Thesis (M.Fam.Med.)--University of the Witwatersrand, Faculty of Health Sciences, 2014. / Background The combined influence of processes of care, lifestyle advice and drug treatment on glycaemic control in Type 2 diabetes in primary care settings is not well documented. Aim To describe the provision of lifestyle advice, selected processes of care and drug treatment to, and assess the influence of these factors on glycaemic control in, a sample of adults with type 2 diabetes mellitus attending the Johan Heyns Community Health Centre in Sedibeng District, Gauteng. Methods A cross-sectional design was used. Participants consisted of 200, consecutively chosen, adult volunteers with type 2 diabetes. Information on demographics, reported receipt of lifestyle advice and anthropomorphic measurements was collected through questionnaire-based interviews. This was followed by a record review of all participants’ clinic files for information on current drug management, co-morbid medical conditions and documentation of processes of care, in the preceding 12 months, in respect of HbA1c, blood pressure (BP), weight, waist circumference (WC) and body mass index (BMI) monitoring. HbA1c values were used to ascertain glycaemic control. Performance of processes of care was assessed in accordance with Society for Endocrinology, Metabolism and Diabetes of South Africa (SEMDSA) guidelines. Parsimonious models for glycaemic control were constructed through multivariate logistic regression. Results Mean age of the sample was 58 years with 58% in the 50-64 year age group. Blacks (88%) and females (63%) were in the majority. Over two-thirds had diabetes for under 10 years and 98% had at least one co-morbid condition, mainly hypertension (92%). Obesity was noted in 65%, while 95% of females and 83% of males had a WC that conferred substantial cardio-metabolic risk. Receipt of advice on any of diet, exercise or weight control from a health professional in the preceding 12 months was reported by 79%, with 67% reporting receipt of advice on all three. Under 2% of patient records met the SEMDSA standard for processes of care for HbA1c, weight, WC and BMI monitoring, while 93% achieved the standard for BP monitoring. Exclusive oral treatment was prescribed in 62%, and the majority of these were on combined metformin and sulphonylurea; 5% were on insulin monotherapy. Optimal glycaemic control (HbA1c < 7%) was noted in only 25% of the sample. On multivariate analyses, the presence of CCF conferred higher odds of controlled glycaemia (OR = 3.17, P = 0.035). Compared with insulin monotherapy, treatment with either combined metformin and insulin (OR = 0.216, P = 0.02), or with the combination of all 3 drug classes ( metformin, sulphonylurea and insulin) (OR = 0.185, P = 0.027), conferred lower odds of glycaemic control. Conclusions This study highlights substantial shortcomings in the compliance with key processes of care and the achievement of optimal glycaemic control for type 2 diabetes mellitus in the current research setting. An inverse association was noted between glycaemic control and the use of combined oral and insulin drug therapy. Measured processes of care and reported receipt of lifestyle advice showed no association with glycaemic control. CCF co-morbidity conferred improved odds of controlled glycaemia.

Background: Type 2 diabetes mellitus (T2DM) is defined by an increase in serum glucose, however, this leads to the belief that only the serum glucose levels need be monitored and treated. Hence many other risk factors such as obesity, lipids and blood pressure which increase the risk of coronary heart disease, myocardial infarction, stroke and peripheral vascular disease are neglected. Consequently, T2DM patients that are at greater risk of developing cardiovascular disease (CVD), are often not receiving optimal comprehensive care. Aims: To identify the treatment gaps of cardiovascular risk factors in patients with T2DM using both national and international current treatment guidelines. Methods: Using a public sector database, data was obtained on the treatment of 666 T2DM patients. Records of patients were selected on the basis of established T2DM diagnoses, receiving oral hypoglycaemic and/or insulin therapy. The following patient data was recorded: demographics (age, gender, ethnicity), systolic blood pressure (SBP), diastolic blood pressure (DBP), glycated haemoglobin (HbA1c), total cholesterol (TC), triglycerides (TG), HDL-cholesterol (HDL-C), LDL-cholesterol (LDL-C) , family history, cardiovascular history and all chronic medications. The following parameters were applied to the cohort: SBP <130 mmHg, DBP <80 mmHg. In the event of proteinuria: SBP ≤120 mmHg, DBP ≤70 mmHg. HbA1c <7.0%, TC <4.5 mmol/L, LDL-C <2.5 mmol/L, HDL-C >1.0 mmol/L (males), HDL-C >1.2 mmol/L (females) and TG <1.7 mmol/L. In patients with established CVD, LDL-C target: ≤1.8 mmol/L. Results: The study cohort consisted of 666 T2DM-patients. 55% females. Mean age was 63 years (SD: 11.8), mean HbA1c was 8.7% (SD: 2.4). The mean SBP and DBP readings for the cohort were 133.66 (SD: 19.9) and 78.07 mmHg (SD: 11.6), respectively. Mean LDL-cholesterol was 2.6 mmol/L (SD: 0.9). 26.2% reached HbA1c of ≤7%, 45.8% reached ≤130/80 mm Hg blood pressure targets, 53.8% reached LDL-C of ≤2.5mmol/L and all 3 were reached by 7.5% of the cohort. TC ≤4.5 mmol/L was reached by 53.8%, 60.2% reached TG ≤1.7mmol/L, 58.6% males and 52.8% females reached HDL-C targets of ≥1.0 mmol/L and ≥1.2 mmol/L, respectively. There were 17.9% of patients with CVD reaching targets of LDL-C ≤1.8 mmol/L whilst 16.4% of patients with nephropathy reaching targets of ≤120/70 mm Hg. Almost half (48.2%) were not receiving lipid-lowering therapy, yet would be deemed eligible for therapy. Blood pressure targets may have been better reached with appropriate dosage reductions in addition to the introduction of further antihypertensive combination therapy. CVD was present in 15.5%. Conclusions: T2DM patients are at high-risk for CVD. Many trials have demonstrated the benefits of targeting CVD risk factors (HbA1c, blood pressure, serum lipids) in T2DM. Less than 10% of CVD risk factor targets were reached by the study cohort despite treatment guideline recommendations. The data from the study suggests poor control of modifiable cardiovascular risk factors and significant under treatment of T2DM in clinical practice. Whether improvement lies in the form of therapeutic titration adjustment or an increase in patient education, there needs to be a more aggressive multi-factorial therapeutic approach to treating this high risk group of patients in order to reduce overall morbidity, mortality and improve patient outcomes.

Mutations in HNF1A cause Maturity Onset Diabetes of the Young type 3, the second most frequent form of diabetes caused by single gene mutation. We generated human stem cell-derived pancreatic endocrine cells with clinically pathogenic mutations in HNF1A and show that HNF1A deficiency impairs endocrine cell fate, insulin granule maturation and the secretion of insulin in response to glucose. Single-cell RNA sequencing reveals that HNF1A orchestrates a network of genes involved in β-cell fate, granule maturation, glucose metabolism, calcium ion binding and hormone exocytosis. In both patients and stem cell-derived β-cells, HNF1A deficiency altered the stoichiometry of secreted insulin to c-peptide. Sulfonylurea, used in the treatment of these patients, restored both insulin secretion and stoichiometry. The uncoupling of insulin and c-peptide secretion as described here questions the common practice of using c-peptide as a proxy to evaluate β-cell function. We also demonstrate that correction of the HNF1A mutations restores function, providing a path to cell-based replacement therapy.

The calorie restriction (CR) and insulin/IGF-I-like signalling (IIS) are two pathways regulating the lifespan of C. elegans. Recent studies showed that glucose restriction extends the lifespan of C. elegans while excessive glucose shortens the lifespan of the worms. The first step of the glucose metabolism is the transport of glucose across the plasma membrane by the glucose transporters. The work described in this thesis aims to identify glucose transporters in C. elegans and to provide a primary investigation of the in vitro and in vivo function of the identified glucose transporter. Nine putative transporters have been cloned and expressed. Out of the nice cloned putative transporters in the C. elegans genome, H17B01.1 (H17) only is identified as a fully functional glucose transporter using an oocyte expression system in which glucose transport activity is directly measured. The two transcripts of H17 are both capable of transporting glucose with high affinity, as well as transporting trehalose. Heterologous expression of H17 in mammalian CHO-T cells suggests that the protein is localised both on the plasma membrane and in the cytosol. In vitro studies of H17 show that the protein does not respond to insulin stimulation when expressed in mammalian CHO-T cell and rat primary adipocyte systems. In vivo functional studies using H17 RNAi indicate that the worm’s lifespan is not affected by the H17 knockdown. However, glucose metabolism of C. elegans (as measured by glucose oxidation to CO2 and incorporation into fat reserves) is influenced by the decreased expression of H17, especially in the daf-2 mutant strain, e1370. However, the increase of glucose metabolism caused by H17 knockdown observed in daf-2 mutant is inhibited in the age-1 and akt-1 mutant strains. The findings reported in this thesis suggest that the H17 glucose transporter may play an important role glucose metabolism in C. elegans and that this transport and metabolism is influenced by insulin receptor activity and serine kinase cascades.

Thesis (M.S.)--Boston University / PLEASE NOTE: Boston University Libraries did not receive an Authorization To Manage form for this thesis or dissertation. It is therefore not openly accessible, though it may be available by request. If you are the author or principal advisor of this work and would like to request open access for it, please contact us at open-help@bu.edu. Thank you. / This study was undertaken to determine the pharmacodynamics of insulin which nursing students understand at the end of thirty months in a three year diploma program in nursing. This study attempted to answer the following questions: 1. Do nursing students reveal a deficiency in their knowledge of insulin in the following areas? [TRUNCATED] / 2031-01-01

by Patricia Jane Anderson. / "June 1999." / Thesis (Ph.D.)--Chinese University of Hong Kong, 1999. / Includes bibliographical references (p. 300-328). / Electronic reproduction. Hong Kong : Chinese University of Hong Kong, [2012] System requirements: Adobe Acrobat Reader. Available via World Wide Web. / Mode of access: World Wide Web.

by Lee Suk Kuen Zoe. / Thesis (Ph.D.)--Chinese University of Hong Kong, 1998. / Includes bibliographical references (p. 271-314). / Electronic reproduction. Hong Kong : Chinese University of Hong Kong, [2012] System requirements: Adobe Acrobat Reader. Available via World Wide Web. / Mode of access: World Wide Web. / Abstract in Chinese.

O efeito de refeições ricas em carboidratos e lipídeos sobre a sensibilidade à insulina foi avaliado. Além disso, investigou-se o conteúdo da proteína GLUT4 em músculo esquelético e tecido adiposo branco. Ratos foram realimentados por 1, 2, 4 e 6 horas com: refeição balanceada (B); rica em carboidrato (C) e rica em lipídeo (L). O índice glicose/insulina revelou que C e L apresentavam resistência à insulina 2 horas após o início da ingestão. No teste de tolerância à insulina, uma redução (~47%) na sensibilidade à insulina foi observada em C após 2 e 4 horas de realimentação. O teste de tolerância à glicose confirmou a resistência à insulina em C e L após 2 horas de ingestão. Não houve alteração no conteúdo de GLUT4, nos momentos em que se verificou alteração na sensibilidade à insulina. Tais resultados indicam que, em ratos, refeições não balanceadas (alto teor de carboidrato ou alto teor de lipídeo), induzem menor sensibilidade à insulina 2 horas após o início da ingestão, e este fenômeno não envolve alterações no conteúdo de GLUT4 nos tecidos avaliados. / The effect of high carbohydrate and fat meals on the insulin sensitivity was evaluated. Furthermore, it was investigated the content of GLUT4 protein on the skeletal muscle and white adipose tissue. Rats were refed for 1, 2, 4 and 6 hours with: balanced meal (B); high carbohydrate meal (C) and high fat meal (L). The glucose/insulin index shows that C and L meals exhibited insulin resistance after 2 hours of ingestion. In the insulin tolerance test, a reduction (~47%) in the insulin sensitivity was observed in C group after 2 and 4 hours of refeeding. The glucose tolerance test confirmed the insulin resistance in C and L-groups after 2 hours of ingestion and such phenomena did not involve alterations in the GLUT4 content on both skeletal muscle or white adipose tissue.

Zhan Siyan. / "November 2004." / Thesis (Ph.D.)--Chinese University of Hong Kong, 2004. / Includes bibliographical references (p. 133-152) / Electronic reproduction. Hong Kong : Chinese University of Hong Kong, [2012] System requirements: Adobe Acrobat Reader. Available via World Wide Web. / Mode of access: World Wide Web. / Abstracts in English and Chinese.

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