New study on Metformin
London, Aug 8 (IANS):
A study involving over 180,000 people has shown that patients treated with the widely prescribed diabetic drug metformin can live longer than non-diabetics.
The drug has anti-cancer and anti-cardiovascular disease benefits and can offer surprising health benefits to non-diabetics also, indicates a promising research.
"What we found was illuminating. Patients treated with metformin had a small but statistically significant improvement in survival compared with non-diabetics," claimed Craig Currie, professor at Cardiff University's school of medicine. "Those treated with another common diabetes drug called sulphonylurea had a consistently reduced survival compared with non-diabetic patients," he said, adding that this was true even without any clever statistical manipulation.
The life expectancy of these cohorts was also compared against non-diabetics who were matched based on criteria that included age, gender, same general practice, smoking status and clinical status.
Inflammation, defective Insulin signaling, and mitochondrial dysfunction as common molecular denominators connecting Type 2 Diabetes (T2D) to Alzheimer Disease (AD)
A growing body of evidence supports an intriguing clinical/epidemiological connection between AD and T2D. T2D patients have significantly increased risk of developing AD and vice versa. Recent studies have begun to reveal common pathogenic mechanisms shared by AD and metabolic disorders, notably obesity and T2D. In T2D and obesity, low-grade chronic inflammation is a key mechanism leading to peripheral insulin resistance, which progressively causes tissue deterioration and overall health decline. In the brain, proinflammatory signaling was recently found to mediate impaired neuronal insulin signaling, synapse deterioration, and memory loss Here, we review evidence indicating that inflammation, insulin resistance, and mitochondrial dysfunction are common features in AD and T2D.
Clinical take home message:
Dementia and its underlying neuronal dysfunction are exacerbated or driven by peripheral inflammation. Identification of central and peripheral inflammation as potential mediators of brain dysfunction in AD may lead to the development of effective treatments for this devastating disease.
An Evaluation of the Current Type 2 Diabetes Guidelines: Where They Converge and Diverge?Tan E, Polello J, Woodard LJ, et al. Clinical Diabetes. 2014:3(32):132-39.
Key review points:
American Diabetes Association (ADA), the World Health Organization (WHO), the American Association of Clinical Endocrinologists (AACE), the Indian Health Service (IHS) and the Center for Medicaid and Medicare Services (CMS) guidelines are available to support Healthcare Professionals (HCPs) in caring for patients with type 2 diabetes. The article includes guidelines recommendation in the areas of screening, diagnosis, management and prevention of type 2 diabetes. The abstract version will be focused on the management. Management All five sets of guidelines are in agreement that patients can benefit from medical nutrition therapy and diabetes self management education. Diabetes education may help to improve glycemic control, long-term diabetes management and weight management. Target glycemic control- A1C < 7% (ADA, WHO and HIS), A1C = 6.5% (AACE). Stricter A1C goals will benefit for patients with longer-life expectancy, few comorbid conditions and little to no history of hypoglycemia. Elderly patients would benefit from a less stringent A1C goal. Patients with chronic diseases - Immunizations should be kept up-to-date to minimize the risk for complicating infections.
Clinical take home message:
Healthcare professionals should consider the individualized needs of their patients based on each patient's medical history, comorbid conditions, age and other factors. Above all, patients must be the focal point of the decision-making process to increase the likelihood of success.
Brought to you by Dr. Reddy's, the makers of Glimy-M (Glimepiride + Metformin tablets).
*Reference
**For the reference of a registered medical practitioner.
Blockade of Na+ Channels in Pancreatic a-Cells Has Antidiabetic Effects.Dhalla AK, Yang M, Ning Y, et al. Diabetes. 2014;63(10):3545-3556.
Key review points:
Pancreatic a-cells express voltage-gated Na+ channels (NaChs), which support the generation of electrical activity leading to an increase in intracellular calcium, and cause exocytosis of glucagon Ranolazine, a NaCh blocker, is approved for treatment of angina Ranolazine has been shown to reduce HbA1c levels in patients with type 2 diabetes mellitus and coronary artery disease; however, the mechanism behind its antidiabetic effect has been unclear When tested for the hypothesis that Ranolazine exerts its antidiabetic effects by inhibiting glucagon release via blockade of NaChs in the pancreatic a-cells, the results shows that Ranolazine, via blockade of NaChs in pancreatic a-cells, inhibits their electrical activity and reduces glucagon release Glucagon release in human pancreatic islets is mediated by the Sodium voltages (Nav) 1.3 isoform In animal models of diabetes, Ranolazine and a more selective NaCh blocker lowered postprandial and basal glucagon levels, which were associated with a reduction in hyperglycemia, confirming that glucose-lowering effects of Ranolazine are due to the blockade of NaChs.
Clinical take home message:
Major factor contributing to increased glucagon levels may lie at the a-cell level (i.e., hypersecretion of glucagon), which can be corrected by the blockade of Nav1.3 channels.
Diabetic Foot
