The theory is that home glucose monitoring works by helping patients adjust their medications and encourages them to take their diabetes more seriously, motivating diabetics to change their behaviour.
The researchers are suggesting that the current guidelines for self-monitoring among well-controlled, non-insulin dependent (type 2) diabetic patients needs to be reviewed.
The suggestions have come about as a result of a study by Dr. Andrew Farmer and colleagues at the Department of Primary Health Care at Oxford University.
For the study, Farmer's team randomly assigned 453 patients with type 2 diabetes to one of three groups; one group had their blood sugar level checked three times a month; the second group was given a meter to test their blood sugar at home and told to have their doctor interpret the results, while a third group was given meters and taught how to interpret the findings themselves.
As a rule, non-insulin dependent (type 2) diabetes appears in people over 40, particularly when the person is overweight and in most cases a change in diet, loss of weight and oral medication controls the condition, and insulin injections are not needed.
Self monitoring for type 2 diabetes is a costly business but many doctors believe that it helps to control blood glucose levels and commonly recommend it but the researchers say the cost, effort and time involved in the procedures may be better used in other health-related behaviours.
It appears that after a 12 month period the researchers found there was no evidence that blood glucose monitoring, with or without instruction, improved glucose control compared with usual care.
The team also found that half of the people who had been given the glucose monitors stopped using them before the end of the study.
The findings which were presented at the American Diabetes Association Conference in Chicago, do not apply to type 2 diabetics who must take insulin.
These changes contributed to the ability of these mice to fend off weight gain despite a high-fat diet and lack of exercise. Together these results suggest that a CD38 deficiency has a protective effect against high-fat, diet-induced obesity, Dr. Chini says.
Dr. Chini and colleagues also examined the effects of resveratrol in mice. Resveratrol is a naturally occurring substance found in some plants such as mulberries, peanuts and red grapes used to make wine. It has been marketed as a drug that mimics the effects of moderate exercise without the physical act of exercising and also as a longevity drug, despite the lack of evidence that resveratrol is safe and effective in humans.
Mice with CD38 were treated with 30 milligrams (mg) of resveratrol per day. And, to determine the effects of the SIRT genes on obesity, mice without CD38 received the same dose of sirtinol, a drug that shuts down the SIRT genes.
Researchers found that mice with CD38 that were treated with resveratrol for two weeks were protected from high-fat, diet-induced obesity. By contrast, the protective effect against high-fat, diet-induced obesity in the absence of CD38 in mice was invalidated by sirtinol. Mice without CD38 that were treated with sirtinol gained a statistically significant amount of weight when compared with mice without the gene who were not treated with sirtinol.
This data supports the novel notion that CD38 modulates high-fat, diet-induced obesity by a SIRT- dependent mechanism.
Together these results identify a novel pathway regulating body weight and clearly show that CD38 is a nearly obligatory component of the cellular cascade that led to diet-induced obesity, the authors write.
The authors say the study's results are promising and should be explored in follow-up studies that will focus on the quality of life and longevity in mice.
mayoclinic/