Diabetic Updates

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What is the difference between Type 1 and Type 2?

Type 1 diabetes, in the past, was commonly referred to as juvenile onset. Those effected were commonly children and the reason for diagnosis are typically unexplained. Normal care for Type 1 is diet and exercise and always includes the use of Insulin, normally by injection through an insulin pump or syringes. There is no cure for individuals with the affliction.

Type 2 diabetes was commonly referred to as adult onset diabetes and often effects older adults who typically follow poor eating habits and do not exercise throughout their lives. Often this type is hereditary. Type 2, in many cases, can be cured with a lifestyle change which brings about better eating habits and regular exercise. Normal care for Type 2, like Type 1, also includes diet and exercise, but may include insulin injections or pills.

When I was a child I remember learning a comparison that I never forgot. I can't remember where I learned it, but it was likely in one of the many handouts I received from my doctor or some diabetic group I was involved in, so I can't take the credit for it. The idea is: Type 1 diabetes occurs when the pancreas either does not create insulin cells or creates cells which are dead. Thereby the body has no insulin at it's disposal. Type 2 diabetes occurs when the pancreas creates insulin cells which are tired or old (I often picture the cells with little wooden walking sticks trying to get around the body). The cells are only able to do so much in a Type 2 diabetic because the individual has worn out it's body's ability to care for itself. Although not always, often the individual has followed a poor lifestyle for so long the body can no longer care for itself.

All that being said, the trend for disease is becoming much worse, and more aggressive among those affected by diabetes.

The British Journal of Diabetes drafted an article explaining the decreased age of onset for Type 2 diabetes, a previously categorized adult disease. This statement provides a poor outlook for our populous in general, but with small steps such as adding 30 minutes of exercise per day for both children and adults, and eating better, we can all make a big difference. I challenge each of us to make one change a week, I think you will be happy with the outcome!

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A western diet rich in animal products and other acidogenic foods can induce an acid load that is not compensated for by fruit and vegetables; this can cause chronic metabolic acidosis and lead to metabolic complications. Most importantly from a blood-sugar control perspective, increasing acidosis can reduce the ability of insulin to bind at appropriate receptors in the body, and reduce insulin sensitivity. With this in mind, the authors decided to analyse whether increased acidosis caused by dietary acid loads increased the risk of type 2 diabetes. A total of 66,485 women from the E3N study (the French Centre of the European Prospective Investigation into Cancer and Nutrition, a well-known ongoing epidemiological study) were followed for new diabetes cases over 14 years. Their dietary acid load was calculated from their potential renal acid load (PRAL) and their net endogenous acid production (NEAP) scores, both standard techniques for assessing dietary acid consumption from nutrient intake.

During follow-up, 1,372 new cases of incident type 2 diabetes occurred. In the overall population, those in the top 25% (quartile) for PRAL had a 56% increased risk of developing type 2 diabetes compared with the bottom quartile. Women of normal weight (BMI of 25 and under) had the highest increased risk (96% for top quartile versus bottom) while overweight women (BMI 25 and over) had only a 28% increased risk (top quartile versus bottom). NEAP scores showed a similar increased risk for higher acid load. The authors say: "A diet rich in animal protein may favour net acid intake, while most fruits and vegetables form alkaline precursors that neutralise the acidity. Contrary to what is generally believed, most fruits such as peaches, apples, pears, bananas and even lemons and oranges actually reduce dietary acid load once the body has processed them.

"In our study, the fact that the association between both PRAL and NEAP scores and the risk of incident type 2 diabetes persisted after adjustment for dietary patterns, meat consumption and intake of fruit, vegetables, coffee and sweetened beverages suggests that dietary acids may play a specific role in promoting the development of type 2 diabetes, irrespective of the foods or drinks that provide the acidic or alkaline components." They conclude: "We have demonstrated for the first time in a large prospective study that dietary acid load was positively associated with type 2 diabetes risk, independently of other known risk factors for diabetes. Our results need to be validated in other populations, and may lead to promotion of diets with a low acid load for the prevention of diabetes. Further research is required on the underlying mechanisms." -source

Scientists may be getting closer to finding a stem cell cure for Type 1 diabetes—the type that may require insulin injections for life—after conducting stem cell transplants on mice.

A group of researchers in California said they managed to reverse the equivalent of Type 1 diabetes in mice by transplanting stem cells.

"Here, we describe a stepwise method in which pluripotency reprogramming factors were transiently expressed in fibroblasts in conjunction with a unique combination of soluble molecules to generate definitive endoderm-like cells that did not pass through a pluripotent state. These endoderm-like cells were then directed toward pancreatic lineages using further combinations of small molecules in vitro," they said.

They added the resulting pancreatic progenitor-like cells "could mature into cells of all three pancreatic lineages in vivo, including functional, insulin-secreting β-like cells that help to ameliorate hyperglycemia."

"Our findings may therefore provide a useful approach for generating large numbers of functional β cells for disease modeling and, ultimately, cell-based therapy," they said.

Authors of the paper include Ke Li, Saiyong Zhu, Holger A. Russ, Shaohua Xu, Tao Xu, Yu Zhang, Tianhua Ma, Matthias Hebrok, and Sheng Ding.

A separate report on UK's The Guardian said the researchers' experiments replaced cells in the pancreas unable to make insulin after being damaged by diabetes.

Without insulin, the body will have a hard time absorbing sugars such as glucose from blood. Presently, glucose levels can be monitored and regulated with insulin injections.

The researchers from the Gladstone Institutes in San Francisco collected skin cells (fibroblasts) from laboratory mice and treated them with a mix of molecules and reprogramming factors.

The cells were transformed into endoderm-like cells, the type that eventually mature into the body's major organs including the pancreas.

Li, the lead author, said they used another chemical cocktail to turn these endoderm-like cells into cells that mimicked early pancreas-like cells (PPLCs).

"Our initial goal was to see whether we could coax these PPLCs to mature into cells that, like ß-cells, respond to the correct chemical signals and – most importantly – secrete insulin. And our initial experiments, performed in a petri dish, revealed that they did," Li said.

When the team injected these cells into mice genetically modified to have high glucose levels to mimic the Type 1 diabetes in humans, the mice's glucose levels started to decrease and approach normal levels "just one week post-transplant."

"And when we removed the transplanted cells, we saw an immediate glucose spike, revealing a direct link between the transplantation of the PPLCs and reduced hyperglycemia [high glucose level]," Li said.

Even better, the researchers found the pancreas-like cells turned into fully functional insulin-secreting ß-cells, eight weeks after the transplantation.