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  • About
  • The Global ETD Search service is a free service for researchers to find electronic theses and dissertations. This service is provided by the Networked Digital Library of Theses and Dissertations.
    Our metadata is collected from universities around the world. If you manage a university/consortium/country archive and want to be added, details can be found on the NDLTD website.
1

Postprandial lipaemia in type 2 diabetes : relationship to insulin sensitivity

Al-Majali, Khulood January 2004 (has links)
In a detailed study, the effect of sensitizing tissues to insulin with a thiazolidinedione (pioglitazone) on postprandial lipid metabolism was compared to a group of type 2 diabetic patients treated with sulphonylurea (glibenclamide) in a treatment regime designed to achieve equivalent glycaemic control (HbAlc) in both groups. An oral fat tolerance test was administered after a 6 week treatment with diet and after 20 weeks treatment with glibenclamide or pioglitazone. Glycaemic control in both groups was unchanged by either treatment but in the fasting state, insulin sensitization caused a significant reduction in plasma total triglyceride content due to a significant reduction in total VLDL and, in particular, VLDL-2 present. The overall triglyceride response to the fat test showed a significant improvement to control clearance levels in the pioglitazone group that was not observed in the glibenclamide group. Chylomicron and chylomicron remnant clearance improved with insulin sensitization. IDL and LDL-TG was significantly higher in the diabetic patients than the controls and after treatment with thiazolidinedione the triglyceride content of these lipoproteins was reduced by contrast to glibenclamide treatment. Cholesterol content did not change significantly over the postprandial period either overall or in lipoproteins. There were only small effects on the enzymes of lipoprotein remodelling (LCAT, CETP, PLTP, HL or LPL) by insulin sensitization. Insulin release was reduced over the postprandial period by insulin sensitization and a significant reduction of proinsulin and 32-33 split-proinsulin also occurred. The results of this study show that sensitizing tissues to the action of insulin causes a reduction in insulin resistance (HOMA) and a more rapid clearance of postprandial lipoproteins. In addition there is an apparent beneficial effect on ?-cell function which is manifested by lower levels of incompletely processed insulin species probably caused by a less prolonged period of glycaemia.
2

Endogenous insulin secretion in long duration type 1 diabetes

Oram, Richard Anthony January 2014 (has links)
Type 1 diabetes(T1 D) is defined as a disease of progressive autoimmune destruction of pancreatic beta cells, leading to absolute insulin deficiency. In each individual with the disease there is a critical point when the loss of beta cells is sufficiently great that blood glucose can no longer be controlled, and they develop diabetes. Most people have some remaining endogenous insulin after diagnosis with T1 D but this "honeymoon period" is thought to last for a relatively brief period of time (months to 1-2 years) before all remaining beta cells are destroyed. However, there is mounting evidence from autopsy specimens and from recent studies of endogenous insulin in longstanding T1 D, that some people with T1 0 have persistent functional beta cells for many more years than previously thought. Endogenous insulin production is best measured using C-peptide, as C-peptide is secreted in equimolar amounts to insulin from pancreatic beta cells, C-peptide assays do not cross react with insulin, and C-peptide has a longer half-life. Very low levels of C-peptide are now measurable using highly sensitive electrochemiluminescence assays. A new method of measuring endogenous insulin developed by the Exeter team, urine C-peptide creatinine ratio (UCPCR), correlates very well with blood measures of C-peptide and can be posted from home, allowing the study of large numbers of people and repeated measurements of C-peptide. This thesis aims to assess the prevalence of low-level insulin production in people with longstanding T1 D. using a highly sensitive C-peptide assay in blood and urine, and to assess the use of repeated home UCPCR to monitor islet transplant recipients. 3 In Chapter 1 We review the current methods and recent advances in measurement of endogenous insulin in T1 D, and the natural history of endogenous insulin production in T1D. In Chapter 2 we assess the prevalence of low-level detectable serum and urine Cpeptide in 74 patients with long-duration T1 D. We assess whether very low levels reflect functional beta cells by comparing C-peptide levels before and after a meal stimulus. We demonstrate that most patients continue to secrete very low levels of endogenous insulin, which are detectable in either blood or a spot UCPCR sample, and that the detectable low levels of C-peptide increase after meals. In Chapter 3 we further explore the findings from Chapter 2, using a home stimulated UCPCR to assess endogenous insulin in a large cross-sectional, population-based study of patients with T1 D. Our findings provide confirmation that the majority of long duration patients with T1 D have detectable urine C-peptide and that 8% have much higher levels of endogenous insulin secretion. In Chapter 4 we assess if UCPCR posted from home can be used as a marker of islet transplant function. We find that home UCPCR correlates with clinical and metabolic measures of islet transplant function and provides a valid measure of Cpeptide production in islet transplant recipients. In Chapter 5 we test whether UCPCR could be a surrogate measure of insulin resistance by examining the correlation of UCPCR with serum insulin, C-peptide and HOMA2 (Homeostasis Model Assessment 2)-insulin resistance in people without diabetes and a subgroup with chronic kidney disease (CKD). We find in participants with normal renal function, UCPCR may be a simple, practical method for the 4 assessment of insulin resistance, but that in patients with CKD, UCPCR does not correlate with serum C-peptide, insulin or HOMA2-IR. An overview of the major findings of each chapter, their implications and possible future research are discussed in Chapter 6. 5
3

Role of peroxisomal proliferator-activated receptor alpha (PPARα) linked functions in relation to pancreatic Β-cell glucose sensing and insulin secretion

Greenwood, Gemma Kirsty January 2007 (has links)
No description available.
4

The role of the endothelium and oxidative stress in insulin uptake and processing

Bertelsen, Malene January 2003 (has links)
No description available.
5

Altered monocyte cox-1 & cox-2 levels in human type 1 diabetes

Beyan, Huriya January 2004 (has links)
No description available.
6

Catecholamine sensitivity preceding Type 2 diabetes

Forbes, Shareen January 2005 (has links)
No description available.
7

Knowledge-based supervised learning models for the assessment of type 2 diabetes complications

Giardina, Marisol January 2008 (has links)
No description available.
8

Xenobiotic metabolism and human pathology : cytochrome P4502E1-mediated pancreatic cell dysfunction and destruction

Murdock, Diane Joan Lees January 2001 (has links)
No description available.
9

Usability evaluation of a spoken dialogue system for older adults with type 2 diabetes

Black, Lesley-Ann January 2005 (has links)
No description available.
10

Insulin and chromogranin B secretory granules in β cell lines under physiological and stress conditions

Giordano, Tiziana January 2006 (has links)
No description available.

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