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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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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Causal Relationship Between Adiposity And Heart Failure, And Elevated Liver Enzymes

New evidence supports a causal relationship between adiposity and heart failure, and between adiposity and increased liver enzymes, according to a study published this week in PLOS Medicine. The study, conducted by Inga Prokopenko, Erik Ingelsson, and colleagues from the ENGAGE (European Network for Genetic and Genomic Epidemiology) Consortium, also provides additional support for several previously shown causal associations such as those between adiposity and type 2 diabetes, metabolic syndrome, dyslipidemia, and hypertension.

The authors investigated whether adiposity is causally related to various cardiometabolic traits using a Mendelian randomization analysis, in which the variation in genes associated with conditions is used to assess the causal relationship between conditions. It is known that a genetic variant (rs9939609) within the genome region that encodes the fat-mass- and obesity-associated gene (FTO) is associated with increased BMI. Using genetic and health data collected in 36 population-based studies of nearly 200,000 individuals of European descent, the authors measured the strength of the causal association between BMI and cardiometabolic traits and found that higher BMI had a causal relationship with heart failure, type 2 diabetes, metabolic syndrome, dyslipidemia, hypertension, increased blood levels of liver enzymes, and several other cardiometabolic traits.

As with all Mendelian randomization studies, the reliability of the causal associations reported here depends on several assumptions made by the researchers. The authors report, "The present study addressing the role of BMI in 24 traits in up to 198,502 individuals provides novel insights in the causal effect of obesity on heart failure and increased liver enzymes levels."

They also say that this study "provides robust support to the causal relationship between obesity and a number of cardiometabolic traits reported previously. These results support global public prevention efforts for obesity in order to decrease cost and suffering from [type 2 diabetes] and heart failure."

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Helping Prevent Obesity Among Children Via Community-Based Programs

When it comes to confronting childhood obesity, researchers at the Johns Hopkins Bloomberg School of Public Health conclude that community-based approaches are important. A systematic review of childhood obesity prevention programs found that community-based intervention programs that incorporate schools and focus on both diet and physical activity are more effective at preventing obesity in children. The results of the study appear online in Pediatrics.

"In measuring the effectiveness of community-based programs that impact childhood obesity - more comprehensive interventions are definitely better," said Sara Bleich, PhD, associate professor inof Health Policy and Management and lead author on the paper. "The research shows that in order to help prevent obesity among children, we must focus on both diet and exercise in the communities where children live and go to school since the environment is a key contributor to obesity risk. Focusing on the community is especially important for children since they generally have little or no control over their environment."

This shift toward a stronger community focus is echoed in a recent Institute of Medicine (IOM) report, Accelerating Progress in Obesity Prevention, which recommends a comprehensive approach to childhood obesity prevention that includes the community.

Researchers examined nine studies that featured community-based interventions and found that, among those, the two interventions that included a school component effectively prevented obesity or overweight in children. Common characteristics found across most of the nine studies included the use of multiple intervention components (e.g., health education and family outreach), the inclusion of settings other than just the community (e.g., school, home, primary care, child care), and a focus on children at middle school age or younger.

"While additional research is needed to assess the full impact of community-based interventions on the prevention of childhood obesity, our conclusions indicate that more comprehensive approaches, which attempt to modify diet and exercise in the community with engagement from the schools, weigh in everyone's favor," said Bleich.

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