Diabetes’ continued menacing presence on a global scale has led to the release of a smorgasbord of pharmaceutical options available for the treatment of diabetes. The majority of today’s drugs address a variety of diabetes symptoms. While they do keep blood glucose in check for the most part, they fail to address the advancement of the illness. Also, many researches have concluded that over time, the body no longer uses the medication as effectively as it once did.
What modern pharmacological progress has been attempting is the concerted effort to halt the advancement of diabetes. This provides the possibility of a better overall outlook for the patient and current medical practitioners’ ability to tackle the many facets of diabetes.
Let’s review some of the drugs that, while still imperfect, have shown incredible promise for future strategies of diabetes treatment.
Glifozans are a class of drug whose function is to increase the renal absorption of glucose molecules. The kidneys filter blood by absorbing water and cellular waste. The glucose contained within the blood, instead of being filtered and passing through urine, gets returned to our blood stream where it gets “back in line” to await transportation (insulin) into our cells where they are utilized for energy. This is a normal function. However, in diabetes, blood sugar is already too high and so it would not make sense for the body to keep returning glucose molecules back into the bloodstream. What glifozins accomplish is that it forces our kidneys to filter circulating glucose from the blood stream where it becomes part of the urinary waste and they also help to keep cardiac pressure in check. The mechanism in which the drug accomplishes this occurs outside the cell membranes of the nephrons; the functional unit of the kidneys. There is a protein that sits at the outer membrane of the nephron that is responsible for reabsorbing the passing glucose back into the blood stream called SGLT2 (Sodium glucose transport protein). Glifozins are SGLT2 inhibitors and therefore retard glucose reabsorption.
Some side effects of glifozins are hypoglycemia and ketoacidosis
We always read about insulin and how it regulates our blood glucose levels but, how many times have you heard incretins come into the picture? Ever wonder how our pancreas knows when to secrete insulin? The communicating hormones responsible for this are produced in certain parts of our digestive system and are called incretins. One of them is GLP-1 (formerly Glucagon-like Peptide 1) and the other is GIP (Gastric Inhibitory Peptide). Both these hormones serve a special function, that is, they “instruct” the pancreas to begin releasing insulin. Conveniently, this occurs after we eat.
Synthetic GLP-1 drugs have been developed to mimic the function of natural incretins to maximize the amount of insulin released into the blood stream.
Currently, GLP-1 imitating drugs are only available by injecting subcutaneously.
Betatrophins are a type of peptide that have been under scrutiny over the last few years. According to research, betatrophins are major players in the enhancement of insulin creation because they encourage enhanced mitotic division of the beta cells responsible for producing insulin. The thinking here is, if we stimulate beta cells to reproduce more, the greater the amount of insulin the pancreas can secrete.
It was discovered some time ago that mice actually carry a gene that produces betatrophins as well. Scientists recently studied the effects of this drug in the metabolism of glucose in mice and it was found to significantly reduce blood glucose levels. However, as we have seen, glucose regulation is a balancing act and betatrophins have also been known to induce hypoglycemia. If trials in human beings proves successful, it would be a major breakthrough in the current advancement of diabetic’s treatment.