No description available.

No description available.

Class of 2007 Abstract / Objectives: To determine the effect of antihypertensive use on renal function and other diabetic complications in adults over the age of 18 with type 2 diabetes mellitus (DM). Methods: A retrospective secondary analysis of the NIH Pima epidemiologic data included 1,828 individuals with type 2 DM were evaluated for antihypertensive use and DM complications. Statistical analysis was done using general linear model regression (GLM) or logistic regression models controlling for age, sex and DM duration. Three groups were established to evaluate antihypertensive use Group 1 those taking antihypertensives to those not taking antihypertensives, Group 2 those taking more than one (multiple) antihypertensives to those only taking one and Group 3 those taking an angiotensin converting enzyme (ACE) inhibitor to those not taking an ACE. Results: Group 1 those taking antihypertensives were significantly worse for all outcome measures than those taking no antihypertensives as evident with: renal function (ACR 43 mg/mmol versus 15.9 mg/mmol (ρ=0.0003) and albuminuria 55.8% versus 37.6% (p=0.0039), retinopathy, neuropathy and CVD. Group 2 those taking multiple antihypertensives had significantly worse renal function (ACR 69.2 mg/mmol versus 34.5 mg/mmol (p=0.0329) and albuminuria 63% versus 52% (p=0.0396)), CVD while retinopathy and neuropathy were not significantly different. Group 3 those taking ACE had significantly worse renal function (ACR 43.8 mg/mmol versus 35.2 mg/mmol (p=0.0329)) while CVD was improved and no difference was observed in retinopathy and neuropathy. Conclusions: Antihypertensive use had little impact on preventing diabetic complications. This is contrary to well- documented literature that supports the use of antihypertensives to slow disease progression and protect renal function.

No description available.

Mild thiamin deficiency is prevalent in diabetes, and high dose thiamin ameliorates some diabetic complications, but there are no definitive studies addressing thiamin intake, diabetes control and thiamin status in diabetes. Subjects were 113 people with diabetes (58 type 1, 55 type 2), 43 with and 70 without thiamin supplementation. Dietary thiamin was estimated by 24-hour recall, diabetes control by HbA1c. Age, BMI, albumin excretion, activity level and smoking status did not correlate with red cell thiamin (RCT) in either group. RCT correlated with serum thiamin (ST) (p < 0.01). In those unsupplemented, adequate dietary thiamin did not ensure normal RCT, with 15.7 % of subjects below the reference range. Supplementation to intake > 4 mg/d, was significantly associated with normal RCT (p = 0.028), with 97.7% of supplemented subjects having normal RCT. Supplementation was also significantly associated with elevated serum thiamin 24 hours post supplementation, contrary to other reports. HbA1c was not significantly associated with RCT. Conclusions: In diabetes, adequate dietary thiamin does not ensure normal red cell thiamin, but supplementation to > 4 mg/day does, raising questions about actual thiamin requirements in diabetes and supporting evidence that thiamin deficiency in diabetes is not primarily due to dietary deficiency. Diabetes control was not significantly related to thiamin status.

Type 2 diabetes mellitus (T2DM) is one of the leading causes of death from worldwide non-communicable diseases. The prevalence of diabetes in the Mexico (MX)-United States border states exceeds the national rate in both countries. The economic burden of diabetes, due to decreased productivity, disability, and medical costs, is staggering and increases significantly when T2DM-related complications occur. The purpose of this study was to use a modified behavioral risk factor surveillance system (BRFSS) to describe the T2DM self-management behaviors, diabetes care, and health perception of a convenience sample of adults with T2DM in Monterrey, MX. This cross-sectional study design, with convenience sampling, was conducted with a convenience sample (n = 351) of adults in the metropolitan area of Monterrey, MX who self-reported a diagnosis of T2DM. Potential participants were recruited from local supermarkets. Twenty-six diabetes and health-related items were selected from the BRFSS and administered in face-to-face interviews by trained data collectors. Data analysis was conducted using descriptive statistics. The mean age was 47 years, and the mean length of time with T2DM was 12 years. The majority was taking oral medication and 34% required insulin. Daily self-monitoring of feet was performed by 56% of the participants; however, only 8.8% engaged in blood glucose self-monitoring. The mean number of health-care provider visits was 9.09 per year, and glycated hemoglobin level (HbA1c) was assessed 2.6 times per year. Finally, only 40.5% of the participants recalled having a dilated eye exam. We conclude the modified BRFSS survey administered in a face-to-face interview format is an appropriate tool for assessing engagement in T2DM self-management behaviors, diabetes care, and health perception. Extension of the use of this survey in a more rigorous design with a larger scale survey is encouraged.

This thesis examined how and why TRPV1 function is being modulated in sensory neuropathy and explored the potential of its rescue in the urinary bladder of STZ-­‐induced diabetic rats. Diabetes induced a rapid decline in TRPV1 function and changes in neurogenically mediated electrically-­‐evoked responses together with a gradual decline in muscarinic function. Diabetic bladder was also deficient in muscarinic and TRPV1 organ bath temperature-­‐induced changes but not in those affecting spontaneous contractile activity. Exposure to a potential neuropathy causative agent, methylglyoxal was studied and its mechanism of action explored through the use of TRPA1 ligands. Methylglyoxal exposure mimicked some of the effects of diabetes on TRPV1, neurogenic electrically evoked responses and muscarinic function. Methylglyoxal effects were seen to be partly through TRPA1 receptor activation but other as yet undefined pathways were also involved. Use of TRPA1 ligands revealed an unexpected complexity of the interaction of the TRPA1 receptor with TRPV1. Finally the potential of reversing the diminished TRPV1 response was examined through the use of three known sensitising agents, bradykinin, NGF and insulin. Bradykinin was the only agent seen to reverse the TRPV1 diminished response back up to to control equivalent levels and through the use of bradykinin selective ligands, it was seen that the dual activation of BK-­‐1 and BK-­‐2 receptor was necessary to rescue the TRPV1 response. The likely mechanism of action of bradykinin was through prostaglandin production as indomethacin blocked TRPV1 rescue. In the acute stage of diabetes, TRPV1 function is downregulated and may be caused by exposure to a neuropathy-­‐causing metabolite such as methylglyoxal. The TRPV1 function still retains plasticity at this acute stage because function could be enhanced back to control levels by bradykinin receptor activation : a potential for early therapeutic intervention.