World Diabetes Day: PeerJ Research and Academic Editors Highlights
World Diabetes Day is an annual day of awareness, held on the November 14, to keep diabetes firmly in the public spotlight. According to the official website, more than 371 million people have diabetes, and the top 3 countries with diabetics are China, India, and USA. It became an official United Nations Day in 2007, and the day itself marks the birthday of Frederick Banting who, along with Charles Best, first conceived the idea that led to the discovery of insulin in 1922.
In honor of World Diabetes Day, we highlight some of our PeerJ Academic Editors experts in the field, as well as recently published PeerJ articles.
Leif C. Groop, PeerJ Academic Editor, is a Professor of Endocrinology at Lund University and the Director of Lund University Diabetes Centre. He devoted his research to dissect the heterogeneity of diabetes and to explore the pathogenic events leading to type 2 diabetes. As an important tool to achieve this goal, he initiated the Botnia Study at the west coast of Finland, one of the world’s largest family studies on type 2 diabetes. His group has been involved in many of the genetic discoveries on type 2 diabetes during the past 15 years, including one of the first whole genome association studies for type 2 diabetes. We asked Prof Groop to share his hopes on finding a treatment for this disease.
“Diabetes, particularly type 2 diabetes is the fastest increasing disease worldwide with an estimated prevalence of 350 million patients today and a predicted increase to more than 550 million by 2030. The disease results from a collision between a genetic predisposition and a westernized environment. Although we know how to change the lifestyle, we have not been very successful. Therefore, the hope is that by dissecting the genetic causes of type 2 diabetes, we could identify novel treatment targets aiming at the underlying molecular defects.”
Arthur Sherman, PeerJ Academic Editor, is a Senior Investigator at the Laboratory of Biological Modeling, National Institute of Diabetes and Digestive and Kidney Diseases, NIH. We asked him about his research on diabetes and oscillations of insulin secretion.
“Type 2 diabetes results from the confluence of two distinct pathologies, inefficient use of insulin (insulin resistance) and inadequate insulin secretion (relative to the increased demand imposed by insulin resistance). One important aspect of insulin secretion is that it is oscillatory, with pulses approximately every five minutes. These pulses have been shown to be more efficient in controlling glucose metabolism in the liver than steady secretion, and they are disrupted in both people with type 2 diabetics and their non-diabetic relatives. The pulses originate in oscillatory electrical activity in the pancreatic beta cells, which I have been studying for many years with my colleagues Les Satin (University of Michigan) and Richard Bertram (Florida State University) through a combination of experiments and mathematical modeling. We have amassed considerable evidence to support a model in which the oscillations are driven by oscillations in metabolism, specifically glycolysis, in the beta cells. This is natural because the beta cells use their own metabolic rate as a surrogate for the glucose concentration in the circulation in order to regulate how much insulin they secrete. A deeper understanding of the interactions of metabolism and electrical activity may lead to better treatments to enhance insulin secretion in people with diabetes.”
Brian Wells is a Family Physician and Epidemiologist. He is an Associate Staff Member in the Department of Quantitative Health Sciences at the Cleveland Clinic where he trained as a post-doctoral fellow with Michael Kattan, PeerJ Academic Editor, Professor and Chair of the Department.
They have published two articles with us, and today, they comment on “Prediction of morbidity and mortality in patients with type 2 diabetes”.
“Head-to-head comparisons of clinical outcomes between oral hypoglycemic agents for the treatment of type 2 diabetes are lacking, which makes informed treatment decisions difficult. Patients with the best glycemic control do not always experience the best outcomes, and physicians must balance the risk of multiple complications simultaneously while also considering the individual patient’s characteristics. This project used data on 33,000 patients with type 2 diabetes in the Cleveland Clinic electronic health record to create an online calculator that predicts the risk of heart disease, heart failure, mortality, and stroke according to unique patient characteristics. Separate risk is calculated for four commonly used hypoglycemic agents. The calculator outperformed the Framingham model in predicting heart disease and is available for free online at http://rcalc.ccf.org. The tool may aid the clinician’s choice of hypoglycemic agent and motivate dialogue between physician and patient.”
Izuho Hatada is a Professor at the Institute for Molecular and Cellular Regulation, Gunma University, Japan. We asked him to comment on his PeerJ article “MiR-184 regulates insulin secretion through repression of Slc25a22”.
Here is what he said: “Pancreatic islet beta cells play an important role in glucose homeostasis by secreting insulin. Secretion of an inappropriate amount of insulin, as a result of β cells dysfunction, leads to diabetes. MicroRNAs are small non-coding RNAs that function as specific regulators of gene expression. However, the role of these tiny RNAs in insulin secretion and diabetes had not been exhaustively studied. We found that miR-184, a microRNA enriched in islets and its expression negatively correlated insulin secretion, inhibits insulin secretion in the MIN6 pancreatic beta cell line through the repression of its target Slc25a22, a mitochondrial glutamate carrier. Our study provides new insight into the regulation of insulin and a new target for diabetes drug.”