Weight Loss Promoted By Drug Combination In Polycystic Ovary Syndrome

Women with polycystic ovary syndrome, or PCOS, lost significantly more weight when they took two drugs that are traditionally used to treat diabetes, rather than either drug alone, a study from Slovenia demonstrates. The results were presented at The Endocrine Society's 95th Annual Meeting in San Francisco.

PCOS is the leading cause of infertility among women. In the United States, the disorder affects approximately 5 million women, according to the U.S. Department of Health and Human Services Office of Women's Health. This translates to 1 in 10 to 20 women, overall, who are affected. The disease probably is genetic, although the exact causes are still unknown.

In PCOS, the ovaries produce excessive amounts of male sex hormones, or androgens. The name of the disease derives from small cysts that form on the ovaries, which do not produce enough of the hormone that triggers ovulation. When this occurs, the ovarian follicles, which have filled with fluid in preparation for ovulation, remain as cysts when ovulation fails to take place. In addition to infertility, symptoms include excessive hair growth in areas that usually are relatively hairless; obesity; menstrual irregularity; thinning or balding hair on the scalp; prediabetes or diabetes; and anxiety or depression. Weight loss in these women leads to higher chances of conception, improved pregnancy outcomes and improved metabolic profile.

Treatment varies depending upon the severity of the disease, and includes lifestyle modifications and drug therapy. Some of the same medications that are used to treat diabetes also improve PCOS symptoms. One of these medications, metformin, works by regulating the hormone insulin and by suppressing androgen activity, which, in turn, helps control blood-sugar levels and has beneficial effects on ovarian function. The problem with metformin, however, is that it does not always aid with weight loss.

Because of this, investigators examined different drug combinations to see which ones caused the most weight loss. In addition to metformin, they administered another diabetes medication called liraglutide, both alone and in combination with metformin, to determine which approach led to the greatest amount of weight loss.

They found that patients who took the combined drugs lost 6.5 kilograms (kg), or about 14 pounds, on average, compared to about 4 kg, or almost 9 pounds, on liraglutide alone, and 1 kg, or about 2 pounds, on metformin alone. Furthermore, 22 percent of participants on the combined treatment lost a significant amount of weight, defined as 5 percent or more of their body weight, compared to 16 percent of those on liraglutide. No one in the metformin group achieved this amount of weight loss. In terms of body-mass index and waist circumference, the combined-treatment group saw greater improvements than either of the single-medication groups. For both of these measurements, liraglutide alone outperformed metformin alone.

"The effect of metformin on weight reduction in polycystic ovary syndrome is often unsatisfactory," said study author Mojca Jensterle Sever, MD, PhD, who served as lead author with Andrej Janez, MD, PhD, a fellow consultant at the University Medical Center in Ljubljana, Slovenia. "Short-term combined treatment with liraglutide and metformin appears better than either metformin or liraglutide alone on weight loss and decrease in waist circumference in obese women with PCOS who had been previously poor responders regarding weight reduction on metformin alone."

The main side effect was nausea, which occurred more often with liraglutide than with metformin. The nausea did improve with time, however, and was not associated with weight loss.

Study participants comprised 36 women with PCOS who had lost less than 5 percent of their body weight on a six-month course of metformin preceding the study. Their average age was 31 years. Investigators randomly assigned them to one of three treatment groups for the 12-week study, including metformin alone, liraglutide alone, and both medications.

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Research Links Two Genes To Obesity And Health Disorders

Family DNA may influence development of Metabolic Syndrome.

Two genes may be linked to obesity and health disorders according to new research by the TOPS Obesity and Metabolic Research Center at the Medical College of Wisconsin. The study of obese individuals from four generations of families shows that hereditary DNA may influence development of Metabolic Syndrome, a cluster of conditions effecting one in five Americans, which dramatically increases the risk for heart disease and diabetes. So far, the TOPS families' DNA samples have made it possible for researchers to query almost one million variations in genes that are associated with whether or not someone develops the Metabolic Syndrome and how the disease surfaces in different people.

Soon to be published in Obesity, the official journal of The Obesity Society, the report reveals evidence of two new genes that significantly impact weight gain. One gene affects the growth and development of newborn infants, as well as regulation of glucose/insulin response, lipid profiles, and body weight in adults. The other gene affects pro-inflammatory pathways, which are precursors of traits of Metabolic Syndrome.

"Our genome-wide survey could lead to the creation of early diagnostic tools for detecting risks for developing obesity, as well as the discovery of drugs targeted specifically to these genes," said Yi (Sherry) Zhang, Ph.D., instructor, Department of Medicine, Human & Molecular Genetics Center at the Medical College of Wisconsin. "This is the first published work of our genome-wide survey, and we expect a series of reports will soon follow to address other aspects of this complex disease," she added.

Zhang and her colleagues from the TOPS Obesity Center have been working to determine the full picture of the genetic makeup that encourages development of Metabolic Syndrome, including body composition, insulin resistance, and circulating blood levels of the hormone leptin, which is exclusively produced by fatty tissue.

"We've all heard such common expressions as, 'You have your mom's eyes,' or 'I developed high blood pressure in my '40s, just like my grandfather," notes Barbara Cady, TOPS President. "When we discuss 'inheritance' like this, we're relating to a question that scientists have been striving to answer for decades: how does our genetic makeup determine our traits? Knowing which genes are detrimental to our health may help researchers develop a strategic plan to treat or even prevent the symptoms that are caused by these genes."

This research is the latest in a series of papers based on the TOPS Obesity and Metabolic Research samples housed at the Medical College of Wisconsin as part of an ongoing partnership.

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Adolescent Obesity Associated With Hearing Loss

Obese adolescents are more likely than their normal-weight counterparts to have hearing loss, according to results of a new study. Findings showed that obese adolescents had increased hearing loss across all frequencies and were almost twice as likely to have unilateral (one-sided) low-frequency hearing loss. The study was recently e-published by The Laryngoscope, a journal published by the American Laryngological, Rhinological and Otological Society.

"This is the first paper to show that obesity is associated with hearing loss in adolescents," said study first author Anil K. Lalwani, MD, professor and vice chair for research, Department of Otolaryngology/Head & Neck Surgery, Columbia University Medical Center.

The study found that obesity in adolescents is associated with sensorineural hearing loss across all frequencies (the frequency range that can be heard by humans); sensorineural hearing loss is caused by damage to the inner-ear hair cells. The highest rates were for low-frequency hearing loss - 15.16 percent of obese adolescents compared with 7.89 percent of non-obese adolescents. People with low-frequency hearing loss cannot hear sounds in frequencies 2,000 Hz and below; they may still hear sounds in the higher frequencies (normal hearing range is from 20 Hz to 20,000 Hz). Often they can still understand human speech well, but may have difficulty hearing in groups or in noisy places.

"These results have several important public health implications," said Dr. Lalwani, who is also an otolaryngologist at NewYork-Presbyterian Hospital/Columbia University Medical Center. "Because previous research found that 80 percent of adolescents with hearing loss were unaware of having hearing difficulty, adolescents with obesity should receive regular hearing screening so they can be treated appropriately to avoid cognitive and behavioral issues."

Although the overall hearing loss among obese adolescents was relatively mild, the almost 2-fold increase in the odds of unilateral low-frequency hearing loss is particularly worrisome. It suggests early, and possibly ongoing, injury to the inner ear that could progress as the obese adolescent becomes an obese adult. Future research is needed on the adverse consequences of this early hearing loss on social development, academic performance, and behavioral and cognitive function.

"Furthermore, hearing loss should be added to the growing list of the negative health consequences of obesity that affect both children and adults - adding to the impetus to reduce obesity among people of all ages," said Dr. Lalwani.

In the United States, nearly 17 percent of children are obese, defined as having a body mass index (BMI) of =95 percentile. (BMI in children is expressed as a percentile; adult BMI is expressed as a number based on weight and height.) Obesity and its associated morbidities have been identified as a risk factor for hearing loss in adults.

The study analyzed data from nearly 1,500 adolescents from the National Health and Nutrition Examination Survey - a large, nationally representative sample of adolescents between the ages of 12 and 19, conducted from 2005 to 2006 by the National Center for Health Statistics of the Centers for Disease Control and Prevention. Participants were interviewed at home, taking into account family medical history, current medical conditions, medication use, household smokers, socioeconomic and demographic factors, and noise-exposure history.

Dr. Lalwani and his colleagues speculate that obesity may directly or indirectly lead to hearing loss. Although additional research is needed to determine the mechanisms involved, they theorize that obesity-induced inflammation may contribute to hearing loss. Low plasma levels of the anti-inflammatory protein adiponectin, which is secreted from adipose tissue, have been found in obese children, and low levels in obese adults have been associated with high-frequency hearing loss (which affects a person's ability to understand speech). Obesity also may contribute indirectly to hearing loss as a result of its comorbidities, including type 2 diabetes, cardiovascular disease, and high cholesterol - all of which have been reported to be associated with loss of peripheral hearing (relating to the outer, middle, and inner ear).

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Identifying Genetic Markers In Overweight Newborns Could Prevent Obesity In Later Life

Similar genetic variations occur in both overweight newborns and obese adults, a large study finds. The results were presented at The Endocrine Society's 95th Annual Meeting in San Francisco.

"Our data suggest that adult obesity and newborn adiposity share, in part, a common genetic background," said study lead author Reeti Chawla, MD, fellow in pediatric endocrinology at Ann & Robert H. Lurie Children's Hospital of Chicago and the Northwestern University Feinberg School of Medicine, in Chicago, IL. "Allowing earlier identification of high-risk newborns may allow for earlier interventions to take place to possibly prevent obesity later in life. "

Obesity has become an epidemic worldwide. In the United States alone, more than one-third of adults are obese, according to the Centers for Disease Control and Prevention. Excess weight and obesity are related to numerous health problems, including heart disease, type 2 diabetes, stroke and some cancers. Since being obese in childhood increases the risk of adult obesity, medical researchers are interested in identifying early risk factors, or genetic markers, to help predict who is at greater risk for weight gain.

One of these genetic markers is called a single nucleotide polymorphism, or SNP, which is a naturally occurring genetic variant within the general population. In this case, investigators used SNPs related to adult obesity to identify genetic markers associated with higher newborn weight and skinfold thickness.

Investigators were able to identify 144 SNPs associated with birth weight or skinfold thickness. Since some of these 144 SNPs are closely linked and inherited together, they then narrowed the group down to 45 SNPs that are related to higher fat among newborns.

Investigators obtained the genetic data of 4,465 newborns from a large, multi-ethnic study examining the association between maternal blood-sugar levels and risk of poor pregnancy outcome. The study, called the Hyperglycemia and Adverse Pregnancy Outcomes, or HAPO, comprised mothers and infants from diverse ethnic backgrounds, including 1,095 Afro-Caribbean, 1,363 European, 616 Mexican-American and 1,207 of Thai descent.

Chawla said that she and her team now are using the 45 SNPs identified in this study to develop a genetic risk score "to determine whether bearing a large number of these SNPs predicts which newborns are at risk for increased fat at birth and, potentially, obesity later in life."

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Fat Tissues In Sheep Affected By Prenatal Exposure To BPA

New research suggests that fetal exposure to the common environmental chemical bisphenol A, or BPA, causes increased inflammation in fat tissues after birth, which can lead to obesity and metabolic syndrome. Results of the animal study were presented at The Endocrine Society's 95th Annual Meeting in San Francisco.

Found in plastic water bottles, older baby bottles and many other consumer products, BPA is a known hormone disrupter with estrogen-like properties. Prior research has linked BPA in both animals and humans to obesity and the metabolic syndrome, which is a cluster of metabolic risk factors that increase the chance of later developing diabetes, heart disease and stroke.

"This research is the first study to show that prenatal exposure to BPA increases postnatal fat tissue inflammation, a condition that underlies the onset of metabolic diseases such as obesity, diabetes and cardiovascular disease," said the study's lead author, Almudena Veiga-Lopez, DVM, PhD, a research investigator at the University of Michigan, Ann Arbor.

She said the study, which examines the effects of BPA on sheep, improves the understanding of how prenatal BPA exposure regulates the inflammatory response in offspring in the tissues that are relevant to development of metabolic disease. The study was conducted in the laboratory of Vasantha Padmanabhan, MS, PhD, Professor at the University of Michigan, Ann Arbor, with funding from the National Institutes of Health's National Institutes of Environmental Health Sciences. Veiga-Lopez said sheep have similar body fat to that in humans, including visceral (deep belly) fat and subcutaneous fat, which is directly below the skin.

The researchers fed two groups of pregnant sheep corn oil, either with nothing added to it or with added BPA at a dose needed to achieve BPA levels similar to those seen in human cord blood in the umbilical cord blood of the sheep offspring. Of the female offspring from the sheep, half from each group were overfed at approximately 6 weeks of age. All female offspring then were divided into four groups of nine to 12 animals each: (1) non-BPA-exposed controls that received a normal diet, (2) BPA-exposed offspring that received a normal diet, (3) overfed, obese controls and (4) overfed, obese BPA-exposed offspring.

At 15 months of age, sheep underwent a glucose tolerance test, to measure their insulin and blood sugar levels. Seven months later, the researchers collected samples of the animals' visceral and subcutaneous fat tissues to evaluate levels of two biological markers of inflammation. These biomarkers were CD68, a marker for inflammatory cells, and adiponectin, a molecule with a known role in the development of metabolic syndrome. When the adiponectin level decreases or CD68 expression increases, inflammation is worse, according to Veiga-Lopez.

Adiponectin was decreased and CD68 expression was raised in the visceral fat of both obese groups, and CD68 expression also was raised in the subcutaneous fat in normal weight, BPA-exposed female offspring, Veiga-Lopez reported. She said these results suggest that "prenatal BPA exposure and postnatal diet may interact to modulate inflammatory mechanisms in fat deposits."

Both obese groups had hyperinsulinemia, or high insulin levels, a precursor to insulin resistance, which is a prediabetic state, Veiga-Lopez reported. However, she said prenatal exposure to BPA did not lead to insulin resistance in sheep, as was true in a previous mouse study. She speculated that the hyperinsulinemia in obese offspring stems from changes that occurred in the two inflammatory markers in the visceral fat deposit.

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Research Breakthrough Of Essential Molecule Reveals Important Targets In Diabetes And Obesity

Insulin is the most potent physiological anabolic agent for tissue-building and energy storage, promoting the storage and synthesis of lipids, protein and carbohydrates, and inhibiting their breakdown and release into the circulatory system. It also plays a major role in stimulating glucose entry into muscle tissue, where the glucose is metabolized and removed from the blood following meals. But gaps exist in understanding the precise molecular mechanisms by which insulin regulates glucose uptake in fat and muscle cells.

A research team led by Assia Shisheva, Ph.D., professor of physiology in Wayne State University's School of Medicine, has made breakthrough advancements on a molecule that may provide more answers to this mystery.

The conserved phospholipid enzyme, PIKfyve, was discovered in Shisheva's lab in 1999. Based on studies in cultured cells, the lab has implicated PIKfyve in the insulin-regulated glucose transport activation, which led to the development of a unique mouse model with PIKfyve ablation, or removal, in muscle (MPlfKO), the tissue responsible for the majority of postprandial glucose disposal.

In Shisheva's recent paper, "Muscle-specific PIKfyve gene distribution causes glucose intolerance, insulin resistance, adiposity and hyperinsulinemia but not muscle fiber-type switching," published online in the American Journal of Physiology - Endocrinology and Metabolism, Shisheva and her research team characterize whether this new model exhibits metabolic defects.

"Our team found a striking metabolic phenotype in the MPIfKO mice consisting of glucose intolerance and insulin resistance at an early age and on a normal diet," said Shisheva, a resident of Royal Oak. "We also revealed that PIKfyve is essential for normal insulin signaling to GLUT4/glucose transport in muscle and provided the first in vivo evidence for the central role of PIKfyve in the mechanisms regulating healthy blood glucose levels, or glucose homeostasis."

In addition, the research team found that these metabolic disturbances were followed by increased animal fat (adiposity) and elevated levels of insulin (hyperinsulinemia), but not abnormal amounts of lipids or cholesterol in the blood (dyslipidemia).

"The combined phenotype manifested by the MPlfKO mouse closely recapitulates the cluster of typical features in human prediabetes including systemic glucose intolerance and insulin resistance, hyperinsulinemia and increased visceral obesity without dyslipidemia," said Shisheva.

"Therefore, our mouse model, in addition to providing novel mechanisms of insulin resistance, represents a valuable tool for exploring new preclinical strategies to improve treatments in individuals with prediabetes."

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CNIO Researchers Discover A New Gene Involved In Obesity

RAP1 is a gene that also protects telomeres. This is the first time that a link has been found between these structures that shorten with ageing and obesity

The discovery of an unexpected function for a gene that was associated to another process in the organism might be a solution in search of a problem, a clue to unsuspected connections. That is what has happened with RAP1, a gene that protects telomeres - the ends of chromosomes - after researchers from the Spanish National Cancer Research Centre (CNIO) surprisingly discovered its key role in obesity.

"We still don't know what evolutionary significance to attach to it, but it is at the very least interesting that a telomere gene is related to obesity", says Maria Blasco, CNIO director and co-author of the study published in the journal Cell Reports.

RAP1 forms part of the shelterin complex, a group of proteins that make up the protective hood of telomeres - the DNA sequence at the ends of chromosomes that shortens with each cellular division and thus measures the ageing of the organism. There are six shelterins, and CNIO's Telomeres & Telomerase Group, which studies them in-depth, has discovered that RAP1, contrary to the rest, is not essential for the survival of the organism; but that does not mean RAP1 is not important. The reverse is rather the case: when comparing the genomes of different species, it can be observed that RAP1 is the most conserved shelterin of all. Despite the long history of evolutionary changes, RAP1 has not changed; it is present even in yeast. This normally implies an important role in the organism, but which one?

CNIO researchers had discovered that RAP1, in addition to being located in telomeres, is also present in the rest of the chromosome; they supposed it acts regulating the action of other genes. In order to analyse this other potential function, and its importance in the organism, CNIO researchers created a lineage of mice without RAP1 and, to their surprise, discovered a model for obesity.

MICE LACKING RAP1 GAIN MORE WEIGHT

"Mice - especially female mice - without RAP1 do not eat more, but do gain weight. They suffer from metabolic syndrome, accumulate abdominal fat and present high glucose and cholesterol levels, amongst other symptoms", says Paula Martínez, first-author of the study.

The reason is that RAP1 plays an important role in the regulation of genes involved in metabolism. In particular, researchers have discovered that it acts on the same signalling pathway mediated by another protein: PPAR- gamma (PPAR-?). In fact, PPAR-? deficient mice suffer from a type of obesity "surprisingly similar" to that seen in mice without RAP1.

The next step in the research will be to study if RAP1 also plays a role in human obesity. "This discovery adds an element to the obesity equation, and opens up a possible new link between metabolic dysfunction and ageing, via a protein present in telomeres", says Blasco.

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Your Weight, Eating Behavior, Likely Impacted By What You Believe Causes Obesity

Whether a person believes obesity is caused by overeating or by a lack of exercise predicts his or her actual body mass, according to new research published in Psychological Science, a journal of the Association for Psychological Science.

Obesity has become a pressing public health issue in recent years, with two-thirds of U.S. adults classified as overweight or obese and similar trends unfolding in many developed nations. Researchers Brent McFerran of the Ross School of Business at the University of Michigan and Anirban Mukhopadhyay of Hong Kong University of Science and Technology wondered whether individual beliefs might play a role in these trends.

From an initial online survey, they discovered that people seem to subscribe to one of two major beliefs about the primary cause of obesity:

"There was a clear demarcation," says McFerran. "Some people overwhelmingly implicated poor diet, and a roughly equal number implicated lack of exercise. Genetics, to our surprise, was a far distant third."

McFerran and Mukhopadhyay wanted to dig deeper to see if the pattern could be replicated and, if so, what implications it might have for behavior. They conducted a series of studies across five countries on three continents.

Data from participants in Korea, the United States, and France showed the same overall pattern: Not only did people tend to implicate diet or exercise as the leading cause of obesity, people who implicated diet as the primary cause of obesity actually had lower BMIs than those who implicated lack of exercise.

"What surprised me the most was the fact that we found lay theories to have an effect on BMI over and above other known factors, such as socio-economic status, age, education, various medical conditions, and sleep habits," says McFerran.

The researchers hypothesized that the link between people's beliefs and their BMI might have to do with how much they eat.

A study with Canadian participants revealed that participants who linked obesity to lack of exercise ate significantly more chocolates than those who linked obesity to diet. And a study with participants in Hong Kong showed that participants who were primed to think about the importance of exercise ate more chocolate than those primed to contemplate diet.

These findings provide evidence that our everyday beliefs about obesity may actually influence our eating habits - and our body mass.

According to Mukhopadhyay, this is "the first research that has drawn a link between people's beliefs and the obesity crisis, which is growing as fast as people's waistlines are."

The new findings suggest that, in order to be effective, public health campaigns may need to target people's beliefs just as much as they target their behaviors.

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Relationship Between Short-Term Antidepressant Use, Stress, High-Fat Diet And Long-Term Weight Gain

Short-term use of antidepressants, combined with stress and a high-fat diet, is associated with long-term increases in body weight, a new animal study finds. The results were presented Sunday at The Endocrine Society's 95th Annual Meeting in San Francisco.

"Our study suggests that short-term exposure to stress and antidepressants, rather than a high-calorie, high-fat diet alone, leads to long-term body weight gain, accompanied with increased bone and spleen weights," said study lead author Suhyun Lee, a PhD candidate in the medical sciences at the John Curtin School of Medical Research at the Australian National University in Canberra, Australia.

Antidepressants are among the most prevalent medications today, accounting for millions of prescriptions each year. In the United States, physicians wrote more than 1.5 million prescriptions for antidepressants in 2009, while physicians in Australia wrote more than 12 million of these prescriptions in 2008.

At the same time, obesity rates are climbing in developed countries worldwide. Among adults in both the United States and Australia, two-thirds are overweight or obese. Being overweight or obese is a risk factor for many serious diseases, including heart disease, which is the leading cause of death among adults in the United States and Australia.

Unfortunately, weight gain is one of the main side effects associated with antidepressants. The amount of excess weight varies between patients, but some have reported increases as high as 7 percent of the amount they weighed at the start of their antidepressant treatment.

In this study, male rats treated with the antidepressant fluoxetine after induced stress had significantly increased body weight compared to control animals. In addition to greater overall body weight, animals in the antidepressant group also developed greater bone and spleen weights, compared to animals in the control group.

"These findings may implicate different pathophysiological mechanisms in stress and antidepressant related obesity when compared to obesity that is solely diet-induced," Lee said.

During the follow-up, investigators also compared behavior between the drug and control groups. This comparison showed that the antidepressants reduced anxiety among the animals in response to induced stress. After the stressful periods, which involved physical restraint, the fluoxetine-treated animals exhibited significantly fewer symptoms of anxiety, compared to the control animals.

The study involved a two-week period of repeated restraint stress, combined with antidepressant treatment among one group of animals, and saline administration among the control group. After the two-week period, both groups of animals received a high-fat diet for 295 days.

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New Tool To Measure Sugar Consumption

Scientists at the University of Alaska Fairbanks identified a new tool that can dramatically improve the notoriously inaccurate surveys of what and how much an individual eats and drinks. Their research is published in the June 2013 issue of the Journal of Nutrition.

Conventional wisdom says that consumption of sugar-sweetened beverages such as soda and fruit juice is a significant contributor to obesity and chronic disease risk, but the science surrounding this issue is inconclusive. Part of the problem is that in a typical diet survey few people accurately and consistently recall what they consumed. The problem becomes exaggerated when people underreport foods they know are less healthy for them, like sugars.

"We were looking for an objective biomarker that could accurately measure long-term sugar intake from a single blood or hair sample" said Diane O'Brien, project leader and biologist with the UAF Center for Alaska Native Health Research at the Institute of Arctic Biology.

The biomarker O'Brien and her CANHR research group pilot-tested was the ratio of two different carbon atoms (heavy carbon 13 and light carbon 12) which are incorporated into plants during photosynthesis. The ratio, called an isotopic signature, is distinct in corn and sugar cane, which are the sources of nearly all of the sugars found in sugar-sweetened beverages.

"We used the isotopic signature of alanine an amino acid and building block of protein that essentially traps the carbon from dietary sugar so that it can be measured in the protein component of hair or blood," O'Brien said.

Even after foods and beverages are consumed, metabolized, transported in blood and stored in body tissues, these isotopic signatures remain largely intact. The more sugar-sweetened beverages an individual consumes, the greater alanine's carbon isotope ratio will be. Importantly, O'Brien's group found that alanine was uncorrelated with other foods that can contribute to elevated carbon ratios.

Although the use of isotope signatures to study food webs and diet is not new, previous efforts to accurately measure sweetener intake have not been particularly successful. The use of alanine and the technique employed by O'Brien's group makes their findings particularly exciting.

"Even for validated and well-accepted biomarkers of diet, associations with self-reported intake are generally very weak. Our biomarker was able to explain almost half of the variation in self-reported sugar-sweetened beverage intake, which in this field is a very high level of explanatory power," said O'Brien.

The scientists' findings are also being used in other health and diet-related research.

"Diane's research program has provided CANHR with incredibly valuable objectively measured biomarkers of food intake," said CANHR Director Bert Boyer. "These biomarkers are currently being used to help us understand the role polyunsaturated fatty acids play in disease prevention, including the modification of genetic risk."

The tool is not without its drawbacks, caution the authors.

"The gas chromatography-combustion-isotope ratio mass spectrometry process we used isn't inexpensive and or widely available," O'Brien said. "We expect that our findings will be most useful as a calibration tool, either for self-reported dietary data or more high-throughput biomarkers of sweetener intake."

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The Importance Of A Father's Diet Before Conception

When fathers eat a high-fat diet before conception of offspring, the male offspring have increased body weight after weaning and high body fat in midlife despite eating a low-fat diet, a new study in mice finds. The results were presented at The Endocrine Society's 95th Annual Meeting in San Francisco.

"Many researchers have studied the effects of maternal diet on the risk of obesity in their children. We found that the father's diet also affects the offspring in ways that are inherited," said the study's principal investigator, Felicia V. Nowak, MD, PhD, associate professor of molecular endocrinology at Ohio University in Athens.

The inherited differences in metabolism in the offspring of obese fathers appear to be epigenetic - changes in how genes are expressed that are "not hardwired" into the genes, meaning that they are modifiable by internal and external environmental factors, Nowak said. The cause of these changes was not behavioral because the offspring did not observe what their fathers ate nor did they have access to a high-fat diet, she noted.

In their study, the researchers fed male mice a 13-week diet that was either high fat (45 percent of calories derived from fat) or low fat (10 percent of calories from fat; control mice) but contained the same number of calories. The mice that ate the high-fat food became obese. All mice were mated with females that had received the matched low-fat diet. All their offspring received standard laboratory mouse chow.

The mouse pups underwent testing of their body weight and fat at various ages: 20 days, which was right after weaning and is similar in age to human infants or toddlers, according to Nowak; 6 weeks, which is roughly equivalent to adolescence; 6 months, or young adulthood; and finally 12 months, or older adulthood.

Compared with offspring from control mice, the male offspring of paternal mice with diet-induced obesity had higher body weight starting at 6 weeks of age, and the increased weight was still present at 6 and 12 months, the authors reported. In addition, at 6 months, the male offspring of the obese paternal mice had a higher percentage of total body fat than control offspring did. There were, however, no observed differences in the amount of brown fat, the calorie-burning fat that both rodents and humans have.

Surprisingly, male offspring of the high-fat-fed paternal mice also showed increases in voluntary running at 6 weeks. Female offspring ran more than male offspring at 6 months and 12 months, Nowak said. She said they are studying possible causes for this behavior, which might offset the increased body fat and reduce the offspring's risk of metabolic disease such as diabetes and heart disease.

"Increasing numbers of children and adolescents are affected by obesity," Nowak said. "It is essential that we identify markers for early detection and prediction of obesity and diabetes. This will enable individuals to make healthy lifestyle choices and receive targeted health care interventions to delay or prevent the related disabilities and increase life expectancy."

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