Melissa Glim

The annual prevalence of pediatric diabetes and pediatric diabetic nephropathy “markedly increased starting at age 12 years,” a new analysis of insurance data shows.

The results were published online ahead of print on December 17, 2015, and appear in the February 2016 issue of 

A team lead by Lin Li, MD, PhD, Research Assistant Professor of Epidemiology, Boston Collective Drug Surveillance Program, Boston University School of Public Health in Lexington MA, in conjunction with researchers at Bayer Pharma AG in Germany, estimated the prevalence of diabetes and diabetic nephropathy in U.S. commercially insured patients under age 18.

They used the US MarketScan Commercial Claims and Encounters Database to identify 96,171 pediatric patients with diabetes and 3161 children with diabetic nephropathy between 2002 and 2014. From this sample, they estimated the prevalence of pediatric diabetes and diabetic nephropathy in the US population.  

The annual prevalence of pediatric diabetes had increased from 1.86 to 2.82 per 1000 during the period measured. The prevalence of type 1 diabetes went up from 1.48 to 2.32 per 1,000, while type 2 increased from 0.38 to 0.67 per thousand.  

Diabetic nephropathy tripled from 1.16 to 3.44 percent for all cases. Prevalence was highest among patients between 12 and 18 years. Type 1 diabetes prevalence was higher in boys, while type 2 diabetes and diabetic nephropathy was higher in girls.    

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Pediatric diabetes and pediatric diabetic nephropathy rates significantly increase at age 12.

Juvenile Diabetes Rates Increase

Traditional folk art contains small mistakes that affirm the idea that Man’s creations cannot be perfect. So it is with natural and manufactured insulin.

Now researchers in Denmark may have found a way to get the manufactured product a little closer to nature’s original design.

Natural insulin assembles into homogenous grid-like structures called hexameres. The more regular the structure, the more evenly the insulin can be released from the pancreas into the body.

Manufactured insulin, on the other hand, can contain irregularities in its structure.

Knud J. Jenson, PhD, a professor at the University of Copenhagen in Denmark, working with researchers from the Technical University of Denmark and Novo Nordisk, have developed a new technique to design insulin-based drugs with greater uniformity. The resulting drugs could lead to more personalized medicine with fewer side effects.

All insulin molecules have compounds called bipyridines on the ends that serve as a hook to attach to other molecules.

The team has come up with a method to get manufactured insulin to self-assemble in a homogenous chemical grid. By hooking an Iron II atom to the bipyridine, they could control insulin assembly with greater precision. The new Iron II method causes insulin to self-assemble into nanostructures that are well suited to form deposits in fatty tissue, where injected insulin gets stored.'

“It is absolutely clear that this could be a good method for designing medications that release over extended periods of time, from depots beneath the skin," Jensen said in a release, adding "because we are able to control the insulin's self-assembling properties so precisely, I believe that the method can also be used to design insulin with a variety of properties."

In rats, the new insulin caused blood sugar levels to fall, leaving the team optimistic about the new method. The team also imaged the insulin grid structures so that they could state, with certainty, that adding Iron II would really assembled homogenously.

"We have discovered an entirely new method of modifying a molecule - insulin - that is important for 35 million diabetes patients. We are incredibly happy with that," Jensen said in a release.

The report appears in the January 14 issue of 

New insulin caused blood sugar levels to fall in mouse models, creating hope for improved treatment of diabetes.

Research Targets Improved Insulin Development

Treating a rare genetic form of diabetes with oral medications may do more harm than good.

Maturity-onset diabetes of the young (MODY1) is a rare form of diabetes caused by a range of genetic mutations that interrupt beta cell function. Although it differs from type 2 diabetes, it is often misdiagnosed because symptoms appear similar.

A recent study conducted at Washington University School of Medicine suggests that the oral medications used to stimulate beta cells to release more insulin in type 2 diabetes may actually kill those same cells in people with MODY1 by overstressing them.

"People diagnosed with type 2 diabetes are treated with oral medications that make insulin-secreting beta cells very active," said first author Benjamin D. Moore, PhD, a former postdoctoral fellow at Washington University who is now at Massachusetts General Hospital. "But the MODY1 pathway we've uncovered shows that stimulating those cells with those drugs can lead to beta cell death. That means these patients can become dependent on insulin injections much sooner."

Moore, working under Jason C. Mills, MD, PhD, associate professor of medicine at Washington University and his team identified a pathway in which hepatocyte nuclear factor 4-alpha induces expression of a gene involved in regulating the cells that secrete insulin, and that can cause MODY1 when mutated. MODY affects around 3 to 5 percent of people.

"It's important to diagnose patients as accurately as possible and to attempt to target the correct pathway," Moore said. These patients may benefit from therapies designed to target this pathway that regulates the beta cells. Their findings are published in the March 18 issue of the Journal of Biological Chemistry.

The pathway may also affect the secretion of enzymes in the stomach, liver, kidney, and intestines, and Moore and Mills believe the pathway they have identified may also be important in other disorders involving enzyme-secreting cells.

"Nature doesn't re-invent the wheel," Mills said.

"What these different cells secrete is very different, but the machinery is very similar. As with auto plants, although a BMW is very different from a Volkswagen, the factories where those cars are built are not really that different. It appears the same thing may be true for a number of these cells that secrete key enzymes in the gastrointestinal tract."

Maturity-onset diabetes of the young is a rare form of diabetes caused by a range of genetic mutations that interrupt beta cell function. 

Oral Medications May Cause More Harm in Rare Form of Diabetes

Researchers seek to improve treatment for autoimmune diseases, including rheumatoid arthritis, gout, Crohn’s disease, and lupus. 

In autoimmune diseases, one size doesn’t fit all when it comes to tools to encourage adherence to treatment.

Nearly 10% of the US population is affected by 29 autoimmune diseases, including rheumatoid arthritis, gout, Crohn’s disease, and lupus.

Effective therapies are available but many patients struggle to adhere to medication regimens or choose not to due to side effects, cost, or beliefs about their effects. Various studies estimate that as many as 50 percent of patients skip out on their meds at some point.

Online tools have been developed to help with adherence — many are digital versions of traditional paper tools – like diaries and trackers – along with additional feature like social networking. Still, studies show use of these tools often fizzles out fairly quickly. Moreover, there do not appear to be any such apps specifically designed for autoimmune diseases.

In a study published in the June 24 issue of 

, researchers from Evolution Health Systems in Toronto, Janssen Scientific Affairs in Horsham, Penn., and the University of Reading in the UK, conducted an analysis of current literature to identify the particular causes of non-adherence in autoimmune disease treatment and techniques that may be most likely to help.

Using “Grounded Theory,” a stepped approach to identifying, classifying, and analyzing research, they found that the most common modifiable factors affecting adherence were dose regimen, patients not understanding treatment, followed by side effects and a belief that the medication wasn’t effective. Ethnicity was the most common non-modifiable factor (age and gender being other factors).

According to these findings, adherence outcomes and digital attrition in autoimmunology patients could be improved if patients had tailored tools to help them gain a better understanding of their disease, the role of their medications, and information on side effects and the role of the dose regiment.

Lack of understanding, perceived ineffectiveness, and forgetfulness can be addressed through targeted communications — such as emails or texts, shared decision making tools, and regular interactions. Support groups could help with addressing side effects as patients share information and advice for mitigating the effects.

Tremendous cost results from not adhering to treatment — as diseases progress, and patients require more intensive care and hospitalization, as well as the cost due to missed work etc. Studies estimate non-adherence in North America costs $300 billion in avoidable costs each year.

 “A patient’s relationship to treatment is highly personal, and digital interventions should take advantage of technologies that enable tailoring for the unique needs of individuals,” the authors wrote.

Researchers seek to improve treatment for autoimmune diseases, including rheumatoid arthritis, gout, Crohn's disease, and lupus. 