Light shed on triglyceride metabolism

Light Shed on Triglyceride Metabolism


ScienceDaily (Aug. 8, 2010) — New findings reported in the July issue of Cell Metabolism, are offering new leads as to why some people might suffer from high levels of triglycerides. High triglycerides are a risk factor for atherosclerosis and cardiovascular disease. They can also lead to inflammation of the pancreas, the researchers said.



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The team led by Loren Fong and Stephen Young of the University of California, Los Angeles, has identified the component responsible for bringing a key triglyceride-processing enzyme (called lipoprotein lipase or LPL for short) into the capillaries, where it does its work.
"LPL is required for normal metabolism of triglycerides in blood," Fong said. "If there is no LPL, triglycerides accumulate."
Scientists have known for decades that the LPL enzyme is produced in fat and muscle before it makes its way into blood vessels. What they didn't know until now was how it got there.
It seems that a protein known as GPIHBP1 is the key. Mice lacking that protein end up with LPL built up outside of their muscle and fat tissue instead of where it belongs in capillaries. They show that GPIHBP1 normally sits on the surface of capillary cells, where it actively transports LPL.
The new findings offer an explanation for what had been a surprising finding; Gpihbp1-deficient mice develop severe hypertriglyceridemia, even when they eat a normal diet of mouse chow. Very recently, other researchers have also shown that some people with elevated triglyceride levels carry mutations in their GPIHBP1 gene.
Fong and Young say they don't yet know exactly how GPIHBP1 does its job of transporting LPL into capillaries. It's likely that other as-yet unknown players are involved. Their team also suspects that GPIHBP1 may influence triglyceride metabolism in other ways, aside from its transport function.
There is also much left to learn about how the process is regulated in response to diet or other factors. For instance, "if you eat a fatty meal with more lipids, does this transport go faster?" Fong asked.
The findings may help sort out the causes of hypertriglyceridemia, which in many instances remain unclear.
"In humans, mechanisms for severe cases of hypercholesterolemia have come into focus, but the same cannot be said for many cases of severe hypertriglyceridemia," the researchers wrote. Many patients with very high triglyceride levels don't have mutations in any of the genes with known links to the condition and some have no obvious abnormalities in LPL levels either.
"It seems possible that defective transport of LPL into the capillaries could underlie at least some cases of hypertriglyceridemia in humans," they said.
The researchers include Brandon S.J. Davies, University of California, Los Angeles, Los Angeles, CA; Anne P. Beigneux, University of California, Los Angeles, Los Angeles, CA; Richard H. Barnes II, University of California, Los Angeles, Los Angeles, CA; Yiping Tu, University of California, Los Angeles, Los Angeles, CA; Peter Gin, University of California, Los Angeles, Los Angeles, CA; Michael M. Weinstein, University of California, Los Angeles, Los Angeles, CA; Chika Nobumori, University of California, Los Angeles, Los Angeles, CA; Rakel Nyren, Umea University, Umea, Sweden; Ira Goldberg, Columbia University College of Physicians and Surgeons, New York, NY; Gunilla Olivecrona, Umea University, Umea, Sweden; Andre´ Bensadoun, Cornell University, Ithaca, NY; Stephen G. Young, University of California, Los Angeles, Los Angeles, CA; and Loren G. Fong, University of California, Los Angeles, Los Angeles, CA.

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The above story is reprinted (with editorial adaptations by ScienceDaily staff) from materials provided by Cell Press, via EurekAlert!, a service of AAAS.




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Brandon S.J. Davies, Anne P. Beigneux, Richard H. Barnes, Yiping Tu, Peter Gin, Michael M. Weinstein, Chika Nobumori, Rakel Nyrén, Ira Goldberg, Gunilla Olivecrona, André Bensadoun, Stephen G. Young, Loren G. Fong. GPIHBP1 Is Responsible for the Entry of Lipoprotein Lipase into Capillaries. Cell Metabolism, July 7, 2010 DOI: 10.1016/j.cmet.2010.04.016

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Diabetes or not, dietary habits of Aftrican-Americans are similar

Diabetes or Not, Dietary Habits of Aftrican-Americans Are Similar


ScienceDaily (Aug. 6, 2010) — Researchers looking for differences in eating habits of African Americans based on whether or not they had Type 2 diabetes uncovered an unexpected result: No matter what the blood sugar level was, the dietary intakes were pretty much the same.



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According to the study, the average diet of African-American adults is higher in carbohydrates and fat and lower in beneficial minerals and nutrients than are federally recommended for daily consumption. The researchers take that as a sign that culturally relevant nutrition education could benefit all black citizens because of their higher risk for diabetes and would be especially prudent for those already diagnosed with the disease.
African Americans are 1.8 times more likely to develop Type 2 diabetes and 1.4 times more likely to be obese than are non-Hispanic whites, according to federal health agencies. Obesity is a leading risk factor for development of diabetes, a condition that results when the body cannot properly use insulin to transfer sugar from the blood to muscle and fat cells that use glucose for energy.
In general, the study showed that African Americans consume more fat and saturated fat than is recommended and lower-than-recommended levels of minerals associated with bone health -- which can be compromised by diabetes. Blacks with diabetes got about half of their total energy from carbohydrates, and their intake of whole grains was well below recommended levels.
"This means people who do have the condition aren't doing anything different from when they didn't, and those who don't have the condition don't appear to be trying to prevent diabetes," said Jonathan Scott, a graduate student in medical dietetics at Ohio State University and lead author of the study.
"We still don't fully understand why some people get diabetes and some don't, especially if they're eating the same kind of diet. But what we can see from this study is that there is potential to use nutrition education to both improve the chances of preventing diabetes and other diseases and to help those with diabetes better manage the condition with some lifestyle changes."
The study is published in a recent issue of the journal Ethnicity & Disease.
The findings led Scott and his colleagues to assert that nutrition education materials that reflect black culture could help promote overall improvement in the diets of African Americans. Comprehensive nutrition education for diabetics is already hard to come by in the current health-care system, researchers say, and the materials available tend to be geared toward a homogeneous group of consumers eating a generic diet.
The researchers have used these findings to identify dietary habits to target in an intervention led by Leon McDougle, assistant professor of family medicine at Ohio State, with African Americans in central Ohio. The cultural specifics featured in the materials range from the inclusion of photos of African Americans to the acknowledgment that eating soul food is part of many black family traditions. Typically high in fat and calories, these foods can be modified or used in moderation rather than eliminated completely from the diet, Scott noted.
The researchers examined the dietary intake of 2,589 African-American adults recorded in the 1999-2004 National Health and Nutrition Examination Survey. Scott and colleagues organized the research participants into three diabetes status groups with the goal of identifying whether having the disease appeared to influence eating habits among black adults.
The three groups studied were those with normal blood sugar levels, those with pre-diabetes and those with a Type 2 diabetes diagnosis. Pre-diabetes indicates elevated blood sugar levels that haven't crossed the threshold for an actual disease diagnosis. Among the participants, 1,863 had normal blood sugar levels, 321 were in the pre-diabetes range and 405 had diabetes.
Besides the findings of high consumption of carbohydrates and fat among the majority of African Americans in the study, the researchers did find a bright spot: Black adults with diabetes and pre-diabetes ate more dietary fiber than did participants with normal blood sugar.
Overall, however, the intake of nutrients recorded by the national study indicated the average African-American diet tended to be low on fruits, vegetables, whole grains and low-fat dairy, and high on meat and non-whole grains.
Christopher Taylor, senior author on the paper and assistant professor of medical dietetics at Ohio State, noted that the national survey represents a snapshot rather than eating trends over time.
"But the data shows that those with diabetes don't seem to be doing the things that we would educate them to do, such as controlling carbohydrates and eating more fruits and vegetables," Taylor said. "We also don't know why those with normal blood glucose levels are normal. They show up as having normal levels in the data, but that doesn't mean their blood sugar levels will stay normal."
Besides diabetes, the researchers noted another risk associated with these dietary habits: Among the African Americans surveyed, almost half -- 44.6 percent of women and 49 percent of men -- over age 20 had cardiovascular disease.
The researchers also could see from the data what else contributed to diabetes risk: For every one-year increase in age, there was a 7 percent greater likelihood that those studied would have diabetes, and for every centimeter increase in waist circumference came a 5 percent increase in the risk for having diabetes. The data also showed that as income increased, risk for diabetes decreased. For example, among the adults surveyed, if income rose from 100 percent of the federal poverty rate to 200 percent, the risk of having diabetes was cut by 14 percent.
Though dietary habits are just one likely contributor to a higher risk of disease, the researchers say nutrition is an important part of diabetes management that often goes unrecognized.
"Our health-care system in general isn't set up very well to provide nutrition counseling," Taylor said. "For the most part, individuals don't get access to a dietitian that is covered by their insurance. So the ability to get nutrition education out there and get people to change the habits they've had for so long becomes a barrier."
Taylor and Scott have partnered with Ohio State family medicine specialists to manage a community-based diabetes education program for African Americans living in central Ohio. The local and national projects inform each other, Taylor said.
"We looked at dietary intake habits locally as well. It gives us a comparative piece and has helped us identify what some of the major dietary habits are that can be addressed," he said. "And on a national scale, we wanted to identify some of the most important trends that we could then address through the local education program."
The program has helped the researchers identify other barriers to educating the African-American community about nutrition, which range from the lack of fresh foods in certain neighborhood markets to misconceptions -- expressed in focus groups -- about what it means to manage Type 2 diabetes.
"Some people think prevention of diabetes is getting their blood sugar checked. But that doesn't tell you how to prevent the disease from happening," Taylor said. "And because medications exist, people might think they don't have to eat better because they have a pill that takes care of blood sugar. So there is a big behavioral side to this."
Co-authors on the paper include McDougle and Kent Schwirian, of Ohio State's Departments of Sociology and Family Medicine (emeritus), who also helped design and operate the central Ohio nutrition education program.

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The above story is reprinted (with editorial adaptations by ScienceDaily staff) from materials provided by Ohio State University. The original article was written by Emily Caldwell.




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Jonathan M. Scott, MS; Leon McDougle, MD, MPH; Kent Schwirian, PhD; Christopher A. Taylor, PhD. Differences in the Dietary Intake Habits by Diabetes Status for African American Adults. Ethnicity & Disease, Vol 20, No 2 [link]

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Obesity prevention begins before birth: Excess maternal weight gain increases birth weight after controlling for genetic factors

Obesity Prevention Begins Before Birth: Excess Maternal Weight Gain Increases Birth Weight After Controlling for Genetic Factors


ScienceDaily (Aug. 4, 2010) — Expectant mothers who gain large amounts of weight tend to give birth to heavier infants who are at higher risk for obesity later in life. But it's never been proven that this tendency results from the weight gain itself, rather than genetic or other factors that mother and baby share.



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A large population-based study from Children's Hospital Boston, looking at two or more pregnancies in the same mother, now provides evidence that excess maternal weight gain is a strong, independent predictor of high birth weight.
The study, published Online First in The Lancet, highlights the importance of weight management efforts even before birth.
"Since high birth weight, in turn, increases risk for obesity and diseases such as cancer and asthma later in life, these findings have important implications to general public health," says coauthor David Ludwig, MD, PhD, director of the Optimal Weight for Life (OWL) at Children's Hospital Boston. "It's appropriate for a baby to be born with some fat, but a baby born too fat indicates that the fetus developed in an abnormal environment during the most critical nine months of life."
Ludwig and collaborator Janet Currie, PhD, of the Department of Economics at Columbia University, used statewide birth records to examine all known singleton births in Michigan and New Jersey from 1989 through 2003. They identified mothers with two or more live births, allowing a comparison of pregnancies in the same mother. Infants born before 37 weeks or after 41 weeks of gestation were excluded, as were mothers with diabetes and infants with extremely low or high birth weights. This left 513,501 women and 1,164,750 infants for analysis.
On average, the women gained an average of 30 pounds during their pregnancies, but with much variation; 12 percent of pregnancies involved weight gains of more than 44 pounds. High-birth-weight babies (8.8 lbs or more) accounted for 12 percent of all births.
"When comparing between siblings to control for genetic influences, we found that increasing amounts of maternal weight gain led to the birth of progressively heavier infants," says Ludwig.
Compared to those gaining just 18-22 pounds, expectant mothers gaining 44-49 pounds were 1.7 times more likely to have a high-birth-weight baby, and those gaining more than 53 pounds were 2.3 times more likely to do so. The pattern was the same after excluding women who had ever smoked, those who delivered by caesarean section, and those who had any pregnancy of less than 39 weeks or more than 40 weeks.
Animal studies suggest that excess maternal weight or excess weight gain during pregnancy affects the uterine environment, producing changes in the hypothalamus, pancreatic islet cells, fat tissue and other systems that regulate body weight. "Hormones and metabolic pathways, and even the structure of tissues and organs that play a role in body weight maintenance are affected," says Ludwig.
Recently updated guidelines from the Institute of Medicine suggest that women gain 28 to 40 pounds if underweight at the start of pregnancy, 25 to 35 pounds if they are normal weight, 15 to 25 pounds if overweight, and 11 to 20 pounds if obese.
The study was funded by the National Institutes of Health.

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The above story is reprinted (with editorial adaptations by ScienceDaily staff) from materials provided by Children's Hospital Boston, via EurekAlert!, a service of AAAS.




Journal Reference:

David S Ludwig, Janet Currie. The association between pregnancy weight gain and birthweight: a within-family comparison. The Lancet, 2010; DOI: 10.1016/S0140-6736(10)60751-9

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Eliminating diabetes and depression, and boosting education, most likely to ward off dementia

Eliminating Diabetes and Depression, and Boosting Education, Most Likely to Ward Off Dementia


ScienceDaily (Aug. 5, 2010) — Eliminating diabetes and depression, as well as increasing education and fruit and vegetable consumption, are likely to have the biggest impact on reducing levels of dementia in the coming years, should no effective treatment be found, concludes a study published on the British Medical Journal website.



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These findings suggest priorities for future public health interventions.
While the exact cause of dementia is still unknown, several modifiable risk factors have already been identified. These include vascular risk factors (heart disease, stroke, high blood pressure, obesity, diabetes, and high cholesterol), a history of depression, diet, alcohol consumption, and education level.
Based on this knowledge, a team of researchers based in France and the UK estimated which of these risk factors might be most effective in reducing the future burden of dementia, should no effective treatment be found.
Their analysis involved 1,433 healthy people aged over 65 years living in the south of France and recruited between 1999 and 2001. Participants underwent cognitive testing at the start of the study and again at two, four and seven years. A reading test (the Neale score) was also used as an indicator of lifetime intelligence.
Medical history and information on measures such as height, weight, education level, monthly income, mobility, dietary habits, alcohol consumption, and tobacco use was obtained. An individual's genetic risk of dementia was also measured: although it's not a factor that can be changed it served as a useful benchmark for dementia risk.
Results showed that eliminating depression and diabetes and increasing fruit and vegetable consumption were estimated to lead to an overall 21% reduction in new cases of dementia, with depression making the greatest contribution (just over 10%). However, the researchers point out that the direct (causal) relationship between depression and dementia remains unclear.
Increasing education would also lead to an estimated 18% reduction in new cases of dementia across the general population over the next seven years. By contrast, eliminating the principal known genetic risk factor from the general population would lead only to a 7% reduction in the number of new cases over the next seven years.
Given these findings, the authors suggest that public health initiatives should focus on encouraging literacy at all ages irrespective of ability, prompt treatment of depressive symptoms, and early screening for glucose intolerance and insulin resistance (early stages in the development of diabetes).
While these calculations can only provide a crude estimate of impact on incidence, they do make a significant statement about public health priorities in disease prevention in the face of current knowledge, conclude the authors. Further studies including younger adults are clearly needed to test the impact of intervention measures.
A second study, also published on the British Medical Journal website August 5, finds that death rates are more than three times higher in people with dementia than in those without dementia in the first year after diagnosis. The study also says that earlier and better detection of dementia in primary care is needed. An accompanying editorial suggests that key areas to focus on include better education and training in primary care, developing more integrated systems of care, and ensuring that policy makers and commissioners plan services that reflect the effects of dementia on primary care and other services.

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The above story is reprinted (with editorial adaptations by ScienceDaily staff) from materials provided by BMJ-British Medical Journal, via EurekAlert!, a service of AAAS.




Journal Reference:

K Ritchie et al. Research Designing prevention programmes to reduce incidence of dementia: prospective cohort study of modifiable risk factors. BMJ, 2010;341:c3885 DOI: 10.1136/bmj.c3885

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Solving the mystery of bone loss from drug for epilepsy and bipolar disorder

Solving the Mystery of Bone Loss from Drug for Epilepsy and Bipolar Disorder


ScienceDaily (Aug. 4, 2010) — Scientists are reporting a possible explanation for the bone loss that may occur following long-term use of a medicine widely used to treat epilepsy, bipolar disorder, and other conditions. The drug, valproate, appears to reduce the formation of two key proteins important for bone strength, they said. Their study, which offers a solution to a long-standing mystery, appears in ACS' Journal of Proteome Research.



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Glenn Morris and colleagues point out that use of valproate, first introduced more than 40 years ago for the prevention of seizures in patients with epilepsy, has expanded. Valproate now is prescribed for mood disorders, migraine headache, and spinal muscular atrophy (SMA), a rare genetic disease that causes loss of muscle control and movement. Many SMA patients develop weak bones as a result of the disease itself, making further bone loss from valproate especially undesirable. Doctors have known about the bone-loss side effect, but until now, there has been no molecular explanation.
In an effort to determine why bone loss occurs, the scientists profiled valproate's effects on more than 1,000 proteins in the cells of patients with SMA. They found that valproate reduced production of collagen, the key protein that gives bone its strength, by almost 60 percent. The drug also reduced levels of osteonectin, which binds calcium and helps maintain bone mass, by 28 percent. "The results suggest a possible molecular mechanism for bone loss following long-term exposure to valproate," the article notes.

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The above story is reprinted (with editorial adaptations by ScienceDaily staff) from materials provided by American Chemical Society.




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Fuller et al. Valproate and Bone Loss: iTRAQ Proteomics Show that Valproate Reduces Collagens and Osteonectin in SMA Cells. Journal of Proteome Research, 2010; 100722144125012 DOI: 10.1021/pr1005263

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Chew on this: Six dental myths debunked

Chew on This: Six Dental Myths Debunked


ScienceDaily (Aug. 5, 2010) — Brushing, flossing, and twice-yearly dental check-ups are standard for oral health care, but there are more health benefits to taking care of your pearly whites than most of us know. In a review article, a faculty member at Tufts University School of Dental Medicine (TUSDM) debunks common dental myths and outlines how diet and nutrition affects oral health in children, teenagers, expectant mothers, adults and elders.



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Myth 1: The consequences of poor oral health are restricted to the mouth
Expectant mothers may not know that what they eat affects the tooth development of the fetus. Poor nutrition during pregnancy may make the unborn child more likely to have tooth decay later in life. "Between the ages of 14 weeks to four months, deficiencies in calcium, vitamin D, vitamin A, protein and calories could result in oral defects," says Carole Palmer, EdD, RD, professor at TUSDM and head of the division of nutrition and oral health promotion in the department of public health and community service. Some data also suggest that lack of adequate vitamin B6 or B12 could be a risk factor for cleft lip and cleft palate formation.
In children, tooth decay is the most prevalent disease, about five times more common than childhood asthma. "If a child's mouth hurts due to tooth decay, he/she is less likely to be able to concentrate at school and is more likely to be eating foods that are easier to chew but that are less nutritious. Foods such as donuts and pastries are often lower in nutritional quality and higher in sugar content than more nutritious foods that require chewing, like fruits and vegetables," says Palmer. "Oral complications combined with poor diet can also contribute to cognitive and growth problems and can contribute to obesity."
Myth 2: More sugar means more tooth decay
It isn't the amount of sugar you eat; it is the amount of time that the sugar has contact with the teeth. "Foods such as slowly-dissolving candies and soda are in the mouth for longer periods of time. This increases the amount of time teeth are exposed to the acids formed by oral bacteria from the sugars," says Palmer.
Some research shows that teens obtain about 40 percent of their carbohydrate intake from soft drinks. This constant beverage use increases the risk of tooth decay. Sugar-free carbonated drinks and acidic beverages, such as lemonade, are often considered safer for teeth than sugared beverages but can also contribute to demineralization of tooth enamel if consumed regularly.
Myth 3: Losing baby teeth to tooth decay is okay
It is a common myth that losing baby teeth due to tooth decay is insignificant because baby teeth fall out anyway. Palmer notes that tooth decay in baby teeth can result in damage to the developing crowns of the permanent teeth developing below them. If baby teeth are lost prematurely, the permanent teeth may erupt malpositioned and require orthodontics later on.
Myth 4: Osteoporosis only affects the spine and hips
Osteoporosis may also lead to tooth loss. Teeth are held in the jaw by the face bone, which can also be affected by osteoporosis. "So, the jaw can also suffer the consequences of a diet lacking essential nutrients such as calcium and vitamins D and K," says Palmer.
"The jawbone, gums, lips, and soft and hard palates are constantly replenishing themselves throughout life. A good diet is required to keep the mouth and supporting structures in optimal shape."
Myth 5: Dentures improve a person's diet
If dentures don't fit well, older adults are apt to eat foods that are easy to chew and low in nutritional quality, such as cakes or pastries. "First, denture wearers should make sure that dentures are fitted properly. In the meantime, if they are having difficulty chewing or have mouth discomfort, they can still eat nutritious foods by having cooked vegetables instead of raw, canned fruits instead of raw, and ground beef instead of steak. Also, they should drink plenty of fluids or chew sugar-free gum to prevent dry mouth," says Palmer.
Myth 6: Dental decay is only a young person's problem
In adults and elders, receding gums can result in root decay (decay along the roots of teeth). Commonly used drugs such as antidepressants, diuretics, antihistamines and sedatives increase the risk of tooth decay by reducing saliva production. "Lack of saliva means that the mouth is cleansed more slowly. This increases the risk of oral problems," says Palmer. "In this case, drinking water frequently can help cleanse the mouth."
Adults and elders are more likely to have chronic health conditions, like diabetes, which are risk factors for periodontal disease (which begins with an inflammation of the gums and can lead to tooth loss). "Type 2 diabetes patients have twice the risk of developing periodontal disease of people without diabetes. Furthermore, periodontal disease exacerbates diabetes mellitus, so meticulous oral hygiene can help improve diabetes control," says Palmer.
This article appears in the July/August issue of Nutrition Today.

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Palmer et al. It's More Than Just Candy : Important Relationships Between Nutrition and Oral Health. Nutrition Today, 2010; 45 (4): 154 DOI: 10.1097/NT.0b013e3181e98969

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Pancreatic cancers use fructose, common in the Western diet, to fuel their growth

Pancreatic Cancers Use Fructose, Common in the Western Diet, to Fuel Their Growth


ScienceDaily (Aug. 2, 2010) — Pancreatic cancers use the sugar fructose, very common in the Western diet, to activate a key cellular pathway that drives cell division, helping the cancer to grow more quickly, a study by researchers at UCLA's Jonsson Comprehensive Cancer Center has found.



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Although it's widely known that cancers use glucose, a simple sugar, to fuel their growth, this is the first time a link has been shown between fructose and cancer proliferation, said Dr. Anthony Heaney, an associate professor of medicine and neurosurgery, a Jonsson Cancer Center researcher and senior author of the study.
"The bottom line is the modern diet contains a lot of refined sugar including fructose and it's a hidden danger implicated in a lot of modern diseases, such as obesity, diabetes and fatty liver," said Heaney, who also serves as director of the Pituitary Tumor and Neuroendocrine Program at UCLA. "In this study, we show that cancers can use fructose just as readily as glucose to fuel their growth."
The study appeared in the Aug. 1 issue of the peer-reviewed journal Cancer Research.
Sources of fructose in the Western diet include cane sugar (sucrose) and high fructose corn syrup (HFCS), a corn-based sweetener that has been on the market since about 1970. HFCS accounts for more than 40 percent of the caloric sweeteners added to foods and beverages, and it is the sole sweetener used in American soft drinks.
Between 1970 and 1990, the consumption of HFCS in the U.S. has increased over 1,000 percent, according to an article in the April 2004 issue of the American Journal of Clinical Nutrition. Food companies use HFCS -- a mixture of fructose and glucose -- because it's inexpensive, easy to transport and keeps foods moist. And because it is so sweet, it's cost effective for companies to use small quantities of HCFS in place of more expensive sweeteners or flavorings.
In his study, Heaney and his team took pancreatic tumors from patients and cultured and grew the malignant cells in petri dishes. They then added glucose to one set of cells and fructose to another. Using mass spectrometry, they were able to follow the carbon-labeled sugars in the cells to determine what exactly they were being used for and how.
Heaney found that the pancreatic cancer cells could easily distinguish between glucose and fructose even though they are very similar structurally, and contrary to conventional wisdom, the cancer cells metabolized the sugars in very different ways. In the case of fructose, the pancreatic cancer cells used the sugar in the transketolase-driven non-oxidative pentose phosphate pathway to generate nucleic acids, the building blocks of RNA and DNA, which the cancer cells need to divide and proliferate.
"Traditionally, glucose and fructose have been considered as interchangeable monosaccharide substrates that are similarly metabolized, and little attention has been given to sugars other than glucose," the study states. "However, fructose intake has increased dramatically in recent decades and cellular uptake of glucose and fructose uses distinct transporters ... these findings show that cancer cells can readily metabolize fructose to increase proliferation. They have major significance for cancer patients, given dietary refined fructose consumption."
As in anti-smoking campaigns, a federal effort should be launched to reduce refined fructose intake, Heaney said.
"I think this paper has a lot of public health implications," Heaney said. "Hopefully, at the federal level there will be some effort to step back on the amount of HFCS in our diets."
Heaney said that while this study was done in pancreatic cancer, these finding may not be unique to that cancer type.
Going forward, Heaney and his team are exploring whether it's possible to block the uptake of fructose in the cancer cells with a small molecule, taking away one of the fuels they need to grow. The work is being done in cell lines and in mice, Heaney said.
The study was funded by the National Institutes of Health, the Hirschberg Foundation and the Jonsson Cancer Center.

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The above story is reprinted (with editorial adaptations by ScienceDaily staff) from materials provided by University of California - Los Angeles, via EurekAlert!, a service of AAAS.




Journal Reference:

Haibo Liu, Danshan Huang, David L. Mcarthur, Laszlo G. Boros, Nicholas Nissen, and Anthony P. Heaney. Fructose Induces Transketolase Flux to Promote Pancreatic Cancer Growth. Cancer Research, August 1, 2010 70:6368-6376; Published OnlineFirst July 20, 2010 DOI: 10.1158/0008-5472.CAN-09-4615

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