Diabetes Research

Diabetes 2001;50: 1691-1697 reports that Israeli researchers have derived cells from human embryonic stem (hES) cells that are capable of producing insulin and share several markers of pancreatic islet beta-cells. This research finding has been called "exciting" by the President of the ADA, who went on to say, "Up until this point, we had just thought it was possible. Now we know it can be done." We all know the President has made up his mind about this type of research. Maybe now is the time to e-mail the President president@whitehouse.gov to thank him and ask him to enlarge the program. While you're at it, contact your Senators and Congressmen. We in the US have never done federally funded research, so this type of research is slow in the US. We need major funding, so keep the pressure on as the Congress will be funding this research for all of us. Never should a child be subjected to what I, as an adult, must do 24/7. It's time for us to fund the "cure."

American Medical News, Vol 44, No.29 has an article on education being the key to safety in substituting diabetic supplies and talk about the growing substitution of generic supplies in some drug stores. You can read of concerns by visiting www.amednews.com.

The Associated Press has reported that scientists may have found a hormone that helps fight diabetic insulin resistance. The hormone, called adiponectin or Acrp30, helped diabetic mice overcome insulin resistance in tests done in Japan and New York. Phillip E. Scherer at Albert Einstein College of Medicine and Takashi Kodowaki' s team at the University of Tokyo both got similar results. Although the results are preliminary, and the researchers differ in their assessment of how the hormone works, their papers show that fat is more than just a storehouse for energy. It also produces needed chemicals such as adiponectin. The main message from this research "is that fat tissue can release factors that influence insulin sensitivity in other tissues. Activation of this protein or its receptor may offer a way to improve insulin sensitivity in insulin resistant patients and may offer a complementary therapeutic approach to existing treatments" reported Scherer. Researchers found adiponectin is reduced in obese mice, making them unable to use insulin.

"Levels are usually inversely correlated with fat mass-that is, the more fat, the less adiponectin, which is surprising for a protein which exclusively originates in fat" said Scherer.He concluded that adiponectin works on the liver causing it to secrete less sugar into the bloodstream. The Japanese believe the primary effect of adiponectin to be in skeletal muscle, where it causes fat to burn. The reduction in fat led to a reduction in fatty acids circulating in the blood and the liver, and that led to the drop in blood sugar. Researchers will continue to look into these findings. Genset, a French pharmaceutical company, has found that adiponectin caused obese mice to lose weight and plans to conduct further trials on the hormone as a weight-loss drug. Keep tuned and we will too.

Our second abstract comes form Diabetes Care 24:1384-1389,2001 and is titled The Marital Relationship and Psychsocial Adaptation and Glycemic Control of Individuals with Diabetes by Paula M. Trief, Ph.D. et al. The objective of the multi-site study was to explore the relationship between marital relationship domains (i.e., intimacy and adjustment) and glycemic and psychosocial adaptation to diabetes. The research design included a total of 78 insulin-treated adults with both type 1 and type 2 diabetes who were assessed on a single occasion. They completed two marital quality measures and four quality of life measures. Glycemic control was assessed by HbA1c. Demographic data of age, sex, type and duration of diabetes, years married, other medical conditions, family history, disability, and years of education were gathered from the patient charts and questionnaires.

The results indicated that psychosocial adaptation, both the marital quality measures were predictors of aspects of adaptations. Better marital satisfaction was related to higher levels of diabetes-related satisfaction and less impact, as well as less diabetes-related distress and better general quality of life. Higher levels of marital intimacy were related to better diabetes-specific and general quality of life. Concerning glycemic control, there was a nonsignificant trend for marital adjustment scores to relate to HbA1c. The researchers concluded that for insulin-treated adults with diabetes, quality of marriage is associated with adaptation to diabetes and other aspects of health-related quality of life. Marital adjustment may relate to glycemic control and warrants further study. Further work should also explore the impact of couples-focused interventions on adaptations, adherence, and glycemic control.

Diabetes Care 24:1384-1352, 2001 has an article titled Long Term Trends in Childhood Diabetes Mortality:1968-1998 by John H. DiLiberto, MD, Ph.D. and Rodney A. Lorenz. MD. The objective was in the context of recent improvements in type 1 diabetes therapy, to describe longitudinal trends in mortality attributable to childhood diabetes and to investigate socioeconomic and health services correlatives of mortality. They extracted motality data for 1968-1998 from the National Center for Health Statistic files and covariates from the Bureau of Health Professions Area Resource File. Analytical techniques included linear and Poisson regression, and standard descriptive statistics. The results indicated that childhood (defined as 1-19 years of age) age-adjusted mortality from diabetes declined from 9.5 (1968) to 3.0 (1984) deaths per 10 million but remained relatively constant subsequently. All-cause childhood mortality, however. continued to decline. Older children experienced higher mortality rates, as did those living in countries with higher levels of unemployment. The researchers concluded that despite recent improvements in therapy, diabetes-related mortality among children has not declined for 14 years. This finding may be partially attributable to sociodemographic factors influencing access to care, but the remaining mortality may defy available treatment methods. Reducing childhood diabetes mortality rates below the current apparent plateau may require prevention and/or treatment strategies.

The Archives of Internal Medicine, Vol.262 no 12, June 25, 2001 has an article titled Physical Activity and Television Watching in Relation to Risk for Type 2 Diabetes Mellitus in Men by Frank B. Hu, MD et al in which the researchers, knowing that TV watching as a major sedentary behavior in the US has been associated with obesity, hypothesized that prolonged TV watching may increase the risk for type 2 diabetes. In 1986, 37,918 men aged 40 to 75 years of age and free of diabetes, cardiovascular disease, and cancer completed a detailed physical activity questionnaire. Starting from 1988, participants reported their average weekly time watching TV on biennial questionnaires. The results indicated that a total of 1058 cases of type 2 diabetes were diagnosed during 10 years of follow-up. After adjustment for age, smoking, alcohol use, and other covariates, the relative risk (RRs) for type 2 diabetes across increasing quintiles of metabolic equivalent hours per week were 1.00, 0.78, 0.65,0.58, and 0.51. Time spent watching TV was significantly associated with higher risk for diabetes. After adjustment for age, smoking, physical activity levels, and other covariates, the RRs of diabetes across categories of average hours spent TV per week were 1.00, 1.66, 1.64, 2.16, and 2.87 respectively. This association was somewhat attenuated after adjustment for body mass index, but a significant positive gradient persisted. The researchers concluded that increasing physical activity is associated with a significant reduction in risk for diabetes, whereas a sedentary lifestyle indicated by prolonged TV watching is directly related to risk. Their findings suggest the importance of reducing sedentary behavior in the prevention of type 2 diabetes.

JAMA 2001;286:327-334 had an article titles Inflammation May Have a Pathogenic Role in Diabetes Mellitus by Paul M. Ridker, MD et al. As we reported to you researchers are looking at an association between two markers of inflammation, C-reactive protein (CRP) and interleukin 6 (IL-6), and the development of type 2 diabetes. In this study this relationship emerged in a prospective, nested case-control study involving participants in the ongoing Woman's Health Study, a primary prevention study launched in 1992. The association was reported that baseline levels of CRP and IL-6 were significantly higher in 188 woman who developed diabetes than in 362 matched controls who did not develop the disease according to the report. Women in the highest quartiles of CRP and IL-6 have relative risks of developing diabetes of 15.7 and 7.5, respectively, compared with women in the lowest quartiles. On adjusted multivariate analysis, elevated CRP remained a "powerful independent" risk factor for diabetes, but the impact of elevated IL-6 dropped to borderline statistical significance. Dr. Ridker's team notes that these findings were "robust in sensitivity analysis limited to subjects with a baseline HbA1c of 6% or less and were consistently in both obese and nonobese individuals." In comments Dr. Ridker said that "the data are very exciting because they suggest that there may be new ways to both detect and prevent diabetes. The data should also point us in several directions in that they raise the possibility that anti-inflammatory strategies may hold promise for diabetes."

BSP