Cause Of Type 1 Diabetes'

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FDA Approves Aegerion's Cholesterol Drug Juxtapid

Editor's Choice
Main Category: Regulatory Affairs / Drug Approvals
Also Included In: Cholesterol
Article Date: 26 Dec 2012 - 0:00 PST Current ratings for:
FDA Approves Aegerion's Cholesterol Drug Juxtapid
2 stars1 star
Aegerion Pharmaceuticals announced that the U.S. Food and Drug Administration has approved use of Juxtapid (lomitapide) pills as an accompaniment to a low-fat diet and other lipid-lowering treatments.

Juxtapid is for patients with homozygous familial hypercholesterolemia (HoFH), a critical, uncommon genetic disease that inhibits the function of the receptor that eliminates bad cholesterol from the body. This loss of function of the LDL receptor function causes high levels of cholesterol in the blood.

HoFH is characterized by untimely atherosclerosis, a blocking of the arteries and can result in heart attacks at an early age.

Katherine Wilemon, president and founder of The FH Foundation. says:

"The FDA approval of JUXTAPID is a major step forward for HoFH patients and their families, who have long been waiting for new therapies. New treatments, combined with further understanding and awareness of this disease, can bring much needed hope to the HoFH community."

Juxtapid has a warning label, known as a "boxed warning", the strongest warning a drug can carry, and will only be available through a restricted program because of its liver damage risks.

The approval was based on Aegerion's Phase III study which examined the effectiveness and safety of Juxtapid. When used in combination with current lipid-reducing therapy, Juxtapid helped decrease LDL cholesterol from an average of 336 mg/dL to 190 mg/dL, a 40 percent drop.

The most common side effects were gastrointestinal issues. Frequent reactions included:

These drug injections could cost up to $300,000 each year and will require strict safety measures.

This drug is Aegerion's first on the market and FDA will decide whether or not to accept a similar drug made by Sanofi and Isis Pharmaceuticals Inc. called Kynamro.

Written by Kelly Fitzgerald
Copyright: Medical News Today
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posted by nomad on 25 Dec 2012 at 12:14 pm

For some reason, I can't shake the feeling that pharmaceutical companies own the FDA..

Making up fake diseases with long confusing names instead of telling people the simple truth, that our ancestors walked and ran at least 10 miles a day every day for a million years; thus our bodies are tuned to work properly only if we walk and run relatively long distances every day. (This is an evolutionary fact. Fish gotta swim and land predators gotta run.)

So, what happens when we don't? Cholesterol and all that other mumbo jumbo. Don't want to be fat? Run 5-6 kms a day; It'll only take an hour away from your 4 hours a day of TV time. (Go ahead, deny it.)

Here's to good health.. and the pharmaceuticals that are making it possible for everyone.

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posted by les on 25 Dec 2012 at 6:47 am

SAY NO TO POISON!You dont need poison.apple cider vinegar lowers cholesterol guaranteed!

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posted by barry on 25 Dec 2012 at 6:35 am

OK we need ground breaking drugs to save lives, thats the accepted norm of our society today, but $300K/Yr? How can they justify that they made a life saving drug, yet to be seen mind you, only for the rich! I guess the rest of us will just have to settle for our mediocre Lipitor and die a slow death`

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'FDA Approves Aegerion's Cholesterol Drug Juxtapid'

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Insulin Plus Growth Factor Inhibitor Limits Vision Damage In Diabetic Mice

Main Category: Eye Health / Blindness
Also Included In: Diabetes
Article Date: 21 Dec 2012 - 1:00 PST Current ratings for:
Insulin Plus Growth Factor Inhibitor Limits Vision Damage In Diabetic Mice
1 starnot yet rated
A new therapeutic approach to diabetes that combines insulin and an inhibitor of the epidermal growth factor (EGF) betacellulin could limit the progression of diabetic macular edema (DME), Cleveland Clinic researcher Bela Anand-Apte, MD, PhD, said at the American Society for Cell Biology Annual Meeting, on Dec. 17 in San Francisco.

The study, conducted with insulin-dependent diabetic mice, showed that by thwarting "cross-talk" between insulin and betacellulin (BTC), which promotes the regeneration of pancreatic beta cells that stores and releases insulin, the EGF inhibitor preserved the animals' vascular integrity, she explained.

"These studies suggest that a combinatorial treatment of insulin and EGF inhibition might be a useful therapeutic combination to prevent macular edema, but needs to be determined in people with diabetes," said Dr. Anand-Apte.

Dr. Anand-Apte's idea for disconnecting diabetic progression from retinopathy was suggested by studies in people with type II diabetes whose blood sugar control was no longer stable on oral medications, requiring them to be treated with insulin. She noted that insulin therapy appeared to result in some patients' retinopathy progressing much faster, at least for a time. There was a correlation between starting insulin therapy and developing DME, she said.

Another clue came from an observation made by Judah Folkman, MD, then at Boston Children's Hospital, about pancreatic cancer patients who had undergone a pancreatectomy. Without a pancreas to produce and regulate insulin, these patients developed severe diabetes but rarely if ever developed proliferative retinopathy, even when they survived for more than 10 to 20 years. In the pancreas of people with diabetes, the researchers hypothesized that "cross-talk" occurred between injected insulin and the secretion of a vascular permeability-inducing factor.

Working with collaborators at Case Western Reserve University and the University of Wisconsin, the Anand-Apte lab used a mouse model for diabetes to look at BTC produced in the pancreas by proliferating beta cells. In previous studies, Dr. Anand-Apte had linked BTC to increased vascular permeability in the retina. Treating diabetic mice with insulin produced a spike in levels of a soluble form of betacellulin in the retina. Simply injecting BTC into the vitreous fluid of both hyperglycemic and normal mice also increased vascular permeability.

Looking more closely, the researchers determined that insulin was disrupting tight junctions between retinal pigment cells (RPEs), the barrier layer wrapped around retinal nerves, by driving up BTC expression. Injecting insulin first increased the production of ADAM10, a protein that weakens molecular cell-cell glues. The increase in ADAM10 was followed by up-regulation of BTC. By blocking the production of BTC and ADAM10 with short interfering RNA (siRNA), the researchers discovered they could protect these cell-cell tight junctions.

Substituting a BTC-targeted EGF inhibitor, the researchers finally thwarted the cross-talk between BTC and insulin. The EGF inhibitor preserved vascular integrity in the diabetic mice.

The association of visual impairment and the progression of both type I and type II diabetes appears to strengthen over time. The National Diabetes Information Clearinghouse estimates that of the 25.8 million American who have diabetes, 4.2 million have diabetic retinopathy, and in 675,000 of them, it progresses to its most severe form, proliferative diabetic retinopathy in which abnormal - and leaky blood vessels intrude into the eyeball's clear vitreous gel, causing retinal traction and bleeding that results in decreased sight.

Many people with diabetes with proliferative retinopathy also develop DME, a thickening of the center of the retina. Increased vascular permeability in the blood-retinal barrier allows leakage of lipoproteins into the macula at the center of the retina, reducing sharp vision. The main risk factors for DME, according to the American Academy of Ophthalmology, are increasing duration of diabetes, high blood sugar and blood pressure. Over 10 years, 20% of patients diagnosed with early-onset diabetes and 40% with older-onset diabetes will develop DME.

Article adapted by Medical News Today from original press release. Click 'references' tab above for source.
Visit our eye health / blindness section for the latest news on this subject. This work was supported in part by National Institutes of Health (EY016490, CA106415, and EY015638), Research to Prevent Blindness (RPB) Challenge Grant, and RPB Lew Wasserman award to BA-A.

"Regulation of retinal vascular leakage by insulin: Implications for patients with diabetic retinopathy," Monday, Dec.17, 2012, 12:30-2 pm, Session: Cell-Cell Junctions II, presentation 1351, poster B927, Exhibit Halls A-C

American Society for Cell Biology

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Temple Researcher Shows Diabetes, Blood Pressure Link To Colon Cancer Recurrence, Survival

Main Category: Colorectal Cancer
Also Included In: Diabetes;  Hypertension
Article Date: 24 Dec 2012 - 1:00 PST Current ratings for:
Temple Researcher Shows Diabetes, Blood Pressure Link To Colon Cancer Recurrence, Survival
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By all accounts, a combination of colon cancer, diabetes and high blood pressure can be a recipe for medical disaster. Now, a new study led by a surgical oncologist and researcher at Temple University School of Medicine and Fox Chase Cancer Center has shown just how deadly this mix can be. In a retrospective analysis of more than 36,000 patients with colon cancer, investigators showed that those with early stage disease and diabetes or high blood pressure - two components of metabolic syndrome - have a greater risk for the cancer returning after treatment and of dying compared to patients with colon cancer who do not have either condition.

"Although metabolic syndrome has been linked to colon cancer, the third leading cause of cancer death in the U.S., previous work looking at its effect on mortality has not adequately accounted for cancer stage or treatment," said senior author Nestor Esnaola, MD, MPH, MBA, Chief of the Division of Surgical Oncology, Professor of Vice-Chair of Clinical and Academic Affairs in the Department of Surgery at Temple University School of Medicine. "Our results suggest that patients with early stage colon cancer who also have diabetes or hypertension may need to be followed more closely for recurrence and could potentially benefit from broader use of adjuvant chemotherapy." Dr. Esnaola and his team reported their findings December 20, 2012 in an early online publication in the journal CANCER.

Metabolic syndrome is a cluster of conditions that affects one in five American adults and which can include diabetes, obesity, high blood pressure, low levels of good cholesterol and high amounts of lipids in the blood.

To better understand the effect of metabolic syndrome on colon cancer outcomes, Dr. Esnaola and his team linked data from the National Cancer Institute's Surveillance, Epidemiology and End Results (SEER) program, a large population-based database, to Medicare data from 1998 to 2006 on 36,079 patients with colon cancer, including 7,024 patients (19.5 percent) who were identified as having metabolic syndrome. They analyzed the effect of metabolic syndrome and its components on colon cancer recurrence and overall survival, controlling for various sociodemographic factors, tumor factors, other medical conditions and cancer treatment received.

"Metabolic syndrome as a whole had no apparent effect on colon cancer recurrence or survival," said Dr. Esnaola, who is also an attending surgeon at Fox Chase Cancer Center. "When we teased out and analyzed the effect of each of its components, however, the data told a different story."

The researchers found that among patients with early stage disease, patients with diabetes or high blood pressure had a significantly greater risk of cancer recurrence rate and death after treatment. For example, 47.7 percent of patients who did not have diabetes were still alive five years after diagnosis compared to only 41.3 percent of patients with diabetes. When the researchers looked more closely, they also found that cancer recurrence rates at five years were approximately 8 percent higher in patients with diabetes or hypertension.

In contrast, the analysis showed that patients with abnormally high levels of lipids in the blood had a lower risk of recurrence and death from colon cancer. Overall, 39 percent of patients with normal lipid levels were still alive after five years, compared to 52.7 percent of patients with abnormal levels. Cancer recurrence rates were approximately 11 percentage points lower in patients with abnormal lipid levels.

"Although we did not have data on medication for these patients, we suspect that the higher survival and lower recurrence rates observed in patients with high lipid levels in our study group were likely due to the protective effects of statins," Dr. Esnaola said. Statins are drugs that are widely used to lower cholesterol and lipid levels and have been shown to lower the risk of developing colon cancer in people.

"To our knowledge, this is the largest study to date controlling for cancer stage and treatment that has analyzed the effect of metabolic syndrome and its components on colon cancer recurrence and survival," said Dr. Esnaola. "The adverse effects of diabetes and hypertension in early stage patients and apparent protective effect of high blood lipids observed in our cohort suggest that when it comes to metabolic syndrome and cancer outcomes, the devil is in the details."

Dr. Esnaola currently is investigating the effect of metabolic syndrome and its components on other cancer types, and plans to confirm these results in a larger set of data that contains information on cancer stage, treatment and medication. "In the interim, our results underscore the need for clinical trials to define the true benefits of (the diabetes drug) metformin and statins in patients with early stage colon cancer," he said.

Article adapted by Medical News Today from original press release. Click 'references' tab above for source.
Visit our colorectal cancer section for the latest news on this subject. Other investigators contributing to this research include: Yang Yang and Baorui Liu, Comprehensive Cancer Center of Drum Tower Hospital, Medical School of Nanjing University, Nanjing, China; and Patrick D. Mauldin, Myla Ebeling, Thomas C. Hulsey, Melanie B. Thomas, and E. Ramsey Camp, Medical University of South Carolina, Charleston.

This research was supported in part by the Nanjing Drum Tower Hospital Health, Education, and Research Foundation.

Temple University Health System

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Diabetic Patients May Benefit From The Antidepressant Paroxetine

Main Category: Diabetes
Also Included In: Vascular;  Depression
Article Date: 20 Dec 2012 - 0:00 PST Current ratings for:
Diabetic Patients May Benefit From The Antidepressant Paroxetine
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University of Texas Medical Branch at Galveston researchers have discovered that the commonly used antidepressant drug paroxetine could also become a therapy for the vascular complications of diabetes.

The scientists made their discovery after screening 6,766 clinically used drugs and pharmacologically active substances.

"We developed this assay and used it to test literally every single existing drug and a good selection of other biologically active compounds," said UTMB professor Csaba Szabo, senior author of a paper on the research published online by Diabetes. "We were quite surprised when paroxetine came out as an active compound - a result, we later determined, of what seems to be a completely new effect unrelated to its antidepressant actions and not shared by any other known antidepressant drug."

The initial screening process tested the ability of different compounds to protect the cells that make up the inner linings of blood vessels from the destructive effects of the high sugar levels produced by diabetes, known as hyperglycemia. In people with diabetes, hyperglycemia causes these endothelial cells to generate toxic molecules known as reactive oxygen species (ROS), which ravage blood-vessel linings and lead to diabetic endothelial dysfunction, the key factor in such destructive diabetic complications as heart attacks, strokes, retinopathy, nephropathy and neuropathy.

In subsequent test-tube studies, researchers found that paroxetine - which is sold as an antidepressant under the trade name "Paxil" - prevents hyperglycemia-initiated ROS damage to endothelial cells in two ways. First, it directly reduces concentrations of superoxide, a powerful ROS. Second, it suppresses superoxide production by mitochondria, tiny structures whose real job is making the energy-transfer molecules needed for most cellular processes. In a hyperglycemic environment, mitochondria are cells' biggest source of superoxide. According to the researchers' findings, paroxetine inhibits this activity without interfering with the mitochondria's vital normal function.

Further experiments yielded still more evidence that paroxetine protects endothelial cells under hyperglycemic conditions. Reactive oxygen species cause significant damage to DNA, RNA and proteins, but cell-culture experiments showed that paroxetine significantly reduced this effect. The drug had similarly beneficial results when tested on rat "aortic rings" - small pieces of blood vessel kept alive with tissue-culture techniques. When treated with the vasodilator acetylcholine, these rings dilated just as if they were still part of a functioning circulatory system; endothelial dysfunction caused by diabetic hyperglycemia normally interferes with this function, but paroxetine restored it.

Finally, the researchers tested paroxetine in rats that had been injected with streptozotocin, a chemical that induces diabetes. The animals given paroxetine developed hypoglycemia, but like the aortic rings, their arteries retained the ability to dilate - an indication that the drug had prevented damage to their epitheliums.

"The future potential of this study is that we may be able to 're-purpose' paroxetine for the experimental therapy of diabetic cardiac complications," Szabo said. "We'll need to carefully characterize its safety profile in diabetic patients, but I think there's definite potential here."

Article adapted by Medical News Today from original press release. Click 'references' tab above for source.
Visit our diabetes section for the latest news on this subject. Other authors of the Diabetes paper include instructor Dr. Domokos Gerö, research fellow Petra Szoleczy, postdoctoral fellow Kunihiro Suzuki, postdoctoral fellow Katalin Módis, faculty associate Dr. Gabor Oláh and postdoctoral fellow Ciro Colletta. This research was supported by the Juvenile Diabetes Foundation, the American Heart Association and the James W. McLaughlin Endowment.
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Monday, December 31, 2012

Combo-Snacks Of Cheese And Vegetables Cut Kids Calories

Main Category: Obesity / Weight Loss / Fitness
Also Included In: Pediatrics / Children's Health
Article Date: 22 Dec 2012 - 0:00 PST Current ratings for:
Combo-Snacks Of Cheese And Vegetables Cut Kids Calories
4 stars5 stars
Almost everyone is familiar with the alarming trend of childhood obesity. 32% of U.S. children are overweight or obese according to the National Health and Nutrition Examination Survey. One of the many factors leading to the obesity epidemic is increased snacking in children. Today children eat around three snacks daily while thirty years ago they ate only one. Parents want to ensure that their children snack healthfully, but restricting or limiting children's snacking can backfire. Children in homes where parents carefully regulate snacking were found to eat more unhealthy snacks in an unregulated environment than children with less restrictive parents.

Researchers Brian Wansink, Ph.D., Mitsuru Shimizu, Ph.D., and Adam Brumberg set out to discover whether certain types of snacks would lead children to feel full while consuming fewer calories. 201 students in the third through sixth grade were given either a plate of potato chips, a plate of vegetables, a plate of cheese, or a plate of vegetables and cheese while watching some of their favorite afterschool cartoons. They were asked about their fullness at the beginning of the experiment, after watching one episode of a cartoon, and again after watching a second episode of a cartoon.

Children who ate the vegetable and cheese snack plate needed significantly fewer calories than the children who ate the plate of potato chips to achieve satiety. Further, children from low-involvement families (families which spent less time eating meals together or interacting with each other while eating) ate more potato chips than other children when given potato chips to snack on. However, children from low-involvement families and overweight children showed the greatest reduction in the amount of calories consumed when eating the cheese and vegetable snack instead of potato chips. Overweight and obese children ate 76% fewer calories when they were given the cheese and vegetable snack while other children averaged a 60% reduction in calories eaten. Both groups reported being as full when eating the Cheese and veggie snack as they did when eating chips.

Use these results to help your child eat fewer calories when snacking, try: Having more nutritious snacks available instead of eliminating snacking Substituting a healthier snack like veggies and cheese in place of chips on a regular basis Offering smaller quantities of a variety of healthy snacks (multiple kinds of vegetables or fruit) on a plate. Variety tends to stimulate consumption; increasing the healthy options available can lead to more of them being selected and eaten. Encouraging children to be mindful of internal cues and stop eating when they feel full Written by Sandra Cleveland and Adam Brumberg Article adapted by Medical News Today from original press release. Click 'references' tab above for source.
Visit our obesity / weight loss / fitness section for the latest news on this subject. Association of Nutrient-Dense Snack Combinations With Calories and Vegetable Intake, Brian Wansink, PhDa, Mitsuru Shimizu, PhDa, and Adam Brumberg, BS, Pediatrics, Published online December 17, 2012, doi: 10.1542/peds.2011-3895

Cornell Food & Brand Lab

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Host Cholesterol Secretion Likely To Influence Gut Microbiota

Main Category: Cholesterol
Also Included In: GastroIntestinal / Gastroenterology
Article Date: 25 Dec 2012 - 0:00 PST Current ratings for:
Host Cholesterol Secretion Likely To Influence Gut Microbiota
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For more than half a century, researchers have known that the bacteria that colonize the gastrointestinal tract of mammals influence their host's cholesterol metabolism. Now, Jens Walter and colleagues of the University of Nebraska show that changes in cholesterol metabolism induced by diet can alter the gut flora. The research was published online ahead of print in the journal Applied and Environmental Microbiology.

In the study, the researchers added plant sterol esters to the diets of hamsters. The overall effect of this was to inhibit several bacterial taxa, from the families Coriobacteriacea and Erysipelotrichaceae, says Walter. But the immediate effect of the plant sterols was to physically block cholesterol absorption by the intestine. That decreased cholesterol levels in the liver and the plasma, prompting the hamster's body to respond by synthesizing more cholesterol. That, in turn, boosted cholesterol excretion into the gut, and that extra cholesterol was the direct inhibitor of those bacterial families.

"The abundance of these bacterial taxa and the levels of cholesterol in the fecal samples followed a mathematical model of bacterial inhibition," says Walter.

Practically speaking, the microbial inhabitants of the gut are part of the metabolic system. Researchers have shown that certain health problems are related to changes in the gut flora, such as can be induced by overuse of antibiotics. Since changes in diet can influence composition of the gut flora, health problems such as obesity might be targeted by dietary interventions designed to suppress bacteria that contribute to weight gain. "However, for these to be successful, we need to know which bacterial patterns not only are associated with disease, but actually contribute to it," says Walter, noting that his research showed that some alterations associated with metabolic disease might be the consequence, rather than the cause of the disorder.

Walter says that the work was a real student project. Among the coauthors, three were graduate students, and two were undergraduates. "As a supervisor, it is extremely nice to see young scientists work as a team, and staying dedicated through the five years that this project took to complete," he says.

Article adapted by Medical News Today from original press release. Click 'references' tab above for source.
Visit our cholesterol section for the latest news on this subject. A copy of the manuscript can be found online at http://bit.ly/asmtip1212b. Formal publication is scheduled for the January 2013 issue of Applied and Environmental Microbiology.

(I. Martinez, D.J. Perdicaro, A.W. Brown, S. Hammons, T.J. Carden, T.P. Carr, K.M. Eskridge, and J. Walter, 2012. Diet-induced alterations of host cholesterol metabolism are likely to affect gut microbiota composition in hamsters. Appl. Environ. Microbiol. 2012 Nov 2. [Epub ahead of print])

American Society for Microbiology

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