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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

The hypertension-prone man a study on the pathogenesis of hypertension with regard to insulin sensitivity /

Endre, Tomas. January 1997 (has links)
Thesis (doctoral)--Lund University, 1997. / Added t.p. with thesis statement inserted.
2

The hypertension-prone man a study on the pathogenesis of hypertension with regard to insulin sensitivity /

Endre, Tomas. January 1997 (has links)
Thesis (doctoral)--Lund University, 1997. / Added t.p. with thesis statement inserted.
3

Nitric oxide at the nucleus tractus solitarii and rostral ventrolateral medulla in protection against the high fructose diet-induced hypertension by peroxisome proliferator-activated receptor activators

Tsay, Shiow-jen 01 February 2010 (has links)
Insulin resistacne and hyperinsulinemia are important risk factors for development of type 2 diabetes mellitus and hypertension. Recently, accumulating evidence has shown that endothelial dysfunction, increases in peripheral vessel resistnce and overactivation of the sympathetic neruvous system contribute to the development of insulin resistance-associated hypertension. The signigicance of cardiovascular regulatory center in the brain stem in pathophysiology of the insulin resistance-induced hypertension, however, has not been explored. Previously studies have proved that increases in superoxide anion (O2£»−) production in peripheral tissue and suppression of nitric oxide (NO) expression in the endothial cell are involved in insulin resistance and hypertension. The nucleus tractus solitarius (NTS) and rostral ventrolateral medulla (RVLM) are involved in neural regulation of blood pressure by serving respectively as the primary baroreceptor afferent terminal sites and the location of sympathetic premotor neurons for cardiovascular regulation in the brain stem. Clinically, the peroxisome proliferator-activated receptor (PPAR) agonist is commonly prescribed for the treatment of type 2 diabetes mellitus by activate PPAR£^ to enhance peripheral tissue insulin sensitizing ability, to maintain blood glucose homeostasis. Intriguingly, both animal and human studies revealed that PPAR£^ agonist also possesses blood pressure lowering effect, although the underlying mechanism is not clear. We therefore investigated in the present study the role of NO and O2£»− in the NTS and RVLM in the pathophysiology of the high fructose diet-induced insulin resistacne and hypertension, and to evaluate the potential central antihypertensive effect of PPAR£^ agonist in rats subjected to high fructose diet. The normotensive male Wistar Kyoto rats (WKY) were divided into 4 groups, including 3 experimental group that received 60% high fructose diet for 8 weeks and one control group that received regular chow diet for the same period of time. Within the 3 experimental groups, two of them received oral administration of rosiglitazone or pioglitazone (10 mg/kg/day) at the last two weeks (from week 6 to week 8) and the third group received saline ingestion. Systemic blood pressure was measured by tail vein sphygmomanometer very week and venous blood was drawn every other week to measure blood sugar and insulin level. At the end of the experiment, oral glucose tolerance test (OGTT) was tested and O2£»− and NO production in the NTS and RVLM were quantified. In adult male WKY rats I found that high fructose diet induced insulin resistance, hypertriglycemia and hypertension. Oral administration of rosiglitazone or pioglitazone significantly blunted the hypertension, hypertriglyceridemia, and ameliorated insulin resistance induced by high fructose diet. The high fructose diet also increased tissue level of O2£»− in the NTS and RVLM. PPAR£^ agonist treatment for two weeks did not affect the induced oxidative stress in these two nuclei. NO production was also increased in the NTS and RVLM after high fructose diet for 6 weeks. Oral treatment of rosiglitazone or pioglitazone significantly attenuated NO production after high fructose diet. At the molecular level, protein expressions of the NADPH oxdase subunits (p40phox, p47phox and gp91phox) and superoxide dismutase (cupper/zinc SOD, mitochondrial SOD, extracellular SOD) were not altered in the NTS or RVLM after high fructose diet alone or in addition with rosiglitazone or pioglitazone treatment. In the RVLM, there was a significant increase in neuronal NO synthase (nNOS) expression with concomitant decrease in inducible NOS (iNOS) expression. Oral treatment of PPAR£^ agonist for two weeks significantly suppressed the induced nNOS upregulation and attenuated the induced downregulation of iNOS expression in the RVLM. Together these results suggest that overproduction of O2£»− and NO in the NTS and RVLM may related to the development of insulin resistance-associated hypertension. Oral treatment of PPAR£^ agonist, including rosiglitazone and pioglitazone, may provide antihypertensive protection by superssing the induced-nNOS expression and increasing the induced-iNOS expression in the RVLM.
4

Postprandial Metabolic Responses to Macronutrient in Healthy, Hyperinsulinemic and Type 2 Diabetic Subjects

Lan-Pidhainy, Xiaomiao 10 January 2012 (has links)
The literature comparing macronutrient metabolism in healthy and diabetic subjects is abundant; however, little data exists on how non-diabetic subjects with insulin resistance handle macronutrient. We did two studies to investigate the postprandial responses to macronutrient in healthy, hyperinsulinemic and type 2 diabetic (T2DM) subjects. In the first study, twenty-five healthy, non-diabetic subjects [9 with fasting serum insulin (FSI) <40pmol/L; 8 with 40 ≤ FSI < 70pmol/L; and 8 with FSI ≥ 70 pmol/L] were fed eleven test meals (50g oral glucose with 0-30g doses of canola oil or whey protein) after an overnight fast. There were no significant FSI × fat (p=0.19) or FSI × protein (p=0.08) interaction effects on glucose response, suggesting that the effects of fat or protein on glycemia were independent of FSI of the subjects. In addition, the changes in relative glucose response per gram of fat (r = -0.05, p = 0.82) or protein (r = 0.08, p = 0.70) were not related to FSI of the subjects. In the second study, Healthy (FSI < 40pmol/L), Hyperinsulinemic (FSI ≥ 40pmol/L), and T2DM were fed five foods with 50g available carbohydrate. Among the subject-groups, the Glycemic Index (GI) values were not significantly different for each food, and the mean (±SEM) GI values of all foods were not significantly different (p>0.05). However, the mean (±SEM) Insulinemic Index of the foods was higher in T2DM (100±7, n=10) than those of Healthy (78±5, n=9) and Hyperinsulinemic subjects (70±5, n=12) (p=0.05). The Insulinemic Index was inversely associated with insulin sensitivity (r=-0.66, p<0.0001), positively related to fasting- and postprandial-glucose (both r=0.68, p<0.0001) and hepatic insulin extraction (r=0.62, p=0.0002). The oral-glucose data were pooled from the two studies to investigate whether there was any relationship between GLP-1 and insulin sensitivity, β-cell function and hepatic insulin extraction. No significant correlation was observed (p>0.05). The results suggest that the glucose-lowering effect of fat and protein is not affected by insulin sensitivity. GI is independent of the metabolic status of the subjects; however, unlike GI, Insulinemic Index is influenced by the metabolic status of the subjects, and thus may have limited clinical utility.
5

Postprandial Metabolic Responses to Macronutrient in Healthy, Hyperinsulinemic and Type 2 Diabetic Subjects

Lan-Pidhainy, Xiaomiao 10 January 2012 (has links)
The literature comparing macronutrient metabolism in healthy and diabetic subjects is abundant; however, little data exists on how non-diabetic subjects with insulin resistance handle macronutrient. We did two studies to investigate the postprandial responses to macronutrient in healthy, hyperinsulinemic and type 2 diabetic (T2DM) subjects. In the first study, twenty-five healthy, non-diabetic subjects [9 with fasting serum insulin (FSI) <40pmol/L; 8 with 40 ≤ FSI < 70pmol/L; and 8 with FSI ≥ 70 pmol/L] were fed eleven test meals (50g oral glucose with 0-30g doses of canola oil or whey protein) after an overnight fast. There were no significant FSI × fat (p=0.19) or FSI × protein (p=0.08) interaction effects on glucose response, suggesting that the effects of fat or protein on glycemia were independent of FSI of the subjects. In addition, the changes in relative glucose response per gram of fat (r = -0.05, p = 0.82) or protein (r = 0.08, p = 0.70) were not related to FSI of the subjects. In the second study, Healthy (FSI < 40pmol/L), Hyperinsulinemic (FSI ≥ 40pmol/L), and T2DM were fed five foods with 50g available carbohydrate. Among the subject-groups, the Glycemic Index (GI) values were not significantly different for each food, and the mean (±SEM) GI values of all foods were not significantly different (p>0.05). However, the mean (±SEM) Insulinemic Index of the foods was higher in T2DM (100±7, n=10) than those of Healthy (78±5, n=9) and Hyperinsulinemic subjects (70±5, n=12) (p=0.05). The Insulinemic Index was inversely associated with insulin sensitivity (r=-0.66, p<0.0001), positively related to fasting- and postprandial-glucose (both r=0.68, p<0.0001) and hepatic insulin extraction (r=0.62, p=0.0002). The oral-glucose data were pooled from the two studies to investigate whether there was any relationship between GLP-1 and insulin sensitivity, β-cell function and hepatic insulin extraction. No significant correlation was observed (p>0.05). The results suggest that the glucose-lowering effect of fat and protein is not affected by insulin sensitivity. GI is independent of the metabolic status of the subjects; however, unlike GI, Insulinemic Index is influenced by the metabolic status of the subjects, and thus may have limited clinical utility.
6

EVIDENCE THAT THE ASSOCIATION BETWEEN EXERCISE INTENSITY AND INSULIN SENSITIVITY IS SEX DEPENDENT

Hougham, Kaitlyn 16 June 2011 (has links)
The purpose of this study was to determine if, after adjusting for the contribution of exercise dose, exercise intensity was associated with the improvement of insulin sensitivity. Abdominally obese, sedentary men (n = 16, [mean±SD] age: 45.0±7.5 yr; waist circumference: 108.6±5.3 cm) and women (n = 18, [mean±SD] age: 42.3±6.2 yr; waist circumference: 100.1±8.2 cm) performed daily, supervised exercise for 3 and 4 months, respectively. Exercising at a self selected exercise intensity, men were required to expend expended 700 kcal per session and women 500 kcal per session. Exercise intensity and dose were determined using heart rate and oxygen consumption data obtained from repeated graded exercise tests. Insulin sensitivity was determined by hyperinsulinemic euglycemic clamp. Insulin sensitivity improved in both men and women (change score: men = 7.2±5.4 mg/kgskm/min, women = 5.8±7.1 mg/kgskm/min) (p < 0.05). Exercise intensity was associated with the improvements in insulin sensitivity in men (unstandardized regression coefficient (β) = 0.43, p = 0.02). Adjusting for exercise dose, the change in abdominal adipose tissue (AT), or the change visceral AT did not alter this association (p < 0.05). Exercise intensity was not associated with the improvement of insulin sensitivity in women (β = - 0.11, p = 0.7). Adjusting for exercise dose, the change in abdominal or visceral AT did not change the association in women (p > 0.05). Our findings suggest that exercise intensity is independently associated with the improvement of insulin sensitivity in abdominally obese men but not women. / Thesis (Master, Kinesiology & Health Studies) -- Queen's University, 2011-06-13 19:56:40.465
7

Metabolic syndrome and insulin resistance in overweight/obese women in early postpartum

Lu, Hongxing 20 August 2010 (has links)
Metabolic syndrome includes several metabolic and hormonal disorders, such as abdominal obesity, insulin resistance, and lower blood ghrelin. Women with breastfeeding history exhibit a reduced risk for metabolic syndrome in later life. The purpose of aim 1 was to determine the incidence of metabolic syndrome in low income, overweight/obese women in early postpartum and to assess its relationship to lactation status. It has been found that the incidence of metabolic syndrome is much higher in formula feeding women than that of the breastfeeding ones (44.3% vs. 22.4%, p < 0.01). The breastfeeding mothers had reduced triglycerides (109.07 mg/dl vs. 143.10 mg/dl, p < 001) and elevated serum high-density lipoprotein (HDL)-cholesterol (58.59 mg/dl vs. 51.76 mg/dl, p < 0.01). The goal of aim 2 was to explore associations between ghrelin, metabolic syndrome and infant feeding methods in low income, overweight/obese women in early postpartum. In our study, the breastfeeding mothers in early postpartum had higher plasma ghrelin, as compared to those who formula fed (584.73 pg/ml vs. 450.77 pg/ml, p < 0.01). Additionally, it is found that plasma ghrelin was negatively associated with incidence and numbers of risk factors for metabolic syndrome, before and after controlling for body mass index (BMI). After adjusting for ghrelin in logistic regression analyses, significant relationships between lactation status and metabolic syndrome disappeared. Thus, the protective function of breastfeeding against metabolic syndrome in overweight/obese women in early postpartum may related to the plasma ghrelin values. The purpose of aim 3 was to detect the influence of weight loss on insulin resistance and plasma adiponectin, zinc (Zn), manganese (Mn) and copper (Cu) in low income, overweight/obese women in early postpartum. After an eight-week weight loss intervention, plasma levels of adiponectin, Zn and Mn were significantly enhanced, and plasma concentrations of insulin (7.53±0.56 vs. 6.23±0.49, p <0.01) and insulin resistance (1.84±0.15 vs. 1.44±0.12, p <0.01) were reduced. The increase of adiponectin, Zn and Mn was positively associated with weight reduction. However, the plasma Cu was not significantly affected. The relationships between weight loss and reduced insulin resistance disappeared after adjusting the increases of adiponectin, Zn and Mn during weight loss. Thus, weight loss had beneficial effects on insulin resistance, plasma values of adiponectin Zn and Mn. It is plausible that the influence of weight loss on insulin resistance may be associated with improvements of plasma of adiponectin, Zn and Mn. Collectively, the results of this study demonstrate the important benefits of breastfeeding on prevention of metabolic syndrome in overweight/obese women in early postpartum. This study also emphasizes the influence of ghrelin on risk factors of metabolic syndrome and lactation status. / text
8

The role of tyrosine, serine and threonine phosphorylation in the regulation of the insulin receptor tyrosine kinase activity

Lynch, Deborah Frances January 1995 (has links)
No description available.
9

The regulation of triglyceride metabolism in the liver and adipose tissue

Crawford, Lynne Mary January 1998 (has links)
No description available.
10

Aspects of cell membrane function in adult polycystic kidney disease

Vareesangthip, Kriengsak January 1997 (has links)
No description available.

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