Bariatric Times

NOV 2017

A peer-reviewed, evidence-based journal that promotes clinical development and metabolic insights in total bariatric patient care for the healthcare professional

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28 News and Trends Bariatric Times • October 2017 t eam showed that, with electronic SNAP purchases, the average per- purchase spending on fresh produce rose from $4.19 to just over $8, with most of the increase s pent on fruit. For the latest survey, respondents were offered a free transit ticket to complete a questionnaire and allow their food p urchases to be documented. Eighty-four percent of the survey participants were female, and over one-half were Hispanic-American. Some 87 percent said they paid o nly in cash for their food purchases. Researchers caution that while this analysis to date suggests that the Green Carts program has i mproved healthy food-purchasing habits, they cannot confirm what anyone actually ate or any health benefit from improved nutrition. Other surveys have shown that m ost Americans—particularly the poorest—do not eat enough fruits and vegetables to meet the recognized standards of a healthy diet, says Elbel, Associate Professor in the Department of Population Health at NYU School of Medicine and at the NYU Wagner Graduate School of Public Service. He says the goal of his team's research is to figure out how best to use the Green Carts program to encourage better, lifelong food-eating habits. Elbel and lead study investigator Andrew Breck, MPA, a doctoral candidate at NYU Wagner Graduate School of Public Service, say follow- up studies would help identify whether those who buy fruits and vegetables from the carts in fact eat more of them. "Our research should help the city officials decide whether and how to expand EBT-enabled Green Carts, especially in neighborhoods with few stores selling fresh produce," says Breck. In addition to Elbel and Breck, other NYU Langone researchers involved in this study are Kamila Kiszko, MPH; Olivia Martinez; and Courtney Adams, MA. Funding for the study was provided by United States Centers for Disease Control and Prevention grant U48DP001904. MICROBIOME MANIPULATION DECELERATES OSTEOARTHRITIS PROGRESSION Study suggests link between gut microbiome and joint health in obese mice ROSEMONT, Illinois—The gastrointestinal microbiome is currently a hot topic of research concerning serious diseases affecting large portions of the world's population. It has been implicated in a variety of conditions, such as asthma, obesity, and now osteoarthritis (OA). R ecent work presented at the Orthopaedic Research Society 2017 Annual Meeting by Eric Schott, Robert Mooney, Steve Gill, Michael Zuscik and colleagues at the Center f or Musculoskeletal Research at the University of Rochester Medical Center have shown that prebiotic manipulation of the gut microbiome might lead to decelerated p rogression of OA. The work utilized a mouse model of high-fat diet-induced obesity along with an injury to the medial meniscus to initiate degeneration in the knee. S pecifically, mice that were fed a high-fat diet along with the prebiotic supplement, oligofructose, demonstrated reduced systemic inflammation and decelerated c artilage degeneration after meniscal injury. Prebiotic supplements are intended to nourish and support particular bacterial strains present i n the gut. This is in contrast to probiotic supplements, often found in yogurt, which attempt to confer specific bacterial cultures directly to the gut. In the experiment reported by Schott et al, researchers believe that an increased abundance of microbes from the genus Bifidobacterium, resulting from prebiotic supplementation, might be responsible for the reduction in systemic inflammation and deceleration of OA symptoms. A link between altered gut microbiome and systemic inflammation in obesity has previously been established; however, the mechanisms by which the gut microbiome affect joint health are still largely unknown. Schott speculates that either the increased numbers of Bifidobacteria are crowding out other inflammation-inducing strains, or that these Bifidobacteria are producing a metabolic byproduct(s) that has positive effects on the host, including supporting healthy joints. Answers to these questions might provide the first evidence connecting the gut microbiome to joint health. Future work in the Zuscik lab will further investigate the gut microbiome in OA without obesity as a comorbid factor. They hope to determine if patients with OA have an altered gut microbiome compared to healthy individuals. If the microbiome is altered in OA, perhaps correction of the abnormalities will protect against or even reverse OA symptoms. Additional clarification of the gut- joint connection might lead to novel therapeutic strategies involving the manipulation of the intestinal microbial community to treat or prevent OA. Results from this work might help to address a clinical problem of enormous scope f or which no effective disease- modifying therapy has been established. Visit r eleases/microbiome-manipulation- decelerates-osteoarthritis- progression-300523008.html for the full release. INDIVIDUALS WITH OBESITY LACK CELLS WITH SATIETY HORMONES BASEL, Switzerland—Individuals with severe overweight have an i nhibited sense of satiation—they release fewer satiety hormones than people of normal weight. The reason: the responsible cells in the gastrointestinal tract of people with o besity are severely reduced. Researchers believe surgical weight loss procedures can repair this disorder. The mucous membrane of the u pper gastrointestinal tract is home to highly specified cells, the so- called enteroendocrine cells, that constantly analyze our intestinal contents. During a meal, they release satiety hormones into the bloodstream. This signals to the body that enough food has been taken in and that the meal can be ended. The sense of satiation is created in the central nervous system. R esearchers from the Department of Biomedicine at the University and University Hospital Basel and the St. Claraspital Basel, together with colleagues from the U niversity of Liverpool, have studied the reasons for this reduced release of satiety hormones from individuals with obesity. They examined tissue s amples of the gastrointestinal tract of 24 lean volunteers and 30 patients with obesity before and after weight-loss surgery. The team of researchers led by D r. Bettina Wölnerhanssen was able to show that the number of enteroendocrine cells in people with obesity is significantly lower than in people with normal weight. T his leads to a reduced release of satiety hormone, which in turn leads to altered appetite. People with obesity also showed alterations in the pattern of the so- c alled transcription factors, which are responsible for the development of enteroendocrine cells from stem cells. After surgery, the number of enteroendocrine cells and the pattern of transcription factors were almost entirely restored. Visit to access the full article 598-017-08487-9

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