Abstract Background: Individuals with type 2 diabetes mellitus (T2D) face many challenges in self-management of their current disease state. Nutrition education has been identified as a key component in managing metabolic control in individuals diagnosed with T2D. The purpose of this study is to investigate the effect of a 4-week nutrition intervention on glycated hemoglobin (HbA1c) and nutrition knowledge by food security status in individuals with T2D who attend the Family Health Centers of Georgia (FHCGA) located in West Atlanta. Methods: Subjects enrolled in the study (n=6) completed a nutrition knowledge survey at the beginning of the intervention and had their HbA1c values extracted from the FHCGA medical record. Subjects then entered a 4-week group nutrition intervention program. The program consisted of four lessons that focused on the basic diet for diabetes, food label reading, grocery store shopping and eating out with diabetes. Subjects took a nutrition knowledge survey after the intervention and were asked to return to have a follow-up blood draw for HbA1c levels. Results: Two out of six subjects completed the entire protocol. The HbA1c for this subject was higher after the nutrition intervention. An additional two subjects completed all of the lessons and the post survey, but did not have a follow-up HbA1c drawn. The mean nutrition knowledge score pre-intervention (72.33 + 5.13) was lower than the mean post-intervention score (78.67 + 4.04) but was not significantly different. When subdivided by food security status, subjects with a higher food security status had a lower baseline HbA1c. Conclusion: Nutrition knowledge scores increased after nutrition education but not significantly. The effect of nutrition education on HbA1c by food security status could not be determined due to low participation. Future studies with a larger sample size and incentives for compliance are needed to investigate how group nutrition education influences metabolic control in food insecure and secure people with T2D.

Background: A marked increase of type 2 diabetes and associated morbidity and mortality rate over the last 10 years has been recorded in Malaysia. Ineffective diabetes management and a lack of self-care practice among type 2 diabetic patients have been identified as the major reasons for this problem. Research in other countries has highlighted a range of factors influencing effective self-care of type 2 diabetes including patients' perspectives of diabetes, sociocultural issues, religious beliefs and support from healthcare. Nevertheless, there is paucity of research conducted in Malaysia. Therefore, the exploration of self-care practice and self-care support provision in patients with type 2 diabetes in Malaysia is needed to understand the problem. Aims: To understand the self-care practice of patients with type 2 diabetes in Malaysia and the factors that influence the patients' self-care practice. To understand the type 2 diabetes’ self-care support provision in Malaysia from the perspective of patients, healthcare professionals, and healthcare system. Methods: A qualitative, single embedded case study design was utilised. Eighteen patients with type 2 diabetes and 19 healthcare professionals (physicians, diabetes educators, nurse, pharmacist and dietician), involved in self-care support provision primary- and secondary-care settings in Kuala Lumpur and Putrajaya, Malaysia, participated in in-depth semi-structured interviews between November 2012 and June 2013. In addition, data were collected through participant-observation of clinic consultations, and analysis of relevant documents used in the provision of diabetes management in the respective clinics. The framework technique supported analysis of data. Data were stored and managed using Nvivo 9 software. Findings: The findings indicate that patients with type 2 diabetes had a good understanding of diabetes and self-care, but a lack of self-care support meant that effective self-care was difficult to sustain. Healthcare professionals’ (HCPs’) provision of self-care support was restricted due to several factors, including lack of opportunity to provide self-care support, unsuitable clinic environment and a fragmented management within primary and secondary care. Additionally, barriers in patient–HCP communication, a combination of the personal, interpersonal and inter-professional HCP factors, and a traditional medical model adopted by Malaysian healthcare system, seem to have influenced the practice and quality of the service delivered. Conclusion: It is clear that the increased incidence of uncontrolled type 2 diabetes is not merely due to poor self-care practice by patients, but also due to constraints in service delivery and underdevelopment of self-care support provision. The evidence generated can assist in the development of strategies to improve the quality of care and facilitate changes in the self-care support provision in Malaysia.

Type 2 diabetes mellitus (T2DM) is a widespread metabolic disorder that continues to grow in prevalence both in the United States and worldwide. T2DM is an immense public health crisis and has been declared an epidemic by the United States Centers for Disease Control and Prevention. T2DM is a heterogeneous disease that is characterized by chronic hyperglycemia that is caused by dysfunction of the insulin transduction pathway. Particularly in T2DM, individuals with the disease experience a progressive loss of insulin production by pancreatic β cells in the setting of peripheral insulin resistance. Due to the dysfunction of insulin’s actions, glucose in circulation is unable to enter insulin’s target cells and remains in the bloodstream. Formerly known as adult-onset diabetes, T2DM has recently become more commonplace in youthful populations, particularly in adolescents during puberty. Several risk factors have been identified for T2DM, which defines a population of study to determine the underlying pathogenesis of T2DM and possible therapeutic interventions. While extensive research on T2DM has been performed, the heterogeneous nature of the disease makes it difficult to understand the relationship between genetic susceptibility and environmental triggers. The trend of reaching younger populations is extremely worrying as the loss of glycemic control in T2DM is associated with various medical complications. The most commonly seen complications in T2DM include neuropathy, nephropathy, retinopathy, and cardiovascular disease. These complications come with a significant burden that greatly increases mortality and reduces one’s quality of life. One of the underlying causes of the growing prevalence of youth-onset T2DM is the growing pediatric obese population. The increasing prevalence of pediatric obesity, in turn, is likely tied to adolescents getting less sleep, having diets high in carbohydrates, and having insufficient physical activity. Compared to T2DM that precipitates later in life, youth-onset T2DM appears to have a more aggressive nature, where glycemic control is quickly lost, and complications arise sooner in the disease course than adults. Unfortunately, compared to the various drug classes available to adults, options for youths with T2DM are limited. Currently, the only pharmacologic therapies available to youths are metformin and insulin and given that youths quickly lose metabolic control, new therapies are desperately needed to combat this epidemic. Lifestyle interventions are also widely used in pediatric populations, but success with lifestyle monotherapy is limited. Adherence to treatment plans is a barrier to positive outcomes in youthful populations, which may be improved by having patients and their families attend diabetes education programs. The aggressive nature of youth-onset T2DM and the limited amount of available therapies make it difficult to maintain control diabetes in this youthful population, which is concerning given the huge costs associated with diabetes for both individuals and health care systems. To combat this epidemic of youth-onset T2DM, aggressive monitoring is needed to identify high-risk populations and to prevent and delay T2DM in these populations. Reducing the prevalence of youth-onset T2DM will require efforts to increase the physical activity of youths and to reduce the consumption of foods that greatly increase blood sugar. Additionally, efforts should be made to ensure that youths are getting adequate amounts of sleep. Bariatric surgery has been demonstrated positive results in remission of T2DM in youths, but such an invasive procedure may be an extreme solution in a vulnerable population.

Type 2 Diabetes Mellitus (T2DM), a metabolic disorder denoted by elevated blood glucose levels and insufficient insulin action, is growing in prevalence worldwide . Barriers to improving disease outcome resolve primarily around identifying and intervening during the preliminary stages of insulin resistance, a state clinically referred to as pre-diabetes. Emerging evidence suggests that mitochondrial dysfunction may underlie , and potentially precede, progressive insulin resistance, suggesting that biomarkers indicative of mitochondrial dysfunction could predict disease risk and status. In this study, we examined epigenetic modifications, in the form of DNA methylation, in the promoter region of peroxisome proliferator activated receptor gamma coactivator 1 alpha (PGC-1α), a known regulator of mitochondrial biogenesis. Following the initiation of a high fat diet, we observed significant genotypic (DNA methylation) and phenotypic (mitochondrial copy number) alterations in C57/BL6 rodent models. These changes preceded overt disease onset, as classified by clinically utilized indices, which included the homeostatic model assessment for insulin resistance (HOMA-IR), the homeostatic model assessment for β-cell dysfunction (HOMA- β), and the quantitative insulin-sensitivity check index (QUICKI). Our data indicate that methylation analysis may serve as an effective clinical parameter to use in conjunction with physiological criterion for the diagnosis of pre-diabetes and the assessment of T2DM disease risk, and adds to the growing body of work seeking to elucidate the role. / Doctor of Philosophy / High blood glucose, referred to as type 2 diabetes (T2DM), increases the risk for heart and kidney disease, blindness, stroke, and death. Efforts to prevent T2DM have centered primarily around behavioral interventions, which include increased physical activity and decreased caloric intake. Importantly, the interventions are most effective when implemented early on in disease progression. In this study, we sought to examine the effects of a high fat diet on the epigenetic profile of PGC-1α, a gene responsible for maintaining mitochondrial biogenesis. The mitochondria, the powerhouse of the cell, is responsible for maintaining the energy systems in the body. Therefore, we examined how increasing in caloric intake resulted in changes in the epigenetic profile of the PGC-1α promoter, and how these changes impacted mitochondrial number. Further, we sought to examine how hypermethylation of PGC-1α led to changes in gene and protein expression in the mitochondria. Results from our study indicate that DNA methylation changes preceded disease onset, as characterized by the homeostatic model assessment for insulin resistance (HOMA-IR), the homeostatic model assessment for β-cell dysfunction (HOMA- β), and the quantitative insulin-sensitivity check index (QUICKI). Our data indicate that methylation analysis may serve as diagnostic and risk assessment tool for pre-diabetes and T2DM in conjunction with physiological measures.

The use of telehealth in healthcare has grown in recent years; however, little is known about the effectiveness of this delivery method in the management of Type 2 diabetes mellitus (T2DM). Guided by the chronic care model and telehealth in chronic disease model, the purpose of this systematic literature review was to explore evidence related to lowering hemoglobin A1c levels and managing T2DM using telehealth in the outpatient setting. The practice-focused questions explored telehealth interventions used in T2DM management and their effectiveness. The Joanna Briggs Institute (JBI) method for conducting systematic literature reviews was the process, and data were compiled using the PRISMA evidence-based minimum set for reporting. Eighteen studies met the inclusion criteria for this project. Data were extracted, analyzed, and synthesized using JBI tools for data extraction and critical appraisal. Article appraisals revealed numerous telehealth interventions for management of T2DM including telephone, Internet-based, clinical video, remote monitoring, and smart phones/applications. Overall, telehealth interventions showed statistically significant improvement in the hemoglobin A1c levels of participants compared to traditional outpatient care. Success of the interventions is associated with components of evidenced-based diabetes management such as education, self-management, support, and feedback loop. The implications of this project for positive social change include the integration of telehealth interventions in the outpatient setting to manage T2DM with enhanced access to care, reduction in health disparities, and improved health outcomes for society.

No description available.

Adolescent type 2 diabetes (T2D) diagnoses are on the rise. Consistent with the adult literature, preliminary evidence in adolescents suggests that T2D is associated with reduced brain volume and white matter microstructural integrity. As part of the Cognitive Performance in Adolescents with T2D (CPAT2D) study, this project aimed to test whether T2D diagnosis is associated with poorer cognitive performance in adolescents. Five adolescents with obesity and T2D (60% female; body mass index [BMI] percentile 98.2 ± 2.0; age 16.7 ± 1.1 years) were recruited and matched to two control adolescents with obesity but without T2D (50% female; BMI percentile 99.9 ± 0.2; age 15.9 ± 1.3 years) on at least three of the following characteristics: age, sex, pubertal stage and habitual sleep duration. All participants wore a wrist actigraphy device for seven consecutive nights to measure sleep at home and then completed two neuromotor cognitive tasks at a laboratory testing session assessing motor preparation (simple reaction time task) and executive functioning (affective shifting task [AST]). Control data were available through the Sleep Manipulation in Adolescents at Risk of Type 2 Diabetes (SMART2D) study. Premotor reaction time outcomes in either task and proportions of commission and omission error trials in the AST were subsequently analyzed. Based on this preliminary participant sample, there is no evidence to suggest that adolescents with compared to without T2D perform differently on the neuromotor cognitive tasks. The results should be confirmed once the intended sample size is reached. In the meantime, clinicians should monitor for changes in cognitive function in adolescents with T2D, perhaps by asking about academic achievement. The majority of our sample exhibited sub-optimal movement behaviours; to preserve overall health, adolescents with obesity and/or T2D should strive to meet sleep, physical activity and screen time recommendations for their age group.

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)

Metformin is the most common type 2 diabetes therapy, and may also reduce colorectal cancer growth. Currently, two mechanisms driving reduced cancer growth are considered: 1) Regulation of glucose and insulin levels, which may support cancer growth, and 2) Direct entry into cancer cells to activate the AMP-activated kinase (AMPK) protein, and inhibit cell growth pathways. The gut microbiome is the community of commensal microorganisms in the gastrointestinal tract. It is also affected by metformin, and may elevate production of short-chain fatty acids (SCFAs). Therefore, this thesis aimed to clarify how metformin may inhibit colorectal cancer growth and if the microbiome is involved. The hyperglycemic-responsive, murine-derived MC38 colon cancer cell line was used to test these effects. This model was confirmed to experience growth stimulation caused by high-fat diet (HFD) feeding in mice. Daily i.p. injections of metformin (100mg/kg) had no measurable effect on glucose and insulin sensitivity, or MC38 tumor growth. Oral metformin (250mg/kg) improved glucose tolerance and inhibited MC38 tumor growth in HFD-fed mice. To see if the gut microbiome is required for this effect, the antibiotic ampicillin was used to limit the gut microbiome. The addition of ampicillin blunted metformin’s glucose sensitization and tumor inhibition effects. A fecal microbiome transfer model was then used to isolate the role of the microbiome. Conventional mice fed HFD and gavaged with feces from metformin-treated donors experienced no glucose or insulin tolerance improvements. However, tumor growth was decreased by 30%, and serum SCFAs concentrations were elevated. The SCFA butyrate inhibited in vitro MC38 colony growth, but did not activate AMPK. These data suggest that metformin alters the gut microbiome, and fecal transfer from metformin-treated animals can uncouple MC38 tumor growth inhibition from the glucose homeostasis effects of metformin. These novel findings support a new mechanism for metformin to prevent cancer growth and development. / Thesis / Doctor of Philosophy (PhD) / Metformin is the most commonly used type 2 diabetes therapy, and may also reduce colorectal cancer growth. Anti-cancer effects may be caused by: 1) decreased glucose and insulin levels, which support cancer growth; or 2) entry into cancer cells to directly decrease cell growth. The gut microbiome, microorganisms that live symbiotically in the gastrointestinal tract, is also affected by metformin. This thesis aimed to clarify how metformin can inhibit cancer, and if the microbiome is involved. Mice treated with metformin had improved glucose metabolism and decreased colorectal tumor growth; when an antibiotic was introduced, this effect was lost. A fecal microbiome transfer model was used to determine if the microbiome is driving this effect. Mice receiving feces from metformin treated mice also experienced tumor growth inhibition. This suggests that the gut microbiome is involved in the anti-cancer effects of metformin, and is a new potential mechanism of action.