Prolonged immunosuppression and euglycaemia with beta-cell allograft, does not dramatically improve native beta-cell function, according to a report in the journal Diabetologia.

A number of studies support persistent beta-cell survival years after Type 1 diabetes onset.

To test the hypothesis that long-term treatment for autoimmunity and beta-cell failure would provide the best environment for native islet recovery, David Harlan (National Institutes of Health, Bethesda, Maryland, USA) and colleagues measured native pancreatic C-peptide production in people with Type 1 diabetes who had undergone islet or whole-pancreas transplantation.

C-peptide levels were measured in 141 potential participants for the islet transplant study.

Three islet and four whole pancreas allograft recipients with successful clinical outcomes (insulin-independent euglycemia for at least 1 year following the procedures) underwent selective arginine stimulation (SAS), which can discriminate between the C-peptide produced by the native pancreas and that produced by the beta-cell allograft.

A basal or arginine-stimulated C-peptide level of at least 0.167 nmol/l (normal range in healthy individuals is 0.30??”1.33 nmol/l) was reported in 54 of 141 (38%) potential study participants.

“These data suggest that pancreatic insulin function persists in over a third of individuals with long-standing Type 1 diabetes, but is minimal and often detectable only after appropriate stimulation and with sensitive C-peptide assays,” write the authors.

Following the SAS technique all three islet allograft recipients displayed some evidence of native pancreatic C-peptide production at least 2 years after their last islet allograft infusion.

To determine whether longer term (at least 4 years) immunosuppression and euglycemia might promote clinically significant regeneration, the SAS technique was repeated in four successful pancreas allograft recipients.

While all recipients displayed evidence that their native pancreas secreted C-peptide, the magnitude of the effect was very small, similar to that seen in the islet recipients.

“Our present study suggests that vigorous beta-cell regeneration does not occur in patients with long-term Type 1 diabetes after islet or pancreas transplantation,” conclude the authors.

“While beta-cell regeneration cannot be completely ruled out, these data suggest that the process is not robust given allograft-mediated restoration of glucose metabolism and currently available immunosuppression,” they add.

MedWire (www.medwire-news.md) is an independent clinical news service provided by Current Medicine Group, a part of Springer Science+Business Media. © Current Medicine Group Ltd; 2009

Free abstract

Diabetic neuropathy patients with high triglycerides have increased myelinated fiber density (MFD) loss compared with neuropathy patients with lower triglycerides, report researchers.

Peripheral neuropathy, involving damage to nerves in the hands, arms, legs, and feet, is the most common complication of diabetes, affecting 60% of Type 1 and 2 diabetic patients.

In this study, Eva Feldman (University of Michigan, USA) and colleagues investigated mechanisms underlying the progression of diabetic neuropathy in 427 patients (78% Type 2 diabetes) using indices of sural nerve morphometry obtained at baseline and after 1 year.

Progression of neuropathy was defined as a loss of 500 fibers/mm² or more in sural nerve MFD over 1 year. The researchers found that individuals who had progressing MFD had a 25% decrease in MFD from baseline compared with those whose condition was unchanged.

As reported in the journal Diabetes, the researchers found that elevated triglycerides and decreased peroneal motor nerve conduction velocity (NCV) at baseline were significantly associated with MFD loss at 1 year.

The association with raised triglycerides was independent of disease duration, age, diabetes control, or other variables.

Of note, peroneal NCV, although significant, was only 5% different between groups and therefore did not contribute much to the predictive model.

“These results set the stage for clinicians to be able to address lowering lipid counts with their diabetes patients with neuropathy as vigilantly as they pursue glucose control,” said Feldman.

Co-investigator Rodica Pop-Busui, also from the University of Michigan, added: “Our findings in this study reinforce the tight links between cardiovascular disease and peripheral neuropathy in patients with diabetes.

“We demonstrated that the same lipid particles that contribute to the progression of atherosclerosis are also very important players in peripheral nerve fiber loss.”

MedWire (www.medwire-news.md) is an independent clinical news service provided by Current Medicine Group, a part of Springer Science+Business Media. © Current Medicine Group Ltd; 2009

Free abstract

They say misconceptions can kill. Well, Diabetes misconceptions have killed and will continue to kill many for years to come. We know so much about diabetes. We get information from many sources. From TV, from magazines, from the internet, from a neighbor, from the barber and from many other reliable and not-so-reliable sources.

This is precisely the reason why despite the fact that we know so much, still many more keep dying from this disorder. Because we fail to filter the chaff from the grain. And if we want to avoid Diabetes complications, we have to correct our deep-seated misconceptions.

1.”I’m not fond of sweets.”

Although a penchant for sweets will hasten your membership to the Honey Club, an aversion to it does not guarantee immunity from the disorder. First of all, sugar can be found NOT ONLY in sweets. ALMOST ALL the carbohydrates we take will be converted into sucrose (table sugar) by our intestinal enzymes and ultimately into glucose (blood sugar) before being absorbed into the blood. This would include bread, rice, root crops, and even unripe fruits. So, if your attention is focused only on sweets, you’ll have been shot from behind and you’ll never know what hit you.

2. “We don’t have a history of Diabetes!”

It would be difficult to trace all our relatives up to the 4th degree. And although advances in travel have made migration easier, it has also made recognition of distant relatives more difficult, and increasingly irrelevant. Until we find the need to trace our lineage.

3. “My blood sugar was normal last year.”

With the average western diet these days, yearly blood sugar monitoring is probably inadequate to guard against the onslaught of Diabetes in any individual. And besides, by the time your blood sugar goes up, Diabetes has been doing damage to your tissues for the past 10 yrs. An increase in blood cholesterol leading to hardening and narrowing of the arteries begins years before the blood sugar even starts to go up. It’s a Trojan Horse that does the damage while you snugly sleep, oblivious to the web of complications that this illness cunningly weaves.

4. “My cuts easily heal.”

Just like in No. 3, delayed healing of wounds is a late complication of Diabetes. So why wait to be a candidate for amputation? Landmines have done enough damage to innocent lives.

5. “My urine sugar is normal.”

Sugar in the urine is an effect of “filtration overflow”. When the sugar in the blood exceeds the kidney’s capacity to filter it, the sugar overflows into the urine. So in kidneys with high filtering capacity, the urine sugar may be negative in spite of a very high blood sugar. Are you going to wait for the bucket to spill before turning off the tap?

There are many other misconceptions regarding this terrible disease. Too many, in fact to occupy too many Ezine articles. But I suppose I have made my point. And if we are able to change our notion of this terrible disease, we might be able to transform our reaction to it from that of “What’s in it for me?” to “What can we do?”.

So if we think that we are exempted from this dreaded disease, that would be another misconception. Why don’t we take more time to learn more about it? And with the right information, we might be lucky enough to indeed get exempted.