The Hispanic population has an elevated prevalence of diabetes, resulting in large part from a lack of self-management skills required to obtain glycemic control. The purpose of this project was to determine whether diabetes self-management knowledge was improved through the use of a culturally-based diabetes self-management program for Hispanic adults with diabetes using elements of the Hispanic culture. The research question asked whether a researcher-developed diabetes self-management education program that incorporated elements of the Hispanic culture improved diabetes knowledge in the Hispanic population when compared to a non-culturally based diabetes self-management program. The project was conducted using a quasi-experimental control group pre-test/post-test design using the stages of change transtheroretical model as its theoretical framework. Twenty-three Hispanic adults who had a diagnosis of diabetes and a Hemoglobin A1c level of greater than 7%, were recruited for the project. All project participants were recruited through a referral process from a local community clinic located in Montgomery County Texas. Pre/post-test data for the project were obtained through use of the University of Michigan's Diabetes Knowledge Test. A paired-sample t test was conducted to compare the pre-test and post-test results of the experimental group and the control group The project data results showed a significant difference (p < 0.05) between the pre/post-test scores of the experimental group but showed no difference between the 2 scores for the control group, leading to the recommendation that diabetes self-management education should be culturally based. Positive social change was gained from this project through the empowerment of Hispanics in the self-management of diabetes.

This document only includes an excerpt of the corresponding thesis or dissertation. To request a digital scan of the full text, please contact the Ruth Lilly Medical Library's Interlibrary Loan Department (rlmlill@iu.edu).

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This document only includes an excerpt of the corresponding thesis or dissertation. To request a digital scan of the full text, please contact the Ruth Lilly Medical Library's Interlibrary Loan Department (rlmlill@iu.edu).

No description available.

Objectives: To describe the profile of Canadian adults with type 2 diabetes mellitus (T2DM), examine the prevalence of diabetes-related complications and investigate the factors associated with having common diabetes-related complications. Methods: Self-reported data from Statistics Canada’s 2011 Survey on Living with Chronic Diseases in Canada (SLCDC) – Diabetes component were available to describe the prevalence of T2DM, related complications and co-morbidities. Associations with diabetes-related complications were evaluated using logistic regression models. Survey weights and bootstrapping resampling method were applied to account for the complex survey design. Results: 2,341 T2DM respondents (weighted Canadian population estimate n=1,365,165) had a mean age of 62.9 years and diabetes duration of 10.6 years. The prevalence of diabetes-related complications and comorbidities were high: eye (34.0%), foot or leg (24.4%), cardiovascular (22.6%), renal (15.7%), neuropathy (10.8%), hypertension (68.4%) and high cholesterol (67.2%). Factors associated with diabetes-related complications were: Eye: > 65 years of age (odds ratio [OR] 3.7, 95% CI 2.4 – 5.5, p=<0.0001); household income < $29,999 (OR 1.9, 95% CI 1.1 – 3.2, p=0.01), diabetes duration > 10 years (OR 2.3, 95% CI 1.6 – 3.5, p<0.001), cardiovascular complications (OR 1.8, 95% CI 1.1 – 2.9, p=0.01). Renal: duration of diabetes 6 – 9 years (OR 3.0, 95% CI 1.4 – 6.3, p=0.02), duration of diabetes > 10 years (OR 2.1, 95% CI 1.1 – 3.9, p=0.04) Cardiovascular: male sex (OR 1.9, 95% CI 1.3 – 2.7, p=0.0006), eye complication (OR 1.9, 95% CI 1.2 – 3.0, p=0.007), foot or leg complication (OR 2.0, 95% CI 1.3 – 3.0, p=0.002). Foot or leg: cardiovascular complication (OR 2.0, 95% CI 1.4 – 3.1, p=0.0006). Neuropathy: household income $30,000 - $59,999 (OR 2.1, 95% CI 1.2 – 3.9, p=0.03); duration of diabetes >10 years (OR 1.9, 95% CI 1.1 – 3.8, p=0.01), foot or leg complication (OR 7.0, 95% CI 4.1 – 11.8, p<0.0001), eye complication (OR 2.0, 95% CI 1.1 – 3.7, p=0.006). Conclusions: The presence of diabetes-related complications among Canadians with T2DM is multifactorial. / Thesis / Master of Science (MSc)

The incidence of malformed newborns is higher in human pregnancies complicated by diabetes mellitus, as compared to non-diabetic pregnancies. Neural tube and cardiac defects predominate among the fetal malformations induced by hyperglycemia. Non-specific maternal immune stimulation is protective in mice against birth malformations caused by chemical or physical teratogens, or by maternal diabetes mellitus. Insulin dependent diabetes was induced in ICR females to study the late gestation fetal heart by morphometric analysis. Diabetic females treated with Freund's compete adjuvant (FCA) or interferon-gamma (IFNγ) were also generated to elucidate potential positive effects of maternal immune stimulation during the diabetic pregnancy by morphometric analysis and pathologic scoring. Insulin-dependent CD1 females were generated to analyze late gestation fetal myocardial apoptosis by flow cytometric analysis and by real time-polymerase chain reaction (RT-PCR) analysis of a panel of 5 genes involved in apoptosis/proliferation (Bcl-2, P53, Caspase3, Caspase9 and PkC-e). The morphometric analysis of fetal hearts revealed visibly obvious dilation of ventricular chambers and outflow channel of the left ventricle, and reduction of total myocardial ventricular area in late gestation fetuses, as predominant changes seen in the offspring of diabetic dams. Pathologic scoring revealed that maternal immune stimulation, particularly with FCA, in part alleviated fetal heart changes of cavitary dilation and myocardial reduction. Increased rate of apoptosis/necrosis in the fetal myocardium in late gestation during the diabetic pregnancy was evidenced by flow cytometric analysis. Particularly there was a significant increase in percentage of early apoptotic cells in the fetal myocardium detected by cell markers annexin V and propidium iodide. There was also a significant increase in percentage of late apoptotic/necrotic fetal myocardial cells in the diabetic group compared to the control group. These results suggest that maternal treatment with FCA may in part protect the heart from high hyperglycemia by reducing the number of myocardial cells undergoing apoptosis and necrosis. The RT-PCR analysis revealed subtle changes in gene expression for all the genes except Bcl-2. A paradoxical and dramatic up-regulation of this anti-apoptotic gene was observed in late gestation fetal myocardium from the insulin-dependent hyperglycemic groups. Possibly, this could be a mechanism to protect the fetal myocardial cell from the chronic exposure to a severe hyperglycemic insult and consequent apoptosis. In conclusion, maternal insulin-dependent diabetes caused morphological changes in the late gestation fetal heart. Such changes were in part related to dysregulation of myocardial apoptosis. Maternal immune stimulation with FCA improved fetal heart morphology, by a mechanism that may in part relate to normalizing fetal myocardial apoptosis. / Ph. D.

Diabetic nephropathy is one of the most common causes of end stage renal disease and develops in approximately one third of all diabetes patients. Disease progression is characterized by deteriorating glomerular filtration rate and escalating urinary albumin/protein excretion; both are used as clinical markers for disease progression. Recently, it has been proposed that intrarenal hypoxia is a unifying mechanism for chronic kidney disease, including diabetic nephropathy. Several mechanistic pathways have been linked to the development of intrarenal hypoxia and diabetic nephropathy including increased angiotensin II signaling, oxidative stress and hyperglycemia per se. Furthermore, pathological endothelin signaling has recently immerged as a possible contributing factor for chronic kidney disease and diabetic nephropathy. The overall aims of this thesis were therefore to determine the temporal relationship between development of intrarenal hypoxia and kidney disease as well as elucidate the potential link between endothelin signaling, intrarenal hypoxia and kidney disease in experimental insulinopenic diabetes. It is well established that different mouse strains have different susceptibility for kidney and cardiovascular disease. The first step was therefore to compare four commonly used mouse strains with regards to development of kidney disease after onset of insulinopenic diabetes. From the results of this study, we concluded that the NMRI mouse strain has a disease progression closest to the human disease and this strain was chosen in the subsequent studies in mice. The next step was to adapt and optimize a suitable method for repetitive measurements of intrarenal oxygen tension during the course of disease development. Electron paramagnetic resonance (EPR) oximetry had previously been used in tumor biology and was now adapted and optimized for measurements of kidney oxygenation in our diabetic mouse model. EPR oximetry in normoglycemic control mice recorded cortical oxygen tension values similar to previous reports using invasive techniques. Surprisingly, intrarenal hypoxia developed already within the first 72h after induction of hyperglycemia and persisted throughout the two-week study period. Importantly, this was well before albuminuria developed. The final part of this thesis was to investigate the role of endothelin signaling for the intrarenal hypoxia in a diabetic rat model. Endothelin 1 signals via two distinctly different receptor-mediated pathways. In normal physiology, endothelin 1 binding to endothelin receptor type A (ETA) induces vasoconstriction, which can be blocked by the specific ETA antagonist BQ123, whereas endothelin 1 binding to endothelin receptor type B (ETB) induces nitric oxide-dependent vasodilation. ETB receptors can be selectively activated by Sarafotoxin 6c. The results from blocking ETA and activating ETB receptors demonstrated that endothelin 1 signaling via ETA receptors contributes to intrarenal hypoxia in the rat diabetic kidney, and that ETB stimulation significantly reduces the diabetes-induced intrarenal hypoxia. The beneficial effects on kidney oxygen availability in diabetes by ETA blockade or ETB stimulation were mainly linked to hemodynamic improvements rather than direct effects on kidney oxygen consumption or oxidative stress status. In conclusion, by applying EPR oximetry in a mouse model of insulinopenic diabetes mimicking the human disease, we demonstrated intrarenal hypoxia already within the first couple of days after the onset of hyperglycemia, which is well before detectable signs of kidney disease development. Furthermore, blockade of ETA or activation of ETB receptors significantly reduced intrarenal hypoxia in the diabetic kidney. These results demonstrate involvement of ETA receptor signaling in diabetes-induced intrarenal hypoxia and ETA blockade or ETB activation might provide new therapeutical targets to reduce kidney hypoxia and disease progression in diabetes.

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I dag har cirka 450000 personer i Sverige diabetes. Typ 2 diabetes står för den största delen, cirka 85 procent. Att drabbas av diabetes kan inverka på livet och individen men god egenvård skapar goda förutsättningar för att ändå leva ett gott liv. Det är inte alltid lätt att fullgöra denna egenvård. Kvinnor i de artiklar som använts i denna studie talade om de olika roller de hade och hur de påverkade förmågan att sköta sin diabetes. Syftet med denna studie var att beskriva hur kvinnor upplever det att leva med Typ 2 diabetes. Hur påverkar sjukdomen vardagen för kvinnor som vårdar och sköter om både sig själv och andra? Metoden som använts är Axelssons analysmodell (Axelsson 2012, ss. 203-220) för litteraturstudier. Under detta analysarbete identifierades olika teman och subteman. Dessa behandlar kvinnornas förändrade självbild samt hur de hanterar sin vardag. De behandlar också kvinnornas upplevelser av hälso- och sjukvårdens bemötande  och  hur  det  är  att  sköta  kosten.  Kvinnorna  uttryckte  att  sjukdomen påverkade deras möjligheter att fullfölja sina åtaganden gentemot familjen då de samtidigt skulle sköta sin egen sjukdom. I diskussionen belyses kost ur olika perspektiv och hur kvinnans roller påverkas av hennes sjukdom. Den bristande kommunikationen kvinnorna möter i hälso- och sjukvård diskuteras också. Det är viktigt att kvinnorna får individanpassat stöd och hjälp att hantera sin livssituation, både av hälso- och sjukvård samt av anhöriga. Stödet ska skapa bra förutsättningar för en god egenvård och hälsa. Att främja hälsa och lindra lidande är grunden för vårdvetenskapen.