Excess fructose may play a role in diabetes, obesity and other health conditions

PharmaLive.com (23 November 2010) - more and more people have become aware of the dangers of excessive fructose diets. A new review on fructose in an upcoming issue of the journal of the American Society of Nephrology (JASN) indicates just how dangerous this simple sugar can be.

Richard j. Johnson, MD and Takahiko Nakagawa, MD (Division of kidney disease and hypertension, University of Colorado) provide insight into concise recent experimental studies and clinical understanding how excessive fructose, present in added sugars could play a role in arterial hypertension, diabetes, obesity and chronic kidney disease (CKD).

Dietary fructose is present mainly in food sugars added, honey and fruits.américains ingest more frequently sucrose, fructose syrup high fructose (HFCS), a mixture of free and glucose, fructose generally in a proportion of 55 45-corn and a disaccharide containing 50% 50% of glucose and fructose bound together.With the introduction of HFCS in the 1970s, has been an increased intake of fructose and obesity rates have increased at the same time.

"The link between excessive intake of fructose and metabolic syndrome is becoming more établi.Toutefois, in this literature review, we conclude that it also increased evidence that fructose may play a role in hypertension and renal disease.""Science shows us some there are potentially negative impact of excessive amounts of sugar and corn syrup high-fructose on cardiovascular and kidney health" explains Mr. Johnson.Il continues that "excessive intake of fructose could be seen as an increasingly risky food and beverage additive.

Concerned that physicians may be overlooking this health problem when counsel patients IRC dieting low in protein, Mr. Johnson and Mr. Nakagawa recommends that low-protein diets include an attempt to restrict the added sugars containing fructose.

Mr. Johnson and Mr. Nakagawa listed as inventors on several requests for patents related to the lowering of uric for treatment or prevention of hypertension, diabetes and foie gras.

Editor's note: this article is not intended to provide medical advice, diagnosis or treatment.

Source of the story:

The story above is reproduced (with drafting adaptations by staff at PharmaLive.com) materials provided by American Nephrology Society, via EurekAlert!, a service of AAAS.

Reference of the review:

Richard j. Johnson, MD and Takahiko Nakagawa, MD.Effects of fructose kidney biology and diseases of the American Society of Nephrology, 29 November 2010 .Journal DOI: 10.1681/ASN.2010050506

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HYPERACTIVE AFP gene causes eating and obesity

PharmaLive.com (16 November 2010) - scientists have gained strong confirmation of the direct connection between the AFP gene and obesity, obtaining the first direct evidence that the hyperactivity of the gene leads to eat and obesity in mice.

University of Oxford and the Council of medical research (MRC), the Wellcome Trust and the MRC funded research team have published their results in the journal Nature Genetics.

Results team of suggested that the gene may be a promising target for the development of anti-obesity drugs that Act by turning to the activity of the gene.

"This work we confident that the AFP is an important gene that contributes to obesity," said Frances Ashcroft the Professor of the Oxford University Department of Physiology, Anatomy and genetics, and one of the leaders of research. "Too much activity of this gene can lead to put on weight by overeating.

"We now think the development of drugs that turn down the activity of AFP gene in the form of pills potential anti-obesity b.c ' is a long way off the coast and there is no guarantee of success, but it is an attractive prospect,' she adds."

In 2007, an international team of researchers, including Oxford, scientists announced that they had identified the first genetic variant that may be linked to an increased risk of obesity in a large genome-wide study.

The only change in the DNA sequence of lay of AFP gene.Persons with two copies of this variant genetic (approximately 16% of the population of European origin were two copies) have been the heaviest 3 kg on average than those without.

While it is an important result, genome-wide association studies are often first step allowing then detail to identify the mechanisms behind the observed connection in this case to obesity research.

In particular, surveys genome-scale cannot be certain identified genetic variation directly increases the risk of obesity .the change in DNA could be an indicator or a marker important gene is located nearby, or DNA modification could lie in a control element that regulates a different gene distance.

Researchers of the study, led by Mr. Roger Cox MRC Harwell and Professor Frances Ashcroft, Oxford University, set out determine if there were differences in the activity of the gene of OTF itself directly causing the increase in body weight.

Scientists mimic mice with extra copies of the AFP gene.These mice were in good health, but eat more and becoming fatter than normal mice.

Female with two additional copies of the gene AFP, when subjected to a standard diet, mice has become 22% heavier than normal female mice after 20 weeks.The difference in weight for male mice was 10 lined researchers have also show that the difference came because the mice with AFP hyperactivity consume more food.(There is no suggestion that differences in humans with variants of the AFP weight are or could be almost as large or necessarily affect gender in a similar proportion.)

Chris Church, MRC Harwell and author of the study PhD student, said: "for the first time, we have provided convincing evidence that the FTO gene causes obesity .the ' next step is to understand how it performs, for example if it increases the appetite by influencing our brains or modifies messages from our reserves of fat and other times we know how AFP causes obesity tissus.Une, we have the opportunity to seek to develop drugs for treatment."

Genome-wide association studies did a fantastic job narrowing zones in the genome of the head of obesity.They have provided guides from the place to go, but these areas remain pinning a specific gene as we've done here for the first time with the AFP.Mouse model has allowed us to achieve this goal in only a few years, and we hope the same process will now apply to other areas of genes involved in obesity, allowing scientists to confirm precisely that other genes may predispose us to become overweight.»

From 1 to 3 persons in the United Kingdom are obese or .the ' obesity predisposes people to many diseases, including heart disease, type 2 diabetes and the estimated amount cancer.Le of obesity in the NHS is approximately 1 billion pounds per year, with an additional £ 2.3 to 2.6 billion pounds per year to the economy as a whole.

"This gene is the novel research on obesity and it will be interesting to know how it works," explains Mr Roger Cox, unity of genetics in mammals of the Council of medical research at Harwell and one of the leaders of research. "We now have to address these issues mouse models.»

Editor's note: this article is not intended to provide medical advice, diagnosis or treatment.

Source of the story:

The story above is reproduced (with drafting adaptations by staff at PharmaLive.com) materials provided by The University of Oxford.

Reference of the review:

Chris Church, Lee Moir, Fiona McMurray, Christophe Girard, Gareth T Banks, Lydia Teboul, Sara Wells, Jens C Brüning, Patrick Nolan, Frances M Ashcroft, Roger D. Cox.Tre overexpression leads to an increased food intake and gives rise to obesity .Nature Genetics, 2010; DOI: 10.1038/ng.713

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Fly study discovers molecular link between obesity and heart disease

PharmaLive.com (3 November 2010) - it is no secret that obesity is hard on the heart. More than 30% of Americans are obese, and many of them are also at increased risk of cancer, diabetes and heart disease. However, there are many causes of obesity and other factors of risk for each of these conditions, making it difficult to tease each other.

Sanford-Burnham Medical Research Institute (Sanford-Burnham), a team led by Dr. Sean Oldham, Dr. Rolf Bodmer recently created a simple template bind the diet fat, obese and cardiac dysfunction.Using fruit flies, they discovered that a protein called TOR influences accumulation of fat in the study, published on 3 November in the journal Cell Metabolism, coeur.Leur also shows that manipulation of TOR protects the heart of obese flies from damage caused by a diet rich in fat.

"We have noted previously that reduce the mandate had many beneficial effects on aging", explained Mr. Oldham, co-senior author of the study. " Then we wanted to look at TOR activity in obesity-related diseases, but we didn't have a good system.In this study, we show that the fruit fly as a model for obesity caused by a diet rich in fat. »

The model of the fruit fly is ideal to explore the heart, because most of the basic molecular mechanisms controlling its development are strikingly similar to those of vertebrates - even somewhat interchangeable. In addition, it is relatively easy to remove individual genes in the fly, allowing researchers specifically map each role in the development of heart and function.

In this study, flies on a diet rich in fat the oil of coconut became obese and were of the same side as obese humans, including cardiaque.Ensuite dysfunction symptoms, determining how TOR regulates the effects of grease on the heart, Mr. Oldham and generated colleagues flies which reduces the activity of this protéine.TOR normally takes a damper on an enzyme which breaks down fats. By inhibiting the TOR (or stimulate the enzyme Digest FAT), researchers have reduced fat accumulation in the heart and improve heart health otherwise obese flies. Heart-protection results are the same whether the mandate was stuck in fly together, only adipose tissues or only in cardiac cells.

According to Dr. Bodmer, co-senior author of the study and Professor and Director of development and the program "these results open the possibility that we can respond with the effects of obesity by targeting the TOR and other proteins that it regulates - directly in bold or in a specific organ such as the heart."

This model of fly now allow researchers answer many other questions about diet, obesity and heart. "One thing we would like to know then is that fat themselves are toxic to the heart, or are it metabolic by-products which are harmful?", said Dr. Birse, post-doctoral researcher, first and main author of the study."A good thing about using Drosophila is in theory, we could eat all what we want to screen - different fatty acid molecules, drugs, etc. - to observe their effects on the heart or other systems.»

The study was funded by the Association American Heart (AHA), Ellison and National Heart, Lung and Blood Institute (NHLBI) Medical Foundation at the National Institutes of Health (NIH).Support for this project also offered by the Centre for child health research Sanford Sanford-Burnham.

Editor's note: this article is not intended to provide medical advice, diagnosis or treatment.

Source of the story:

The story above is reproduced (with drafting adaptations by PharmaLive.com staff) to materials provided by the Institute of medical research Sanford-Burnham.

Reference of the review:

Ryan t. Birse, Joan Choi, Kathryn Reardon, Jessica Rodriguez, Suzanne, baking soda Diop, Karen Ocorr, Rolf Bodmer, Sean Oldham.-High fat-diet-induced obesity and cardiac dysfunction are regulated by way of the TOR in Drosophila. metabolism of the cell, 2010; 12 (5): 533-544 DOI: 10.1016/j.cmet.2010.09.014

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Severe obesity during adolescence significantly associated with an increased risk of obesity in adulthood

PharmaLive.com (9 November 2010) - analysis of nationally representative data suggests that being obese adolescents increases the risk of being severely obese in adulthood, with the risk higher in women and highest among black women, according to a study in JAMA 10 November issue.
People suffering from severe obesity (index Bodymass index [BMI] 40 or higher) encounter serious and potentially fatal complications. "In 2000, approximately 2.2 percent of adults, or 4.8 million people, were severely obese, with a prevalence disproportionately high among women and racial and ethnic minorities." However, few national studies follow further to understand the progression of severe obesity overweight people, "the authors write.""Understanding individuals are at risk of severe obesity is essential to determine when interventions should be implemented to prevent the progression toward obesity serious people obèses.Bien observational studies have reported that the prevalence of overweight and obesity severe obesity have increased in recent years, people who are obese early in life have not been studied longitudinally to determine their risk of developing serious adult obesity."
Natalie Dr.., of the University of North Carolina at Chapel Hill, and colleagues conducted a study to determine the incidence and risk of severe obesity in adulthood among people who were obese during adolescence.Study group consisted of 8,834 individuals between the ages of 12 and 21 years, who were enrolled in 1996 in the National Longitudinal Study of Adolescent Health of United States, followed in adulthood II wave (ages 18-27 years waves III [2001-2002]) 24-33 years in the wave IV [2007-09] .i got measurements of size and weight of participants and survey administered in the homes of the participants in the study of standard procedures. New cases of severe adult obesity were calculated by sex, race or ethnic origin and the State of weight among teenagers, and the results were weighted for national representation.
In 1996, 79 adolescents (1.0%) were seriously obèses.60 (70.5%) remains severely obese as adults. In the period of 13 years among adolescents (1996) and age adult (2007-2009), a total of 703 new cases of severe obesity in adulthood were observed, indicating a total rate of 7.9%.Researchers have discovered that people suffering from serious incident obesity in adulthood had a higher adolescents BMI and were more likely to be racial and ethnic minorities compared with people without severe obesity.
"A significant proportion of obese adolescents become severely obese by their beginning in the 1930s, with significant variation in the sexe.Parmi people who were obese as adolescents, severe obesity incident was 37.1% for men and 51.3% among women." Obesity serious incident is highest among black women to 52.4 %.Dans all sexual relations and racial or ethnic groups, less than 5 percent of people who have normal weight in adolescence becomes severely obese as adults, "the authors write."
The analysis indicates that obese adolescents were much more likely to develop severe obesity than adolescents normal weight or excess weight, with a variation on race or ethnic origin and sex.
"The clinical consequences of these observed trends are given co-morbidities and chronic associated with severe obesity the disease."Results highlight the need for interventions before adulthood to prevent the progression of severe obesity, which can reduce the incidence of severe obesity obesity and potentially life-threatening consequences.»
Editor's note: this article is not intended to provide medical advice, diagnosis or treatment.
Source of the story:

The story above is reproduced (with drafting adaptations by staff at PharmaLive.com) materials provided by JAMA and archives of newspapers.

Reference of the review:
Natalie S.Le; Chirayath Suchindran; Kari e. Nord.Barry M. Popkin; Penny Gordon-Larsen.Serious Association adolescent obesity with the risk of obesity in adulthood .JAMA, 2010; 304 (18): 2042-2047 DOI: 10.1001/jama.2010.1635
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