Kidney failure, amputations, blindness, heart attack and stroke complications by delaying insulin therapy among patients with type 2 diabetes
An uncontrolled high blood glucose levels over a period may lead to diabetes complications such as kidney failure, amputations, blindness, heart attack and stroke. A Sanofi funded study by researchers shows 30 percent of the insulin required patients with type 2 diabetes (to control high blood sugar levels) are not starting insulin therapy when their physician advises them. On an average, patients with diabetes are delaying the start of the treatment by about two years and by that time their blood glucose levels had increased further.
Researchers have examined 3,295 patients with diabetes information in the electronic physician notes between 2000 and 2014 at the Brigham and Women's Hospital, Boston, Massachusetts, United States. Their study shows nearly one-third of the patients didn't start the insulin injection therapy when their physician advised them. Patients may be delaying insulin treatment because
Senior author of the study was Dr. Alexander Turchin, MD, MS, Associate Professor, Harvard Medical School, Boston, United States. The study findings were published September 14, 2017, in the Diabetic Medicine. Title of the article was "Decline of insulin therapy and delays in insulin initiation in people with uncontrolled diabetes mellitus."
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Relief for chronic diabetic nerve pain or neuropathy by blocking HCN2 protein
About 25 percent of the diabetic patients were affected with diabetic nerve pain, disorders or damages affecting throughout the body including arms, hands, feet and legs. Normal pain-relieving drugs may not give relief to nerve pain because the pain in the sensory nerves was caused due to high blood sugar glucose levels (type 2 diabetes T2D). Currently, there is no effective treatment for it. A study by the researchers at the King's College London, United Kingdom, confirms the role of hyperpolarization-activated cyclic nucleotide-gated 2 (HCN2) gene or protein in the chronic diabetic nerve pain.
Researchers have conducted experiments with diabetic mice models. They found that overactive HCN2 gene promotes pain sensation by inducing and maintaining electrical signals in nociceptive (a receptor) neurons. Researchers successfully stopped nerve pain sensation by "genetically deleting" or blocking HCN2 channels in nociceptive (a receptor) neurons.
Currently, there are no selective drugs which can suppress HCN2 protein activity without affecting other organ functions (for example heart rate regulation). Researchers say painful diabetic neuropathy or chronic nerve pain may be treated by developing new drugs which can selectively target HCN2 protein without disturbing other molecules.
The first author of the study was Dr. Christoforos Tsantoulas, Department of Pharmacology, King's College London and senior author of the study was Professor Peter McNaughton, Wolfson Centre for Age-Related Diseases, King's College London, United Kingdom. The study findings were published on September 27, 2017, in the journal Science Translational Medicine. Title of the article was "Hyperpolarization-activated cyclic nucleotide-gated 2 (HCN2) ion channels drive pain in mouse models of diabetic neuropathy."
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Published by Jammi Vasista, Chennai, India.