Mouse hormone will win diabetes
It allows the body to independently regulate insulin production.
With the discovery of a new hormone in insulin-dependent diabetics, there was hope to replace the daily three-time injections with one injection of a hormone a week or even a year. The presence of this hormone in the liver increases the rate of reproduction of cells producing insulin thirty times.
Online Cell Magazine April 25th a message appeared on the discovery, which could be a giant breakthrough that could lead to a complete cure in people of type 2 diabetes and a significant relief of life for patients with type I diabetes. This is a new hormone discovered by researchers from the Harvard Stem Cell Institute.
In mice, this hormone, called betatrophin , leads to a rabid multiplication of beta cells responsible for insulin secretion.
It is noteworthy that new cells produce insulin only when the body begins to feel the need for it. In other words, a potential opportunity has been revealed to initiate the natural regulation of insulin in the blood, so far, however, only in mice.
Betatrophin was discovered during experiments on rodents, which artificially caused insulin resistance. Shortly thereafter, scientists have found and the gene, the expression of which leads to the appearance of this hormone.
When an extra copy of this gene was introduced into the liver of normal mice, the beta cells began to multiply 30 times faster than the normal level.
The effect was quite stable – even a week after the injection, animals showed a more than twofold excess of the number of beta cells compared with the normal norm. Curiously, betatrophin had no effect on the growth of the remaining cells.
The authors of the article emphasize that in order to treat human diabetes with the help of betatrophin , a great deal of research work is needed, but even now their discovery is extremely interested in drug manufacturers. There is talk that the Harvard group has already begun to cooperate with one of the German pharmaceutical companies in order to further research betatrophin and begin its clinical trials. And there are a lot of chances for success, as this hormone is present in the human liver and is encoded by the same gene as in mice.
“Of course, we did not set ourselves the goal of curing diabetes mice, – says the main author of the article Douglas Melton. – The goal, naturally, was a human disease.
And if our discovery turns out to be suitable for people, then ultimately three times a day insulin injections can be replaced with weekly or monthly hormone injections. It is even possible that annual injections will suffice. ”
Especially important, according to Melton, the fact that the body will produce its own insulin – this will help to avoid complications, sometimes leading to amputation.
For 15 years, Melton has been researching type 1 insulin-dependent diabetes — mainly because his son (and then his daughter) were victims of the disease. For a long time, the objects of his interest were stem cells that are not directly related to betatrophin . Despite the fact that, as Melton says , the discovery of betatrophin was the fruit of long labors and in-depth analysis, it was not without a bit of luck.Scientists drew attention to a fact that was known for a long time, but did not arouse much interest – that during pregnancy the body’s need for insulin increases due to the increased weight and fetal needs.Starting work with pregnant mice, they found that the betatrophin already discovered by them leads to an increase in the number of cells. Deciding to add an additional copy of the hormone-encoding gene to the mice, they expected that the number of beta cells would increase even more, but a thirtyfold excess of the normal level of reproduction even for them was a complete surprise.
Gene therapy reduces blood sugar
Activating a particular gene allows insulin production to increase, according to research from the Vailor Medical Academy in Houston.
They inserted the neurogenin3 gene into the liver of diabetic mice and revived mature stem cells, forcing them to produce the necessary hormone.
Already a week after the introduction of the gene with the help of an inactivated virus, the blood sugar level in mice with type 1 diabetes reached the norm.
Penetrating into the cells of the liver, neurogenin3 causes them to produce small doses of insulin, sufficient to reduce sugar levels.
“However, these cells lose this ability after six weeks,” – said Dr. Viya Ichor , assistant professor of endocrinology.
Other cells that produce more insulin form later around the portal veins that supply the blood to the liver. They are like insulin producing islands of Langerhans and grow from mature stem cells.
Usually, this reserve is reserved in case of damage to the liver, however, neurogenin3 rebuilds them to produce insulin .
Revision of consensus on the treatment of diabetes mellitus 2
The American Diabetes Association and the European Association for the Study of Diabetes at the end of 2007 promptly updated the guidelines for the treatment of type 2 diabetes. Experts associate such a quick revision with the publication of the results of new clinical trials and studies, according to which the use of thiazolidinediones is associated with a negative effect on the health of some patients with type 2 diabetes.
Several meta-analyzes emphasize that rosiglitazone , one of the modern thiazolidinediones , increases the risk of myocardial infarction by 30–40%. It is also important that one of the meta-analyzes is presented by the manufacturing company ( GlaxoSmithKline ) and one by the organization that regulates the pharmaceutical market, despite the fact that the data presented cannot be considered final. Another study found that taking not only rosiglitazone , but also pioglitazone is associated with an increased risk of cardiovascular events (in particular, pioglitazone – with the risk of sudden death!).
Rosiglitazone or pioglitazone should also be carefully prescribed to patients who, along with type 2 diabetes, have manifestations of congestive heart failure. These drugs almost double the risk of fluid retention in the body. It is this side effect that caused the appearance of a “black square” (a kind of “black tag”) on the packaging of these drugs.
This type of labeling requires more careful familiarization of patients with the instructions for use in order to avoid the development of life-threatening complications. It was also found that rosiglitazone andpioglitazone increases the risk of fractures in women in those parts of the upper and lower extremities (forearm, hand, wrist, foot, ankle, fibula), which are not typical for osteoporosis.
It seemed easier to remove these drugs from the treatment algorithm, and there was no problem. For example, insulin and sulfonylurea drugs can be added to metformino in all cases when its purpose with lifestyle modifications does not allow reaching the target (<7 %) level of HbA1c. However, experts believe that it is thiazolidinediones that, to a lesser extent than other second-line drugs, cause hypoglycemia (a sharp drop in blood glucose), which is why they were left with the above-mentioned restrictions among second-line drugs for the treatment of type 2 diabetes. An updated FDA-approved drug, sitagliptin (a dipeptidyl peptidase-4 inhibitor), is included in the updated guidelines for the treatment of type 2 diabetes . It is expected that his admission will allow for 0.5-0.8% to reduce the level of HbA1c.
The positive properties of the new drug include the lack of influence on the weight of the patient, the negative – insufficient knowledge and high price.