Guardian of the Cell


Scientists unravel the structure, key features of a human immune-surveillance protein, setting the stage for more-precise immune therapies

protein structure
Scientists have identified the key structural and functional features of a critical immune protein in humans that guards against cancer, viral and bacterial infections.

 

The human body is built for survival. Each one of its cells is closely guarded by a set of immune proteins armed with nearly foolproof radars that detect foreign or damaged DNA.

One of the cells’ most critical sentinels is a “first responder” protein known as cGAS, which senses the presence of foreign and cancerous DNA and initiates a signaling cascade that triggers the body’s defenses.

The 2012 discovery of cGAS ignited a firestorm of scientific inquiry, resulting in more than 500 research publications, but the structure and key features of the human form of the protein continued to elude scientists.

Now, scientists at Harvard Medical School and Dana-Farber Cancer Institute have, for the first time, identified the structural and functional differences in human cGAS that set it apart from cGAS in other mammals and underlie its unique function in people.

A report on the team’s work, published July 12 in Cell, outlines the protein’s structural features that explain why and how human cGAS senses certain types of DNA, while ignoring others.

“The structure and mechanism of action of human cGAS have been critical missing pieces in immunology and cancer biology,” said senior investigator Philip Kranzusch, assistant professor of microbiology and immunobiology at Harvard Medical School and Dana-Farber Cancer Institute. “Our findings detailing the molecular makeup and function of human cGAS close this critical gap in our knowledge.” Importantly, the findings can inform the design of small-molecule drugs tailored to the unique structural features of the human protein—an advance that promises to boost the precision of cGAS-modulating drugs that are currently in development as cancer therapies. “Several promising experimental immune therapies currently in development are derived from the structure of mouse cGAS, which harbors key structural differences with human cGAS,” Kranzusch said. “Our discovery should help refine these experimental therapies and spark the design of new ones. It will pave the way toward structure-guided design of drugs that modulate the activity of this fundamental protein.”

The team’s findings explain a unique feature of the human protein—its capacity to be highly selective in detecting certain types of DNA and its propensity to get activated far more sparingly, compared with the cGAS protein in other animals.

Specifically, the research shows that human cGAS harbors mutations that make it exquisitely sensitive to long lengths of DNA but render it “blind” or “insensitive” to short DNA fragments.

“Human cGAS is a highly discriminating protein that has evolved enhanced specificity toward DNA,” said co-first author Aaron Whiteley, a postdoctoral researcher in the Department of Microbiology and Immunobiology at Harvard Medical School. “Our experiments reveal what underlies this capability.”

Location, location, location

In all mammals, cGAS works by detecting DNA that’s in the wrong place. Under normal conditions, DNA is tightly packed and protected in the cell’s nucleus—the cellular “safe”—where genetic information is stored. DNA has no business roaming freely around the cell. When DNA fragments do end up outside the nucleus and in the cell’s cytosol, the liquid that encases the cell’s organelles, it’s usually a sign that something ominous is afoot, such as damage coming from within the cell or foreign DNA from viruses or bacteria that has made its way into the cell.

The cGAS protein works by recognizing such misplaced DNA. Normally, it lies dormant in cells. But as soon as it senses the presence of DNA outside the nucleus, cGAS springs into action. It makes another chemical—a second messenger—called cGAMP, thus setting in motion a molecular chain reaction that alerts the cell to the abnormal presence of DNA. At the end of this signaling reaction, the cell either gets repaired or, if damaged beyond repair, it self-destructs.

But the health and integrity of the cell are predicated on cGAS’ ability to distinguish harmless DNA from foreign DNA or self-DNA released during cell damage and stress. “It’s a fine balancing act that keeps the immune system in equilibrium. An overactive cGAS can spark autoimmunity, or self-attack, while cGAS that fails to detect foreign DNA can lead to tumor growth and cancer development,” said co-first author Wen Zhou, a postdoctoral researcher at Harvard Medical School and Dana-Farber Cancer Institute.

The current study reveals the evolutionary changes to the protein’s structure that allow human cGAS to ignore some DNA encounters while responding to others.

A foe, an accomplice

For their work, the team turned to an unlikely collaborator—Vibrio cholerae, the bacterium that causes cholera, one of humankind’s oldest scourges.

Taking advantage of a cholera enzyme that shares similarities with cGAS, the scientists were able to recreate the function of both human and mouse cGAS in the bacterium.

Teaming up with colleagues from the lab of Harvard Medical School bacteriologist John Mekalanos, the scientists designed a chimeric, or hybrid, form of cGAS that included genetic material from both the human and mouse forms of the protein. Then they compared the ability of the hybrid cGAS to recognize DNA against both the intact mouse and intact human versions of the protein.

In a series of experiments, the scientists observed activation patterns between the different types of cGAS, progressively narrowing down the key differences that accounted for differential DNA activation among the three.

The experiments revealed that out of the 116 amino acids that differ in human and mouse cGAS, only two accounted for the altered function of human cGAS. Indeed, human cGAS was capable of recognizing long DNA with great precision but it ignored short DNA fragments. The mouse version of the protein, by contrast, did not differentiate between long and short DNA fragments

“These two tiny amino acids make a world of difference,” Whiteley said. “They allow the human protein to be highly selective and respond only to long DNA, while ignoring short DNA, essentially rendering the human protein more tolerant of DNA presence in the cytosol of the cell.”

Plotting the genetic divergence on an evolutionary timescale, the scientists determined that the human and mouse cGAS genes parted ways sometime between 10 million and 15 million years ago.

The two amino acids responsible for sensing long DNA and tolerating short DNA are found solely in humans and nonhuman primates, such as gorillas, chimps and bonobos. The scientists hypothesize that the ability to ignore short DNA but recognize long DNA must have conferred some evolutionary benefits. “It could be a way to guard against an overactive immune system and chronic inflammation,” Kranzusch said. “Or it could be that the risk of certain human diseases is lowered by not recognizing short DNA.”

In a final set of experiments, the team determined the atomic structure of the human cGAS in its active form as it binds to DNA. To do so, they used a visualization technique known as X-ray crystallography, which reveals the molecular architecture of protein crystals based on a pattern of scattered X-ray beams.

Profiling the structure of cGAS “in action” revealed the precise molecular variations that allowed it to selectively bind to long DNA, while ignoring short DNA.

“Understanding what makes the structure and function of human cGAS different from those in other species was the missing piece,” Kranzusch said. “Now that we have it, we can really start designing drugs that work in humans, rather than mice.”

Other investigators included Carina de Oliveira Mann, Benjamin Morehouse, Radosław Nowak, Eric Fischer, and Nathanael Gray. The work was supported by the Claudia Adams Barr Program for Innovative Cancer Research, by the Richard and Susan Smith Family Foundation, by the Charles H. Hood Foundation, by a Cancer Research Institute CLIP Grant, by the National Institute of Allergy and Infectious Diseases grant AI-01845, by National Cancer Institute grant R01CA214608, by the Jane Coffin Childs Memorial Fund for Medical Research, by a Cancer Research Institute Eugene V. Weissman Fellow award, and by a National Institutes of Health T32 grant 5T32CA207021-02.

Relevant Disclosures: The Dana-Farber Cancer Institute and Harvard Medical School have patents pending for human cGAS technologies, on which the authors are inventors.

Harvard Medical School Harvard Medical School (http://hms.harvard.edu) has more than 11,000 faculty working in 10 academic departments located at the School’s Boston campus or in hospital-based clinical departments at 15 Harvard-affiliated teaching hospitals and research institutes: Beth Israel Deaconess Medical Center, Boston Children’s Hospital, Brigham and Women’s Hospital, Cambridge Health Alliance, Dana-Farber Cancer Institute, Harvard Pilgrim Health Care Institute, Hebrew SeniorLife, Joslin Diabetes Center, Judge Baker Children’s Center, Massachusetts Eye and Ear/Schepens Eye Research Institute, Massachusetts General Hospital, McLean Hospital, Mount Auburn Hospital, Spaulding Rehabilitation Network and VA Boston Healthcare System.

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Insulin Goes Viral?


New study shows some viruses produce insulin-like hormones that have potential to cause disease

Every cell in your body responds to the hormone insulin, and if that process starts to fail, you get diabetes.

In an unexpected finding, Harvard Medical School scientists at Joslin Diabetes Center have identified four viruses that can produce insulin-like hormones that are active on human cells. The discovery brings new possibilities for revealing biological mechanisms that may cause diabetes or cancer.

“Our research may help open up a new field that we might call microbial endocrinology,” said Emrah Altindis, HMS instructor in medicine at Joslin Diabetes Center and lead author on a paper in the journal PNAS  on the work.

“We show that these viral, insulin-like peptides can act on human and rodent cells. With the very large number of microbial peptides to which we are exposed, there is a novel window for host-microbe interactions. We hope that studying these processes will help us to better understand the role of microbes in human disease,” Altindis said.

“Indeed, the discovery of the viral insulin-like hormones raises the question of what their role might be in diabetes, as well as in autoimmune disease, cancer and other metabolic conditions,” said C. Ronald Kahn, the HMS Mary K. Iacocca Professor of Medicine and Joslin’s chief academic officer.

The key idea for the investigation came when Altindis, whose previous research focused on creating vaccines against bacteria, attended a Joslin seminar that discussed potential causes of the autoimmune reaction that drives type 1 diabetes.

From left, Altindis and Kahn.  Image: Courtesy Joslin Diabetes CenterFrom left, Altindis and Kahn. Image: Courtesy Joslin Diabetes Center

He began to hypothesize whether bacteria or viruses could create insulin-like peptides (small versions of proteins) that could help to trigger the disease.

By analyzing large public research databases that hold viral genomic sequences, he and his colleagues at Joslin found that various viruses can produce peptides that are similar in whole or in part to 16 human hormones and regulatory proteins.

“What really caught our attention were four viruses that had insulin-like sequences,” said Kahn, who was senior author on the paper.

Infecting Fish

These viruses were from a family of viruses known to infect fish. To find out if they could be active in mammals, the Joslin team collaborated with Richard DiMarchi, professor of chemistry at Indiana University, Bloomington, whose lab chemically synthesized these viral insulin-like peptides (VILPs).

Experimenting in mouse and human cells, the scientists studied whether the VILPs could act like hormones. Their experiments proved that the VILPs could indeed bind to human insulin receptors and receptors for a closely related hormone called IGF-1 (insulin-like growth factor 1).

These are the critical proteins on the cells that tell them to take up glucose and to grow. Additionally, the peptides could stimulate all of the signaling pathways inside the cells that were stimulated by human insulin and IGF-1.

Mice injected with the viral peptides exhibited lower levels of blood glucose, another sign of insulin action. Moreover, analysis of databases of viruses found in the human intestine showed evidence that humans are exposed to these viruses.

“These viruses are definitely known to infect fish and amphibians, but they are not known to infect humans,” Kahn pointed out. “However, it’s possible that humans get exposed to these viruses through just eating fish. Nobody has checked directly whether under some conditions the viruses could either infect cells or be at least partly absorbed through the gut intestine.”

The scientists now will broaden their search for other viruses that produce human-like hormones.

“This finding is the tip of an iceberg,” Kahn said. “There are thought to be more than 300,000 viruses that can infect or be carried in mammals, and only 7,500 or so of these, or about 2.5 percent, have been sequenced. Thus, we certainly expect to find many more viral hormones, including more viral insulins, in the future.”

“This research also opens up a new aspect to study in type 1 diabetes and autoimmunity,” he said.

“It may be that these or similar microbial insulin-like molecules could be an environmental trigger to start the autoimmune reaction in type 1 diabetes. On the other hand, you could also imagine that this might desensitize the immune response and could be protective,” Kahn said.

Viral Peptides

A similar question is open for metabolic diseases such as type 2 diabetes and obesity, in which the body fails to respond properly to insulin.

“You could envision that these viral peptides could either protect from or contribute to insulin resistance,” Kahn said.

These or similar viruses might also be a factor in certain human cancers.

“If these viruses are inside the gut, could the VILPs they produce stimulate growth of gut cells so that you get polyps or tumors of the gut?” Kahn asks. “Or if they’re absorbed or become infectious, could they infect any organ in the body?”

Analyzing such viral peptides may eventually help drug companies to design new forms of synthesized human insulins.

“We might be able to learn something, for example, about making insulins that don’t need refrigeration and can be stored for long periods of time, or insulins that are absorbed more quickly or degrade more slowly,” he said.

Given Altindis’s earlier research on infectious disease rather than in endocrinology, “our discovery gives an example of how work in one field can stimulate thought in another field,” Kahn added. “It really underlines the importance of cross-fertilization in the scientific discovery process, which is so valuable but so underappreciated.”

Adjustable gastric band feasible for treatment of type 2 diabetes, obesity


Patients with type 2 diabetes and obesity achieved similar 1-year benefits on diabetes control, cardiometabolic risk and patient satisfaction when undergoing laparoscopic adjustable gastric band or an intensive diabetes medical and weight management program, according to recent research.

Allison B. Goldfine, MD, head of Joslin Diabetes Center section of clinical research and associate professor of medicine at Harvard Medical School, and colleagues conducted a 12-month prospective, randomized clinical trial to evaluate the effects of laparoscopic adjustable gastric band (LAGB; n=18) and an intensive diabetes medical and weight management program (IMWM; n = 22). Participants were aged 21 to 65 years, had a BMI of 30 to 45 kg/m2, a diagnosis of type 2 diabetes more than 1 year before the study period and HbA1c of 6.5% or more on anti-hyperglycemic medications.

Allison B. Goldfine

Allison B. Goldfine

A similar proportion of participants in the LAGB group achieved HbA1c less than 6.5% and fasting plasma glucose level below 7 mmol/L (33%) at 12 months compared with the IMWM group (23%; P = .457). The LAGB group revealed greater weight loss over 12 months (-13.5 kg) compared with the IMWM group (-8.5 kg). However, changes in fat free mass (P = .617) and decreases in waist circumference (P = .856) were similar between the groups.

Over the 12-month period, reductions in HbA1c were similar between the groups at -1.23% for the LAGB group and -0.95% for the IMWM group. The groups also had similar reductions in fasting glucose (P = .975).

The IMWM group had greater reductions in systolic blood pressure from baseline compared with the LAGB group (P = .038). However, no difference was found for change in diastolic BP, total cholesterol, triglycerides, HDL-cholesterol or LDL-cholesterol at 12 months. More participants in the LAGB group achieved LDL-cholesterol levels below 2.59 mmol/L following LAGB (83%) compared with the IMWM group (45%; P = .019).

Researchers used the United Kingdom Prospective Diabetes Study risk engine to determine changes in cardiometabolic risk scores for coronary heart disease, fatal CHD, stroke and fatal stroke, and the scores were similar between the groups 12 months following LAGB and IMWM.

“We can anticipate long-term health benefits from both of these approaches, but they do require different investment of time and energy by the patient and over the short-term our studies show metabolic outcomes are similar in patients comparable to those in our study,” Goldfine told Endocrine Today. “It is important to have different therapeutic options available for patients with a complex disease like type 2 diabetes.” – by Amber Cox

New hormone stimulates pancreatic β-cell proliferation.


Diabetes affects more than 360 million people worldwide and its prevalence is increasing, with 552 million diabetics predicted worldwide by 2030. Scientists recently discovered a hormone that could improve future diabetes management by stimulating replenishment of insulin-producing β cells in the pancreas.

The hormone, which has been named betatrophin, was discovered in studies of a mouse model of severe insulin resistance in which chemical blockade of insulin receptors induced pancreatic β-cell proliferation. Betatrophin was identified in murine liver and fat, and its stimulatory effect on cellular replication was limited to β cells. Its expression was also reported in human liver tissue.

Betatrophin treatment of mice increased proliferation of pancreatic β-cells by an average of 17-fold within a few days, causing an expansion of β-cell mass and increased insulin concentrations in the pancreas.

Betatrophin’s discovery “is a very exciting new development, and is only the beginning of the story”, says C Ronald Kahn (Joslin Diabetes Center, Boston, MA, USA). He adds that unanswered questions include whether “action on islets is direct or indirect. We don’t know how betatrophin works; is it only one growth factor or one of many? There is a lot of future work to be done”.

Senior author Douglas Melton (Harvard University, Cambridge, MA, USA) said: “It’s not often that one finds a new hormone, so it opens up all kinds of possibilities for new treatments”.

The most immediate application for betatrophin is for the “millions of prediabetics who are on their way to getting type 2 diabetes. If these individuals still have β cells, this hormone could give them more β cells and alleviate the need for insulin injections”, Melton continued. Betatrophin may also prove beneficial in type 1 diabetes, which is initiated by an autoimmune process. “If the disease is just starting, one could give an immunosuppressant and this hormone to forestall the onset of type 1 diabetes.”

Melton cautions that results from human studies should not be expected quickly. “We are currently working with our collaborators Evotec and Janssen to make the human betatrophin protein. This will take more than a year.” Results from studies in humans might be available “2—3 years from now, if all goes well”.

Source: Lancet

HbA1c Inadequate to Assess Diabetes Care Across Specialties.


New findings suggest that simply using HbA1clevels to assess the performance of individual physicians or healthcare systems in diabetes management may be misleading or inaccurate.

Endocrinologists typically see more complex patients who require more time to improve their glycemic control, which makes their performance look worse when judged solely by HbA1c levels.

But new data reported here at the American Diabetes Association 2013 Scientific Sessions show that when diabetes patients are grouped by medication use — a proxy for complexity and stage of disease — HbA1c levels for patients cared for by endocrinologists are the same as or better than those for individuals seen by general internists.

Lawrence S. Phillips, MD, professor of medicine in the division of endocrinology at Emory University, Atlanta, Georgia, who reported the findings in a poster at the meeting, said looking at patients by medication group shows there is very little difference between the performance of specialists and generalists.

“The message is really for the payers and the government… They need to do something like this. They need to have some conservative way to give the provider a chance to improve things, and then they need to compare apples to apples. Just looking at A1c is not sufficient,” Dr. Phillips told Medscape Medical News.

Poster session moderator Sanjeev Mehta, MD, MPH, director of quality at Joslin Diabetes Center, Boston, Massachusetts, agrees. “Dr. Phillips’s data demonstrated that endocrinologists, in the practice setting he evaluated, were seeing patients with higher HbA1c levels. While this suggests appropriate referrals by primary-care physicians to optimize glycemic control, it also supports Dr. Phillips’s conclusion that an outcome-based quality measure [such as HbA1c] may be inadequate when assessing the quality of diabetes care across all providers, especially endocrinologists,” he said.

Dr. Mehta noted that the Agency for Healthcare Research and Quality (AHRQ) has endorsed theadoption of more sophisticated quality metrics, including linked action measures such as appropriate medication use, which would assess outcomes in the context of the care provided.

“I strongly believe this is the direction that all stakeholders in the diabetes community need to be [following to evaluate] high-quality diabetes care,” he told Medscape Medical News.

Comparing Apples to Apples Is Best Approach

Dr. Phillips and colleagues obtained Emory Healthcare data for a total of 5880 diabetes patients cared for by 8 endocrinologists and 8 general internists over a 24-month period. The proportion of patients whose most recent HbA1c was 7% or above was higher for the endocrinologists than for the general internists, 51% vs 38%.

Subsequent analysis was restricted to the 3735 patients who had been seen 3 or more times in the past 24 months and at least once in the prior 12 months. This group was divided into 3 groups by medication use: Those using only oral medications and/or incretin-based drugs (1880), those using basal insulin (with or without oral medications/incretins, 324), and those also using mealtime insulin in addition to basal insulin, with or without other medications (1531). The latter group included patients with type 1 diabetes, Dr. Phillips told Medscape Medical News.

Overall control was poorer among the insulin-using patients, with HbA1c levels of 7% or higher in 66% of those using mealtime insulin and 55% of individuals using basal insulin, compared with just 21% of those not using insulin (P < .0001 for trend). And endocrinologists had more patients on insulin than did the general internists, with 53% vs 22% using mealtime insulin (P < .0001), 10% vs 7% using basal insulin (P = .02), and 37% vs 71% not using insulin (P < .0001), respectively.

When examined by treatment group, however, the non–insulin-using patients of the endocrinologists actually had better HbA1cs: 18.8% of their patients had levels at or above 7% vs 23.4% of the general internists’ patients.

For the 2 insulin treatment categories, there was no significant difference between the endocrinologists and the internists. In both groups, just over half of the patients had HbA1cs 7% or above (= .6) as did about two thirds of those using mealtime insulin (= .9).

New Models Needed for Evaluating Care

Dr. Mehta told Medscape Medical News:”I think this poster highlighted the importance of adopting more sophisticated quality metrics, such as linked action measures, and the importance of ongoing collaboration with specialists and specialty centers in the care of adults with diabetes.

“Specialists and specialty centers may have an opportunity to translate best practices to their referring primary-care physicians, who will continue to care for the majority of adults with diabetes in the United States,” he added.

And specialists should be rewarded, not penalized, for their particular patient mix. “Those providers and practices that care for more complex patients need to be recognized, even reimbursed, for their ability to make meaningful improvements in health outcomes in high-risk patients,” he observed.

Dr. Phillips told Medscape Medical News that “diabetes is a heavy-duty proxy for healthcare systems as a whole, because a lot of people have diabetes, and it’s an expensive disease.”

He believes his “apples-to-apples” comparison could have implications for other areas of medicine as well. “I think it’s an important concept. You would think it applies to blood pressure, cholesterol, all the things that doctors do. We think this is a model for how you evaluate care.”

Source: http://www.medscape.com

Diabetes educators review 2012 National Standards.


Last revised in 2007, the National Standards for Diabetes Self-Management Education have served as the acceptable guide for providing consistency and quality through the delivery of diabetes education. At the American Association for Diabetes Educators annual meeting, certified diabetes educators discussed the recently updated standards, emphasizing support and a continuum of self-management, as well as a widened criterion for eligible instructors.

One obvious revision includes a change in the standard’s title. Formerly known as the National Standard for Diabetes Self-Management Education, the guide is now known as the National Standard for Diabetes Self-Management Education and Support (DSMES).

Donna Tomky, MSN, RN, C-NP, CDE, FAADE, immediate past president of AADE and nurse practitioner and diabetes educator from ABQ Health Partners in Albuquerque, NM, said support is a very important part of the change.

 

Donna Tomky

“It really defines those activities that assist the person with prediabetes or diabetes in implementing and sustaining the behaviors needed to manage his or her condition on an ongoing basis. It really looks at the continuum instead of just a one-time effort,” Tomky said during a presentation.

Tomky said there are misunderstandings surrounding the standards. For example, an RN, RD, pharmacist, medical director or CDE are not needed for a diabetes education program. The revisions will be published in the October issue of Diabetes Care, she said.

Co-presenter, Melinda Maryniuk, RD, Med, CDE, director of clinical education programs for the Joslin Diabetes Center in Boston, Mass., said the revisions are aimed to ensure wide applicability and to ensure quality care.

“There aren’t revolutionary new things that have come out, but we have more research to support the information,” Maryniuk said.

In a survey of 225 public comment reviewers consisting of RNs, RDs, pharmacists, MD/DO/Endo, mental health professionals, and other providers, 82% said the standards were applicable to them, Tomky and Maryniuk said. Additionally, 74% agreed the document was clear. Many of the comments received mentioned satisfaction with a wider focus on support and prevention, while looking for more information.

Other revisions include increased clarity to ensure broad-based relevance in institutional and solo-based providers, an increased attention to behavior change and added examples of who can offer diabetes education, including occupational therapists and certified health education specialists. – By Samantha Costa

For more infromation:

Tomky D. #F03. Presented at: The American Association of Diabetes Educators 2012 Annual Meeting & Exhibition. August 1-4, 2012; Indianapolis.

Disclosure: Ms. Tomky and Ms. Maryniuk report no relevant financial disclosures.

Perspective

  • I attended this session so I could be as current and up-to-date with what the new standards will be forthcoming. I thought it was a great overview with realistic discussions in regard to the different organizations that I work with, and what challenges they might potentially have when it comes to interpreting the standards.

The fact that a credentialed CDE person who isn’t a nurse, dietician, or pharmacist can be in solo practice is really great. I have a lot of exercise physiology friends and I can’t wait to share that information with them. They will be so excited. They, too, are potentially masters-prepared and certified.

 

  • Source: Endocrine Today.

 

Diabetes educators review 2012 National Standards.


Last revised in 2007, the National Standards for Diabetes Self-Management Education have served as the acceptable guide for providing consistency and quality through the delivery of diabetes education. At the American Association for Diabetes Educators annual meeting, certified diabetes educators discussed the recently updated standards, emphasizing support and a continuum of self-management, as well as a widened criterion for eligible instructors.

One obvious revision includes a change in the standard’s title. Formerly known as the National Standard for Diabetes Self-Management Education, the guide is now known as the National Standard for Diabetes Self-Management Education and Support (DSMES).

Donna Tomky, MSN, RN, C-NP, CDE, FAADE, immediate past president of AADE and nurse practitioner and diabetes educator from ABQ Health Partners in Albuquerque, NM, said support is a very important part of the change.

 

Donna Tomky

“It really defines those activities that assist the person with prediabetes or diabetes in implementing and sustaining the behaviors needed to manage his or her condition on an ongoing basis. It really looks at the continuum instead of just a one-time effort,” Tomky said during a presentation.

Tomky said there are misunderstandings surrounding the standards. For example, an RN, RD, pharmacist, medical director or CDE are not needed for a diabetes education program. The revisions will be published in the October issue of Diabetes Care, she said.

Co-presenter, Melinda Maryniuk, RD, Med, CDE, director of clinical education programs for the Joslin Diabetes Center in Boston, Mass., said the revisions are aimed to ensure wide applicability and to ensure quality care.

“There aren’t revolutionary new things that have come out, but we have more research to support the information,” Maryniuk said.

In a survey of 225 public comment reviewers consisting of RNs, RDs, pharmacists, MD/DO/Endo, mental health professionals, and other providers, 82% said the standards were applicable to them, Tomky and Maryniuk said. Additionally, 74% agreed the document was clear. Many of the comments received mentioned satisfaction with a wider focus on support and prevention, while looking for more information.

Other revisions include increased clarity to ensure broad-based relevance in institutional and solo-based providers, an increased attention to behavior change and added examples of who can offer diabetes education, including occupational therapists and certified health education specialists. – By Samantha Costa

For more infromation:

Tomky D. #F03. Presented at: The American Association of Diabetes Educators 2012 Annual Meeting & Exhibition. August 1-4, 2012; Indianapolis.

Disclosure: Ms. Tomky and Ms. Maryniuk report no relevant financial disclosures.

Perspective

  • I attended this session so I could be as current and up-to-date with what the new standards will be forthcoming. I thought it was a great overview with realistic discussions in regard to the different organizations that I work with, and what challenges they might potentially have when it comes to interpreting the standards.

The fact that a credentialed CDE person who isn’t a nurse, dietician, or pharmacist can be in solo practice is really great. I have a lot of exercise physiology friends and I can’t wait to share that information with them. They will be so excited. They, too, are potentially masters-prepared and certified.

 

  • Source: Endocrine Today.