URINE TEST FOR DIABETES

Home Urine Test Measures Insulin Production in Diabetes

February 24th, 2011

A simple home urine test has been developed which can measure if patients with Type 1 and Type 2 diabetes are producing their own insulin. The urine test, from Professor Andrew Hattersley's Exeter-based team at the Peninsula Medical School, replaces multiple blood tests in hospital and can be sent by post as it is stable for up to three days at room temperature. Avoiding blood tests will be a particular advantage for children. The urine test measures if patients are still making their own insulin even if they take insulin injections. Researchers have shown that the test can be used to differentiate Type 1 diabetes from Type 2 diabetes and rare genetic forms of diabetes. Making the correct diagnosis can result in important changes in treatment and the discontinuation of insulin in some cases. Jillian, 35 has recently benefitted from the home urine test. She was diagnosed with diabetes aged 19 and put on insulin injections. The urine test identified that she is still making her own insulin 14 years after being diagnosed and a DNA test confirmed that she has a genetic type of diabetes. After 14 years of insulin treatment, Jillian is now off her insulin injections. "Being told I don't have to take insulin injections any more has changed my life", she said. The key studies, led by Dr Rachel Besser and Dr Angus Jones and were funded by Diabetes UK and the National Institute of Health Research, are published in leading diabetes journals, Diabetes Care and Diabetic Medicine. Dr Rachel Besser, who has led the studies on over 300 patients, commented: "The urine test offers a practical alternative to blood testing. As the urine test can be done in the patients own home we hope that it will be taken up more readily, and more patients can be correctly diagnosed and be offered the correct treatment". Dr. Iain Frame, Director of Research at leading health charity Diabetes UK, said: "Dr. Besser's research is an excellent example of Diabetes UK's commitment to fund scientists at the beginning of their careers in diabetes research. With growing numbers of people with diabetes, it's more important than ever to ensure that medically trained graduates are encouraged to enter the field of diabetes research to help improve the lives of people with the condition. Many aspects of diabetes, from diagnosis to treatment, are invasive. Therefore, we welcome Dr. Besser's research and look forward to further developments." Source: Peninsula College of Medicine & Dentistry

AFFECT OF CELL PHONE ON THE BRAIN

Cell phones show effect on brain activity most pronounced near the antenna

February 24th, 2011

In a study of the effects of cell phone usage on brain cell activity, NIH scientists and their colleagues at the U.S. Department of Energy's Brookhaven National Laboratory found that 50 minutes of cell phone usage (with the phone muted to avoid confounding effects from auditory stimulation) elevated brain glucose metabolism significantly in the parts of the brain closest to the phone's antenna. Elevations in glucose metabolism, a measure of brain cell activity, were correlated with the estimated strength of the electromagnetic field emitted by the phone in those regions. The findings are published in the in the February 22, 2011, issue of JAMA. Arrow in the left image shows the location in the orbitofrontal cortex in one subject where glucose metabolism was increased during cell phone use. Red and orange areas shows higher brain metabolic activity. On the right is a baseline image with the cell phone turned off, showing lower activity. "Although we cannot determine the clinical significance, our results give evidence that the human brain is sensitive to the effects of radiofrequency-electromagnetic fields from acute cell phone exposures," said Nora Volkow, the study's lead author. Discrepancies among studies on the effects of RF-electromagnetic fields (RF-EMF) from cell phones on the human brain highlight the need for additional research. Prior studies of the acute effects of cell phone use on human brain function, including measurements of cerebral blood flow monitored by positron emission tomography (PET), have yielded inconsistent results, which might have reflected, in part, the small sample sizes of such studies (the largest studies had 14 subjects). Arrow in the left image shows the location in the orbitofrontal cortex in one subject where glucose metabolism was increased during cell phone use. Red and orange areas shows higher brain metabolic activity. On the right is a baseline image with the cell phone turned off, showing lower activity. The current study, also using PET, provides a more direct measure of brain activity than cerebral blood flow. It uses a radioactively "tagged" form of glucose known as [18F]fluoro-deoxyglucose, or FDG, to measure glucose metabolism in specific regions of the brain. "FDG is a direct substitute for glucose, the brain's fuel. Measuring its concentration in the brain gives a highly specific measure of brain cell metabolism, which is a more direct measure of brain activity than measures of blood flow," Volkow said. Also, because brain glucose metabolic measures obtained with FDG reflect the averaged brain activity occurring over a 30-minute period, this method can assess the cumulative effects of cell phone exposure on resting brain metabolism, unlike blood flow measures, which isolate a more restricted point in time. Scientists conducted the study in 47 healthy individuals. All participants had two scans done on separate days. On both days, prior to the scans, two cell phones, one placed on the left and one on the right ear, were used so subjects wouldn't know which cell phone was active. For one of the days both cell phones were off. For the other day the right cell phone was on but muted while receiving a call from a recorded text. The order of conditions was randomly assigned, and participants did not know when an active phone was being tested. With the cell phones secured to their heads, the subjects sat in a quiet room, not speaking, with eyes open for 20 minutes prior to being injected with the FDG tracer, and then for 30 more minutes, for a total cell phone exposure time of 50 minutes . RF-EMF emissions were recorded once before the call (background) and every five minutes during the "on" phase to ensure that the call was not terminated. Using computational and photographic methods, the scientists were also able to calculate the relative amplitude of the cell phone's electric field at every position in the brain. After the exposure period, the phones were removed and the subjects were placed in the PET scanner for measurements of brain activity. There were no differences in overall brain metabolism between the on and off conditions, but during the on condition, the specific regions of the brain closest to the phone's antenna showed significant increases in brain glucose metabolism. The regions expected to have the greater absorption of RF-EMF from the cell phone exposure were the ones that showed the largest increases in glucose metabolism. "The linear association between cell phone-related increases in metabolism and electric field strength suggests that the metabolic increases are secondary to the absorption of RF-EMF from cell phone exposures," Volkow said. "Further studies are needed to assess if the effects we observed could have potential long-term consequences." This research was funded by the Intramural Research Program of the National Institutes of Health (NIH) using infrastructure supported at Brookhaven Lab by DOE's Office of Science. Source: Brookhaven National Lab

New insight on diabetes

Missing sugar molecule raises diabetes risk in humans

February 24th, 2011

Researchers at the University of California, San Diego School of Medicine and Rady Children's Hospital-San Diego say an evolutionary gene mutation that occurred in human millions of years ago and our subsequent inability to produce a specific kind of sugar molecule appears to make people more vulnerable to developing type 2 diabetes, especially if they're overweight. The findings are published in the Feb. 24 online edition of The FASEB Journal, a publication of the Federation of American Societies of Experimental Biology. Corresponding study author, Jane J. Kim is an assistant professor in the UCSD Department of Pediatrics and a member of the Pediatric Diabetes Research Center and Rady Children's Hospital-San Diego, a research and teaching affiliate of the UCSD School of Medicine. Kim said the findings represent the first documented evidence linking the sugar production to insulin and glucose metabolism problems associated with diabetes. "It opens up a new perspective in understanding the causes of diabetes," said Kim. "Given the global epidemic of obesity and diabetes, we think that these findings suggest that evolutionary changes may have influenced our metabolism and perhaps increased our risk of the disease." Type 2 diabetes is caused by both genetic and environmental factors, such as a fatty diet and lack of exercise, that result in progressively dysfunctional pancreatic beta cells, elevated blood sugar levels due to insulin resistance and eventual health complications, sometimes fatally so. Diabetes is an expanding problem, nationally and globally. In the United States, more than 25 million adults and children � almost nine percent of the population - have diabetes, according to the American Diabetes Association. Another 79 million Americans are estimated to be prediabetic. Worldwide, roughly 285 million people are believed to have the disease. Sialic acids are sugar molecules found on the surfaces of all animal cells, where they act as vital contact points for interaction with other cells and with their surrounding environment. Virtually all mammals produce two types: N-acetylneuraminic acid (Neu5Ac) and N-glycolylneuraminic acid (Neu5Gc). Humans are the exception. For reasons lost in the mists of evolution, a mutation in a gene called CMAH occurred 2 to 3 million years ago, inactivating an enzyme in humans that catalyzes production of Neu5Gc by adding a single oxygen atom to Neu5Ac. Researchers compared two groups of mice: one with a functional CMAH gene, the other with an altered CMAH gene similar to the human mutation. Both groups of mice were fed a high-fat diet. Mice in both groups became obese and developed insulin resistance. However, only mice with the CMAH gene mutation experienced pancreatic beta cell failure � the cells that make and release insulin, a hormone that controls blood sugar levels. Kim said the findings help refine understanding of why obese humans appear to be particularly vulnerable to type 2 diabetes, and also suggest that current animal models used to study diabetes may not accurately mirror the human condition. In clinical terms, she said further research to determine how sialic acid composition affects pancreatic beta cell function may reveal new strategies to preserve the cells, improve insulin production and prevent diabetes. Co-authors of the study are Sarah Kavaler and Alice Jih, UCSD Department of Pediatrics and Rady Children's Hospital-San Diego; Hidetaka Morinaga and WuQuiang Fan, UCSD Department of Medicine; Maria Hedlund and Ajit Varki, UCSD departments of Medicine, Cellular and Molecular Medicine and UCSD Glycobiology Research and Training Center. Funding support was provided by the National Institutes of Health Source: UC San Diego Credit: Eurekalert