News Article | May 9, 2017
DALLAS - May 9, 2017 - UT Southwestern research investigating the blood glucose-regulatory actions of the hormone ghrelin may have implications for development of new treatments for diabetes. Blood glucose is tightly regulated by the opposing actions of the hormones insulin and glucagon. Earlier studies led by Dr. Roger Unger, Professor of Internal Medicine at UT Southwestern Medical Center, demonstrated that experimentally deleting or neutralizing receptors for glucagon can prevent or correct dangerously high blood glucose levels in different models of diabetes. "Dr. Unger's research suggested that high or unopposed glucagon action that results from insulin deficiency is the main culprit in the development of high blood glucose - known as hyperglycemia - in diabetes," said Dr. Jeffrey Zigman, Professor of Internal Medicine and Psychiatry at UT Southwestern and senior author of the study, published online today in the journal Diabetes. "He proposed that blocking or neutralizing glucagon action may serve as a new treatment for Type 1 and Type 2 diabetes. This idea formed the basis of our current study," Dr. Zigman added. Like glucagon and insulin, ghrelin also plays an important role in blood glucose control. But because the hormone was only discovered in the 1990s, ghrelin's actions on blood glucose haven't been studied as much as those of glucagon and insulin. The UTSW research team wanted to learn more about the role of ghrelin in diabetes. "We studied mice that lacks glucagon receptors. When we tried to make these animals diabetic by giving them an agent that destroys insulin-producing cells, the mice did not develop diabetes. Their blood sugar was normal. In addition to these results, we found that their ghrelin levels were high," said Dr. Zigman, who holds the Kent and Jodi Foster Distinguished Chair in Endocrinology, in Honor of Daniel Foster, M.D., the Mr. and Mrs. Bruce G. Brookshire Professorship in Medicine, and The Diana and Richard C. Strauss Professorship in Biomedical Research. In a related set of studies, when the researchers blocked the action of the elevated ghrelin, doing so caused the animals' blood sugar levels to drop below normal, he added. "These findings suggest that when glucagon activity is blocked, circulating levels of ghrelin rise, which helps to prevent dangerously low blood sugars from developing, a condition known as hypoglycemia," Dr. Zigman said. Pharmaceutical companies are now developing drugs targeting glucagon receptors to treat diabetes, including antibodies that will neutralize glucagon receptors or drugs that will block glucagon receptors, he added. "The body's normal ghrelin response should protect diabetic individuals being treated with agents that target glucagon receptors from experiencing hypoglycemia," Dr. Zigman said. Since the current study focused on a Type 1 diabetes model, researchers next plan to examine the coordinated actions of the ghrelin and glucagon systems in a Type 2 diabetes model. They also want to study the impact of ghrelin on hypoglycemia. "A potential side effect with any treatment that lowers blood sugar is that hypoglycemia may develop," Dr. Zigman said. "We would like to determine whether the administration of ghrelin or a compound that mimics the action of ghrelin could help correct that hypoglycemia." Lead author of the study is Dr. Bharath Mani, Instructor of Internal Medicine, and the co-senior authors include Dr. Unger, who holds the Touchstone/West Distinguished Chair in Diabetes Research, and Dr. Eric Berglund, Assistant Professor in the Advanced Imaging Research Center and of Pharmacology. Other contributing UTSW researchers are Dr. Aki Uchida, postdoctoral research fellow; Dr. Young Lee, Assistant Professor of Internal Medicine; and Sherri Osborne-Lawrence, senior research scientist. The study received support from the National Institutes of Health, the Novo Nordisk Foundation Center for Basic Metabolic Research, and the Hilda & Preston Davis Foundation. UT Southwestern, one of the premier academic medical centers in the nation, integrates pioneering biomedical research with exceptional clinical care and education. The institution's faculty has received six Nobel Prizes, and includes 22 members of the National Academy of Sciences, 18 members of the National Academy of Medicine, and 14 Howard Hughes Medical Institute Investigators. The faculty of more than 2,700 is responsible for groundbreaking medical advances and is committed to translating science-driven research quickly to new clinical treatments. UT Southwestern physicians provide care in about 80 specialties to more than 100,000 hospitalized patients, 600,000 emergency room cases, and oversee approximately 2.2 million outpatient visits a year. This news release is available on our website at http://www. . To automatically receive news releases from UT Southwestern via email, subscribe at http://www. .
News Article | March 22, 2017
Fat cells were found to help the liver during fasting and for being responsible for the regulation of glucose and uridine during the fasting stage. Uridine is a metabolite used by the body in a series of bioprocesses such as building RNA molecules. The findings of this study could change the way we treat a number of diseases, among which are diabetes, cancer and neurological disorders. The research was carried out by researchers at the UT Southwestern Medical Center, and its findings were published in the journal Science. The results of this study were replicated in rat, mouse and human studies. Metabolites are important substances which result from a metabolic activity of the body. For instance, the glucose (quantity of sugar in the blood) produced while metabolizing starches or complex sugars is a metabolite. Similar to glucose, every cell in the human body has to use uridine to function properly. The liver produces uridine for the circulatory system, as many textbooks indicate. However, this study found that the liver doesn't just produce uridine, but it's the primary producer of this metabolite, only in the fed state. At the same time, the production of uridine is passed on to the fat cells during the fasted state. According to the study, this new way of understanding the production of uridine in the body is similar to the process of labor division. During fasting, it's the liver that produces glucose, and fat cells help it with the production of uridine for the bloodstream. While uridine is known to have multiple roles inside the human body, the current research was the first to report fat cells producing plasma uridine while the body is going through the fasting stage. Additionally, the finding is that the energy balance of the body is regulated by a fat cell-liver-uridine axis. "It turns out that having uridine in your gut helps you absorb glucose; therefore uridine helps in glucose regulation," noted Dr. Philipp Scherer, senior author of the study and Director of UT Southwestern's Touchstone Center for Diabetes Research. Dr. Yingfeng Deng, the lead author of the research, observed that the levels of uridine in the blood increase during fasting, and drop during feeding. In the feeding process, the liver is responsible for a drop in the levels of uridine, as it secretes it into bile. The uridine is then transported to the gallbladder, and then to the gut, where it plays an important role in absorbing nutrients. "We clarify the mechanism underlying the rapid reduction of plasma uridine upon refeeding, which involves both reduction of uridine synthesis in adipocytes and enhancement of its clearance through the bile," noted the research. Further research starting from these findings will investigate the effects of reducing feeding-induced uridine levels in organs that use mainly uridine from plasma. Additionally, whether or not bariatric surgery affects udirine levels as well is another possible research direction. The results of this question could impact the way we treat the severely obese, as this study also underlined that there is a direct connection between temperature regulation and metabolism. © 2017 Tech Times, All rights reserved. Do not reproduce without permission.
News Article | May 8, 2017
Previous research has demonstrated that saturated fat is more fattening and less muscle building than polyunsaturated fats. A new study shows that the choice of fat causes epigenetic changes which in turn could contribute to differences in fat storage. The so-called "muffin study" received a lot of attention when it was published in 2014. In this study, the participants had eaten three muffins a day, on average, for a period of seven weeks. Half of the muffins had been baked using saturated fat (palm oil) and the other half using polyunsaturated fat (sunflower oil). The carbohydrate and protein content was the same in each muffin, the only difference between them was the type of fat. In a collaboration with the person in charge of the major muffin study, associate professor Ulf Risérus at Uppsala University in Sweden, professor Charlotte Ling at Lund University, Sweden, has now studied the epigenetic changes in the study participants' fat tissue, through biopsies taken before and after the project. The results show that the epigenetic pattern in more than 3 000 genes (out of approximately 25 000 that exists in a human being) had changed differentially, depending on whether the participants had eaten saturated fat or polyunsaturated fat. "We believe that the discovered epigenetic changes, depending on the type of fat they ate, could contribute to the difference in fat storage, in which saturated fat has a more negative impact", says Charlotte Ling. The epigenetic pattern consists of molecules known as methyl groups, which are placed on the genes and affect their function and gene expression. "We have previously shown that exercise can affect the epigenetic pattern in fat tissue. These findings support the fact that through diet and exercise, we can affect our health through epigenetic changes", says Charlotte Ling. Ulf Risérus also finds the results very interesting: "It is fascinating that polyunsaturated fat seems to have completely different molecular effects compared to saturated fat; effects which in turn could potentially have an impact on both the body's fat storage and metabolism", he says. "Compared to saturated fat, polyunsaturated fat, which is the type found in sunflower oil, has recently been linked to an improved carbohydrate metabolism in the body. It would now be interesting to learn whether the epigenetic effects of polyunsaturated fat could be involved in an improved carbohydrate metabolism", concludes Ulf Risérus. The study is published in The American Journal of Clinical Nutrition. It was conducted within the Excellence of Diabetes Research in Sweden (EXODIAB), a strategic collaboration between Lund and Uppsala university In addition to palm oil, saturated fat can be found in butter and other dairy products such as cheese and cream, but also in chocolate, coconut fat and prepared meat products such as sausage and bacon. Polyunsaturated fat can be found in oily fish (salmon, mackerel, herring) as well as in algae, nuts and oil made from rapeseed, corn and sunflower seeds. The increase in body fat and muscle mass, as well as the distribution of fat in the body, were measured using an MRI scanner, before and after the weight gain. Despite a comparable weight gain between the two dietary groups, the overconsumption of saturated fat caused a significant increase in the amount of fat in the liver and gut, compared to the overconsumption of polyunsaturated fat. Furthermore, among the people who consumed saturated fat, their total amount of body fat was subsequently higher, and their increase in muscle mass was three times lower, compared to those who consumed polyunsaturated fat. The study included 39 participants.
News Article | April 17, 2017
Houston dentist, Dr. Behzad Nazari, is commenting on a recent study published in the journal BMJ Open Diabetes Research & Care, that has linked gum disease to type 2 diabetes. Gum disease is a very common oral health condition in American adults, and its advanced effects can range from serious infections to tooth loss. While treatments for gum disease are available, preventing the condition is always preferable. The link between gum disease and type 2 diabetes is information that can help dentists and patients control risks and avoid complications. A primary symptom of uncontrolled diabetes is high blood glucose. Excessive levels of glucose in the blood can raise gum disease risks in multiple ways. Like sugar that is consumed through the diet, sugar in the blood can feed bad oral bacteria. Over time, the bacteria can more easily grow out of control and cause more damage, including to the gums. High blood glucose also suppresses immunity. While the body normally fights against heavy bacterial activity in the gums, a suppressed immune system is less capable of keeping this in check. These factors tie diabetes to gum disease so strongly that detection of the disease sometimes prompts an exam for diabetes instead of the reverse. At Antoine Dental Center, the office of Dr. Nazari, patients can receive many treatments in several dental specialties. Restorations offered at the office include tooth-colored fillings, inlays, onlays, and porcelain crowns. Cosmetic dental treatments at the office include veneers, smile makeovers, and multiple types of teeth whitening treatments. The office provides a variety of tooth replacements, including dental implants, bridges, and dentures. Patients can also visit the office for orthodontic work, such as with Invisalign. Dr. Nazari has been treating Houston patients for eighteen years. Dr. Nazari was originally a registered pharmacist, having graduated from Texas Southern University in 1991. After earning his DDS with honors from University of Texas at Houston Dental Branch in 1998, he began his dental career. In the years since, Dr. Nazari has completed more than 1,800 hours of additional training in several specialties, allowing him to offer a broad array of the latest treatments to his patients. A graduate of the prestigious Kois Center, Dr. Nazari is an active member of the American Dental Association, as well as several professional organizations in his field.
News Article | February 15, 2017
BOSTON - (February 14, 2017) - Joslin Diabetes Center will take part in two clinical trials this year to test artificial pancreas systems designed to automatically monitor and regulate blood glucose levels in people with type 1 diabetes, which would replace traditional methods of managing the disease such as testing blood glucose levels by finger stick or using continuous glucose monitoring systems with separate, non-integrated delivery of insulin by either injections or a pump. Lori Laffel, MD, MPH, Chief of the Pediatric, Adolescent, and Young Adult Section at Joslin Diabetes Center, is Principal Investigator at the Joslin site for the trials, which are among four major research efforts being funded by the National Institute of Diabetes and Digestive and Kidney Diseases (NIDDK) of the National Institutes of Health (NIH) to test and refine artificial pancreas systems. If successful, the trials could lead to applications for regulatory approval for use of the devices by people with type 1 diabetes, helping to improve glucose control and reduce the burden of diabetes self-management. Joslin is a site for the International Diabetes Closed-Loop Trial being led by the University of Virginia in Charlottesville (UVA). The trial will provide clinical results of an automated insulin delivery system that features a reconfigured smartphone running advanced algorithms that link wirelessly to a continuous glucose monitor and an insulin pump that the patient wears, as well as a remote-monitoring site, aimed at keeping blood glucose levels in range. In addition, Joslin will be a site for a trial later this year that will compare a hybrid model of an artificial pancreas approved in September 2016 by the U.S. Food and Drug Administration to a next-generation system. One hundred adolescents and young adults (ages 14-30) will test each system for three months during the trial, which will be led by the International Diabetes Center in Minneapolis and the Schneider Medical Center in Israel. "We are entering an era of exceptional opportunity for patients living with type 1 diabetes, with regard to improving glycemic control and enhancing the quality of life for our patients," said Dr. Laffel. "We are very pleased at Joslin to contribute to advancing this initiative through our participation in this important research." The trials are funded under NIH grant numbers DK108483 and DK108611. Joslin Diabetes Center is world-renowned for its deep expertise in diabetes treatment and research. Joslin is dedicated to finding a cure for diabetes and ensuring that people with diabetes live long, healthy lives. We develop and disseminate innovative patient therapies and scientific discoveries throughout the world. Joslin is an independent, non-profit institution affiliated with Harvard Medical School, and one of only 11 NIH-designated Diabetes Research Centers in the U.S. For more information, please visit http://www. .
News Article | February 21, 2017
Noom, Inc. announced today the successful application and initial results of its Diabetes Prevention Program (DPP) with South Korea’s single payers health care system. Noom’s DPP was deployed with two regional public health centers, Suji gu and Kwangju-si, both supervised by South Korea’s Ministry of Health & Welfare. Participants who completed the 16-week program demonstrated improvements in fasting glucose, triglycerides, and blood pressure. South Korea's single payer system covers the entire population. The Ministry of Health & Welfare supervises 245 public health centers across the country to provide services such as health promotion, health screenings, disease management, and prevention. The two health centers' coaches used Noom’s platform with pre-diabetic patients to enhance quality of life and lower costs, by reducing diabetes risk and improving biometric values. Participants used the Korean version of Noom's mobile platform, Noom Coach, to track their physical activity, log their meals, receive ongoing support from their health coach and peer group, as well as read program-specific content. The health centers performed initial and final blood testing for participants to measure outcomes. Mean fasting blood glucose levels improved from pre-diabetic levels (124.9 mg/dl) to healthy levels (91.1 mg/dl). Triglycerides levels and blood pressure also improved in participants. “Peer reviewed research has already proven that Noom’s Diabetes Prevention Program delivers meaningful weight loss comparable to CDC findings and outcomes. The deployment with two Korean regional health centers has allowed us to further prove the program's impact on improving fasting blood glucose and other cardiometabolic values,” said Noom's Medical Director, Dr. Youngin Paul Kim, M.D. "I'm proud to announce that due to the remarkable success of these deployments, Noom has since expanded its Diabetes Prevention Program to four more public health centers." The British Medical Journal Open Diabetes Research & Care recently published a study about the efficacy of Noom’s Diabetes Prevention Program (DPP); it was the first-ever peer-reviewed study of a fully mobile DPP. The study found 64% of participants who completed Noom’s program lost over 5% of their body weight. The multi-language capability of Noom’s platform expands beyond Korean to include Spanish, Japanese and German, in addition to English. Forty-five million users worldwide have already benefited from Noom’s behavior change programs. “The growing prevalence of obesity-related conditions is a global problem. Noom’s collaboration with employers, health plans and health systems extends well beyond the American healthcare market," said Saeju Jeong, Noom's CEO and co-founder. "Our platform is uniquely positioned to address pre-chronic and chronic conditions such as obesity, pre-diabetes, diabetes, and hypertension in international markets throughout Asia, with structured condition-specific and culturally-adapted programs.” Noom Inc., a leader in mobile health coaching, combines the power of technology with the empathy of real human coaches to deliver successful behavior change at scale. Noom’s direct-to-consumer weight loss and exercise tracking mobile applications have reached more than 45 million users worldwide. Leveraging the success of their ground-breaking health and fitness programs, Noom developed a behavior change platform to treat chronic and pre-chronic conditions, beginning with the CDC’s Diabetes Prevention Program (DPP). On the first day the CDC began recognizing mobile and online DPP providers, Noom was there. Since then, Noom has expanded its curricula across the acuity spectrum and now features programs for pre-hypertension, hypertension and diabetes management in addition to its flagship weight loss and diabetes prevention programs. Noom has offices in New York City, Seoul and Tokyo.
News Article | February 16, 2017
DALLAS - Feb. 16, 2017 - Researchers at UT Southwestern Medical Center, working with a California biotech firm, have developed a potential drug to treat polycystic kidney disease - an incurable genetic disease that often leads to end-stage kidney failure. The drug, now called RGLS4326, is in preclinical animal testing at San Diego-based Regulus Therapeutics Inc. An investigational new drug filing to pave the way for human clinical trials is expected later this year, said Dr. Vishal Patel, Assistant Professor of Internal Medicine at UT Southwestern. Dr. Patel is senior author of a study describing research that led to the drug's development, published online today in Nature Communications. Affecting about 600,000 people in the U.S., autosomal dominant polycystic kidney disease (ADPKD) causes numerous fluid-filled cysts to form in the kidney. An affected kidney, normally the size of a human fist, sometimes grows as large as a football. As their numbers and sizes increase, these cysts eventually interfere with the kidney's ability to filter blood and remove bodily waste. The cysts can quietly grow for decades until symptoms appear such as blood in the urine, Dr. Patel said. About half of those affected with ADPKD suffer kidney failure by age 60, according to the National Kidney Foundation. "There isn't a single drug on the U.S. market right now to treat the disease," Dr. Patel said. "Once your kidneys fail, your only option for survival is to get a transplant or start dialysis." In 2009, Dr. Patel began searching for microRNAs that might underlie progression of ADPKD. MicroRNAs - or MiRs for short - are tiny RNA fragments that interfere with normal gene expression. Proof that such RNA fragments even existed came in the early 1990s; their presence in humans was first reported in 2000. Those discoveries led to a groundswell of interest in developing drugs to treat diseases caused by microRNAs, Dr. Patel said - in part because the process can be straightforward once the problem-causing fragment is identified. "Because miRs are so small, drugs can easily be designed against them. And since we know the nucleotide sequence of every known microRNA, all that is required is to prepare an anti-miR with a sequence that is exactly the opposite of the miR's," he said. In this study, researchers in Dr. Patel's lab focused on microRNA cluster 17~92 following identification of potential miR targets. A National Institutes of Health grant funded the UTSW research. In 2013, Dr. Patel and fellow researchers reported in Proceedings of the National Academy of Sciences that this microRNA cluster indeed appeared to promote kidney cyst growth. Using four mouse models, the researchers next studied whether inhibiting this microRNA could slow cyst growth and thus delay ADPKD progression. They found that genetically deleting microRNA-17~92 slowed cyst growth and more than doubled the life spans of some mice tested. Based on that finding, Dr. Patel's lab collaborated with Regulus Therapeutics to test an anti-microRNA-17 drug. The test drug slowed the growth of kidney cysts in two mouse models and in cell cultures of human kidney cysts, the study showed. In the Nature Communications study, UTSW researchers also reported how miR-17 causes cyst proliferation: the molecule essentially reprograms the metabolism of kidney cells so that cellular structures called mitochondria use less nutrients, freeing up resources to instead make cell parts that become cysts. MiR-17 accomplishes this by repressing a protein involved in making RNA called peroxisome proliferator-activated receptor alpha (PPARα), the researchers found. Other UT Southwestern researchers included lead author Dr. Sachin Hajarnis, a research scientist; Dr. Ronak Lakhia, Instructor in Internal Medicine; Matanel Yheskel and Andrea Flaten, research technicians; Darren Williams, former research associate; Dr. Shanrong Zhang, research engineer; Joshua Johnson, an M.D./Ph.D. student; Dr. William Holland and Dr. Christine Kusminski, Assistant Professors of Internal Medicine; and Dr. Philipp Scherer, Professor of Internal Medicine and Cell Biology, who holds the Gifford O. Touchstone, Jr. and Randolph G. Touchstone Distinguished Chair in Diabetes Research. Also contributing to the study were researchers from the University of Minnesota Medical School, the Mayo Clinic School of Medicine, the University of Montreal, the University of Kansas, and Regulus Therapeutics. Funding was provided by the National Institutes of Health (NIH) and the PKD Foundation. Research reported in this publication was supported by the National Institute of Diabetes and Digestive and Kidney Diseases of the NIH under Award Number R01DK102572. The content is solely the responsibility of the authors and does not necessarily represent the official views of the NIH. UT Southwestern and Regulus Therapeutics have applied for a patent for treatment of polycystic kidney disease with miR-17 inhibitors. In addition, Dr. Patel's laboratory has a sponsored research agreement with Regulus, and Dr. Patel serves as a consultant for Regulus. UT Southwestern, one of the premier academic medical centers in the nation, integrates pioneering biomedical research with exceptional clinical care and education. The institution's faculty includes many distinguished members, including six who have been awarded Nobel Prizes since 1985. The faculty of almost 2,800 is responsible for groundbreaking medical advances and is committed to translating science-driven research quickly to new clinical treatments. UT Southwestern physicians provide medical care in about 80 specialties to more than 100,000 hospitalized patients and oversee approximately 2.2 million outpatient visits a year.
News Article | February 15, 2017
A form of RNA released from fat cells into the blood may help to regulate other tissues. BOSTON - (February 15, 2017) - Fat cells are not simply big blobs of lipid quietly standingby in the body--instead, they send out hormones and other signaling proteins that affect many types of tissues. Scientists at Joslin Diabetes Center now have identified a route by which fat also can deliver a form of small RNAs called microRNAs that helps to regulate other organs. "This mechanism may offer the potential to develop an entirely new therapeutic approach," says C. Ronald Kahn, M.D., Joslin's chief academic officer, Mary K. Iacocca Professor of Medicine at Harvard Medical School and senior author of a paper on the research published today in the journal Nature. The research suggests the possibility, Kahn explains, of developing gene therapy treatments using fat cells that aid in treating metabolic diseases, cancer or other conditions in the liver or other organs. Working in mice and with human cells, he and his colleagues studied the role of microRNAs, a form of small RNAs that are not translated into proteins but can regulate other RNAS that produce protein. They are made by all cells in the body, and it is known that some of these microRNAs may be released from the originating cell into the blood. However, exactly what they do once they enter the bloodstream has been debated. The Joslin scientists focused on microRNAs from fat cells that are released into the blood via tiny sacks called "exosomes". The researchers began with a mouse model that was genetically modified so that its fat cells could not create microRNAs. The Joslin researchers then showed that in these mice which do not make microRNAs in fat, the total population of microRNAs circulating in exosomes dropped significantly. This decrease in circulating miRNAs could be restored when the investigators transplanted normal fat into these mice, a result indicating that many of the microRNAs in circulation were coming from fat. Next, the scientists studied people with two forms of lipodystrophy--a condition in which fat is lost or genetically not present. In both groups of people, they found that levels of microRNAs circulating in exosomes were lower than normal. This suggested that these microRNAs generated by fat might aid in diagnostics for metabolic conditions such as obesity, type 2 diabetes and fatty liver disease, Kahn says. But were these microRNAs also crossing into other tissues and regulating genes there, so that they might potentially be used for therapeutics? The Joslin researchers followed up on this question by looking at a gene whose expression in the mouse liver increases in lipodystrophy. They discovered that this gene expression could be modified by microRNA in exosomes released by fat. They also showed that the mice that couldn't produce microRNAs in fat cells didn't produce that type of microRNA at all. "But if you put back that missing microRNA in exosomes, it does regulate the gene," Kahn says. "So fat is using this as a way to send a signal to the liver." Next, the scientists made a mouse model with fat cells engineered to make a certain microRNA that is found in humans, but not mice, and showed that these human microRNAs could also regulate their target in the livers of the mice and that this was do to these circulating exosomal microRNAs. "We showed in mice that these circulating microRNAs in exosomes can regulate gene expression, at least in liver and perhaps in other tissues," Kahn sums up. His team is now looking to see if this microRNA mechanism also works in other tissues such as muscle and brain cells. Additionally, the scientists will investigate ways the mechanism might be applied in gene therapy. Fat is easy to access, a major advantage for gene therapy, Kahn points out. "We could take out a patient's subcutaneous fat with a simple needle biopsy, modify the fat cells to make the microRNAs that we want, put the cells back into the patient, and then hope to get regulation of genes that the patient is not regulating normally," he suggests. This approach for gene therapy to treat fatty liver disease, for example, might prove both safer and more effective than reengineering cells in the liver itself. "We think it also might be useful for non-metabolic diseases, such as cancer of the liver," Kahn says. Lead author on the Nature paper is Thomas Thomou. Other Joslin contributors include Jonathan Dreyfuss, Masahiro Konishi, Masaji Sakaguchi, Tata Nageswara Rao and Jonathon Winnay. Marcelo Mori of the Federal University of São Paolo in São Paolo, Brazil; Christian Wolfrum of ETH Zurich in Zurich, Switzerland; Steven Grinspoon of Massachusetts General Hospital in Boston; and Phillip Gorden of the National Institute of Diabetes and Digestive and Kidney Diseases also are co-authors. Lead funding was from the National Institutes of Health. Joslin Diabetes Center is world-renowned for its deep expertise in diabetes treatment and research. Joslin is dedicated to finding a cure for diabetes and ensuring that people with diabetes live long, healthy lives. We develop and disseminate innovative patient therapies and scientific discoveries throughout the world. Joslin is an independent, non-profit institution affiliated with Harvard Medical School, and one of only 11 NIH-designated Diabetes Research Centers in the U.S. For more information, visit http://www. or follow @joslindiabetes
News Article | January 31, 2017
A recent study performed by scientists may prove if a link exists between HIV positive patients and their susceptibility to diabetes. According to a new study, people who are HIV positive may be more prone to suffering from diabetes. Similar studies have been undertaken previously but their findings were never concrete. Therefore, the researchers wanted to observe and delve deeper as to whether there really is an increased risk of developing diabetes for HIV positive adults. For the purpose of the study, the scientists considered survey answers from HIV positive individuals listed in the Medical Monitoring Project (MMP). The MMP is basically a database with estimates of the clinical and behavioral features of HIV patients in the U.S. The scientists also took into consideration data from the National Health and Nutrition Examination Survey (NHANES). For the MMP participants, three in four were men and a little less than 60 percent were 45 or above. One in every four had a body mass index (BMI) that was 30 or more and were obese clinically. Moreover, one out five participants were HCV positive, and 90 percent of the subjects underwent treatment via antiretroviral therapy in the previous year. Nearly 56.5 percent of the subjects were over the line of poverty. By comparison, nearly 50 percent of the NHANES subjects were male who were 45 years or older and 91.5 percent of the subjects were above the line of poverty. Of these subjects, 36 percent suffered from obesity and less than 2 percent were HCV positive. The researchers discovered that 1 out of 10 MMP subjects suffered from diabetes. Moreover, less than 4 percent and a little more than 52 percent suffered from Type 1 and Type 2 diabetes, respectively. Four out of 10 participants - which is nearly 44 percent - suffered from an unspecified form of diabetes. By comparison, diabetes for those who are not HIV positive was a little more than 8 percent, this figure accounted people who got Medicaid in the previous year. Even after accounting for all external factors such as obesity, age, and time since an HIV diagnosis, the study revealed that diabetes is at least 3.8 percent higher among HIV positive people than it is among general public. The scientists also added that obesity does increase the risk of developing diabetes in adults. However, even in the absence of obesity, HIV positive adults showed a higher vulnerability to diabetes. "Although obesity is a risk factor for prevalent [diabetes] among HIV infected adults, when compared with the general US adult population, [these] adults may have higher [diabetes mellitus) prevalence at younger ages, and in the absence of obesity," surmised the researchers. Although the study hints that HIV positive people are more likely to be afflicted by diabetes mellitus, scientists are of the opinion that more studies that are similar in nature need to undertaken to establish that the findings portray a true picture. The study has been published online journal BMJ Open Diabetes Research & Care. © 2017 Tech Times, All rights reserved. Do not reproduce without permission.
News Article | February 22, 2017
Severe gum disease, known as periodontitis, may be an early sign of type 2 diabetes, reveals research published in the online journal BMJ Open Diabetes Research & Care. Screening patients visiting their dentist for the treatment of severe gum disease, to try and stave off the complications associated with longstanding diabetes, would be feasible and worthwhile, suggest the researchers. They base their findings on 313 predominantly middle-aged people attending a university dental clinic: 109 had no gum disease; 126 had mild to moderate gum disease; and in 78 it was severe, affecting the supporting structures of the teeth. Weight was significantly higher in those with severe gum disease: they had an average BMI of 27 or higher. But other risk factors for diabetes, including high blood pressure, and high cholesterol levels, were similar among all three groups. And people with mild to moderate gum disease also had more relatives with diabetes than those with no or severe gum disease. Just under 3% of those with no gum disease had already been diagnosed with type 2 diabetes; this was also the case for 4% of those with mild to moderate gum disease, and for nearly 8% of those with the severe form. HbA1C values, which measure the average level of blood sugar in the body over the past 2-3 months, were obtained by analysing dried blood spots, which had been sampled from each of the study participants, using a finger pin-prick test. An HbA1C value of 39-47 mmol/l is considered to indicate 'pre-diabetes,' while values above that indicate diabetes. The analysis of the dried blood spots showed that HbA1C values were highest in those with the most severe form of gum disease. Their average HbA1C value was 45 mmol/l (6.3%), compared with 43 mmol/l (6.1%) in those with mild to moderate gum disease and 39 mmol/l (5.7%) in those with no gum disease. People with suspected diabetes (23% and 14%, respectively) and pre-diabetes (47% and 46%, respectively) were significantly over represented among those with severe and mild to moderate gum disease. Among those with no gum disease, 37% had pre-diabetes, while 10% had suspected diabetes --figures that are relatively high, but which might be explained by the lower threshold of 6.5% rather than 7%, which is commonly used for a diagnosis of type 2 diabetes. Previously undiagnosed cases of diabetes were found in all three groups: 8.5% of those with no gum disease; just under 10% of those with mild to moderate gum disease; and nearly one in five (18%) of those with the severe form. This is an observational study so no firm conclusions can be drawn about cause and effect, but the researchers nevertheless say: "This confirms the assumption that severe periodontitis could be an early sign of undiagnosed diabetes." They suggest that it would be feasible to screen for undiagnosed diabetes in dental practices, focusing on people with the most severe form of gum disease. Picking up diabetes and pre-diabetes early is essential if its associated complications are to be avoided, they add. "The early diagnosis and intervention of (pre) diabetes prevent the common micro vascular and macro vascular complications and are cost effective," they write. Furthermore, early diagnosis and treatment of diabetes might also help to stave off the risk of tooth loss that is associated with longstanding and untreated severe gum disease, they add. Research: Periodontitis as a possible early sign of diabetes mellitus http://bmjdrc. BMJ Open Diabetes Research & Care is one of 60 specialist journals published by BMJ. The title is owned by the American Diabetes Association. http://drc.