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1

Dobson, Lee. "Glucose tolerance in cystic fibrosis." Thesis, University of Exeter, 2004. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.403679.

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2

Legate, Nicola J. "Glucose tolerance in 3 teleost species." Thesis, National Library of Canada = Bibliothèque nationale du Canada, 1999. http://www.collectionscanada.ca/obj/s4/f2/dsk2/ftp01/MQ45235.pdf.

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3

Berrish, Taher S. "Metabolic heterogeneity in impaired glucose tolerance." Thesis, University of Newcastle Upon Tyne, 1995. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.321310.

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4

Krishnaveni, Ghattu Vedamurthy. "Anthropometry, glucose tolerance and insulin concentrations in South Indian children : relationships to maternal glucose tolerance during pregnancy." Thesis, University of Southampton, 2005. https://eprints.soton.ac.uk/210920/.

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Earlier studies have shown that individuals whose mothers were diabetic when they were in utero, have an increased risk of early obesity, and impaired glucose tolerance (lGT) and type 2 diabetes in adult life. This study was designed to test whether adiposity, glucose tolerance and insulin concentrations are altered in Indian children born to mothers with gestational diabetes (GDM), and are related to maternal glucose and insulin concentrations in pregnancy even in the absence of GDM. 830 pregnant women attending the antenatal clinics of the Holdsworth Memorial Hospital (HMH), Mysore, India underwent an Oral Glucose Tolerance Test (OGTT) at 30+/-2 weeks. 674 of these women delivered at HMH. Detailed anthropometry was performed on the offspring at birth, and annually thereafter. 585 mothers returned with their offspring at 5 years of age for detailed investigations including OGTT for glucose and insulin concentrations, bio-impedance for fat estimation and blood pressure measurement. OGTT was administered to mothers and fasting plasma glucose and insulin concentrations were measured in fathers. The Mysore babies were small compared to UK neonates, but the deficit varied for different body measurements. While birthweight (-1.1 SD) was considerably lower, crown-heel length (-0.3 SD) and subscapular skinfold thickness (-0.2 SD) were relatively spared. At five years, subscapular skinfold thickness was larger than the UK standards (+0.23 SD, p
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5

Henareh, Loghman. "Impaired glucose tolerance in ischemic heart disease /." Stockholm, 2005. http://diss.kib.ki.se/2005/91-7140-445-7/.

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6

Page, Renee C. L. "Detection and treatment of impaired glucose tolerance." Thesis, University of Manchester, 1991. https://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.633671.

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7

勞子僖 and Tzu-hsi Terence Lao. "The obstetric implications of gestational impaired glucose tolerance." Thesis, The University of Hong Kong (Pokfulam, Hong Kong), 2002. http://hub.hku.hk/bib/B31981793.

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8

Kushnir, О. Yu. "Glucose tolerance profiles in rats with alloxan diabetes." Thesis, БДМУ, 2020. http://dspace.bsmu.edu.ua:8080/xmlui/handle/123456789/18366.

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9

Lao, Tzu-hsi Terence. "The obstetric implications of gestational impaired glucose tolerance." Hong Kong : University of Hong Kong, 2002. http://sunzi.lib.hku.hk/hkuto/record.jsp?B24463863.

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10

McGarry, Robert Gerard. "Modelling insulin/glucose dynamics and application to the analysis of oral glucose tolerance tests." Thesis, Queen's University Belfast, 1990. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.335562.

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11

Quinn, C. E. "Vascular function in impaired glucose tolerance : Effect of pioglitazone." Thesis, Queen's University Belfast, 2008. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.501394.

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12

Guri, Amir Joseph. "Abscisic acid ameliorates glucose tolerance and obesity-induced inflammation." Diss., Virginia Tech, 2007. http://hdl.handle.net/10919/29433.

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Obesity is a disease characterized by chronic inflammation and the progressive loss in systemic insulin sensitivity. One of the more effective medications in the treatment of insulin resistance have been the thiazolidinediones (TZDs), which act through the nuclear receptor peroxisome proliferator-activated receptor gamma (PPARgamma ). Due to the many side-effects of TZDs, our laboratory sought out a natural phytochemical, abscisic acid (ABA), with chemical similarities to TZDs. Our first study demonstrated that ABA activates PPARgamma in vitro and significantly ameliorates white adipose tissue (WAT) inflammation and glucose tolerance in db/db mice. We next further examined the effect of ABA on the phenotype of adipose tissue macrophages (ATMs). In doing so, we discovered two separate ATM populations which differed in their expression of the macrophage surface glycoprotein and maturation marker F4/80 (F4/80hi vs F4/80lo). Dietary ABA-supplementation significantly reduced F4/80hiCCR2+ ATMs and had no effect on the F4/80lo population. Utilizing a tissue-specific knockout generated through Cre-lox recombination, we were able to determine that this effect was dependent on PPARgamma in immune cells. To further characterize the differences between the ATM subsets that were affected by ABA, we performed a multi-organ assessment (i.e., WAT, skeletal muscle and liver) of the effect of diet-induced obesity on the phenotype of infiltrating macrophages and T cells into metabolic organs. Based on our new data, we formulated a model by which F4/80hiCCR2hi ATMs infiltrate WAT and ultimately induce a CD11c+ pro-inflammatory phenotype in the resident F4/80loCCR2lo subset. Ultimately, our findings provide evidence that ABA has potential as an alternative preventive intervention, expound the role of PPARgamma in immune cells and, in general, expand our knowledge concerning the immunopathogenesis of obesity-induced insulin resistance.
Ph. D.
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13

Inteeworn, Natalie. "The Effect of Hypothyroidism on Glucose Tolerance in Dogs." Thesis, Virginia Tech, 2008. http://hdl.handle.net/10919/32030.

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Background: Canine hypothyroidism is thought to cause abnormalities in glucose homeostasis, but the effect on glucose tolerance and insulin sensitivity has not been determined to date. Hypothesis/Objectives: The purpose of the study was to investigate whether hypothyroidism has an effect on glucose tolerance and insulin sensitivity in dogs. We hypothesized that hypothyroidism causes insulin resistance. Animals: Sixteen euthyroid bitches were randomly selected and allocated into two groups. In 8 dogs, hypothyroidism was induced by administration of 1 mCi/kg I-131. Experiments were performed on non-anesthetized, fasted dogs in anestrous approximately 12 months after hypothyroidism was induced. Methods: The insulin-modified frequently sampled intravenous glucose tolerance test (FSIGT) and minimal model analysis were used to determine basal insulin and glucose concentrations, acute insulin response to glucose (AIRg), insulin sensitivity (SI), glucose effectiveness (SG) and the disposition index (DI). Results: In the hypothyroid group, basal glucose concentrations were mildly decreased (P = 0.0079), whereas basal insulin was increased (P = 0.019). Insulin sensitivity was reduced in the hypothyroid group (P<0.001), whereas AIRg was higher (P=0.01). Other parameters were not different between groups. Conclusions/Clinical Importance: Hypothyroidism negatively affects glucose homeostasis by inducing insulin resistance. In hypothyroid dogs, the disposition index (insulin sensitivity x insulin secretion) remained unchanged due to a compensatory increase in insulin secretion, thereby maintaining glucose tolerance. In cases with impaired insulin secretion, such as canine diabetes mellitus, concurrent hypothyroidism can have important clinical implications in the successful management of the disease.
Master of Science
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14

Farmer, George. "Intravenous glucose tolerance in pregnancy : maternal correlates and fetal outcome." Thesis, University of Aberdeen, 1989. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.254868.

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To study maternal glucose tolerance in pregnancy and its effects on the fetus, a rapid 25g intravenous glucose tolerance test was performed at about 32 weeks gestation in a group of randomly selected women. Full glucose tolerance data was available in 815 cases. The results were withheld from the patients and their obstetricians and paediatricians, and no treatment or advice was offered. Fasting plasma glucose and indices of glucose disposal were distributed unimodally with no evidence of a separate pathological group towards the diabetic end of the distributions. Glucose disposal rate was not, however, signficantly associated with the fasting plasma glucose, suggesting that glucose intolerance associated with elevation of the fasting plasma glucose might be a more clearly defined entity. New reference standards for fasting plasma glucose in pregnancy, which differ from those currently in use, are presented. The major determinants of relatively impaired maternal glucose tolerance in pregnancy were maternal age and obesity. Nonetheless, many cases of relative glucose intolerance occurred in the absence of any preexisting clinical indication. Significant association were found between maternal glucose metabolism and various measures of neonatal size and morbidity, including the incidence of congenital malformations and the occurrence of perinatal asphyxia in post-term infants. These effects were graded through much of the range of maternal glucose tolerance and not of predictive value in individual cases. The available evidence did not indicate that these relationships were mediated by fetal hyperinsulinism. It is concluded that the adverse consequences of impaired glucose disposal with normal fasting plasma glucose in pregnancy do not justify exhaustive measures to identify the condition. Screening for glucose intolerance during pregnancy should seek to identify those cases in which glucose intolerance is associated with elevation of fasting plasma glucose.
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15

Wong, Mei-ling. "Fetal myocardial performance in pregnancies complicated by impaired glucose tolerance /." View the Table of Contents & Abstract, 2005. http://sunzi.lib.hku.hk/hkuto/record/B34885845.

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16

Duwaihy, Mansour Mohammad. "Effect of dietary fat on glucose tolerance in the rat." Thesis, University of Surrey, 2000. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.326901.

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17

Galderisi, Alfonso. "Incretin Effect in Youths with Normal and Impaired Glucose Tolerance." Doctoral thesis, Università degli studi di Padova, 2020. http://hdl.handle.net/11577/3424892.

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Background. Prediabetes includes a broad range of glucose metabolism alterations that increase the risk for diabetes in youths. Analogues of gut-derived hormones (incretins) have been paved as a promising therapeutic option for youths with diabetes. Though, we lack in vivo studies assessing the incretin effect in prediabetes and early diabetes in youths as well as longitudinal assessment of the incretin response in this age. We estimated the incretin effect in obese youths with normal and impaired glucose tolerance, by the use of the gold standard matched oral glucose tolerance test (OGTT) and iso-glycemic intravenous glucose tolerance test (iso-IVGTT). Methods. We enrolled 30 overweight/obese youths with normal (NGT) and impaired (IGT) glucose tolerance. Each participant underwent a 180-minutes OGTT and an iso-IVGTT to quantify the incretin effect, followed by a hyperglycemic clamp to measure glucose and arginine induced insulin secretion. Seriated samples for plasma glucose, insulin, C-peptide and active GLP-1(7-36) were collected. The minimal model and deconvolution were adopted to estimate insulin secretion based on glucose and C-peptide. The hyperglycemic clamp-derived indices were A) M/I for insulin sensitivity, B) acute (0–10 min [first phase]) C-peptide response to glucose (ACPRg), C) steady-state C-peptide concentrations at plasma glucose of 11.1 mmol/L, and D) arginine-stimulated maximum C-peptide response at plasma glucose >25 mmol/L (ACPRmax). Results. We completed the three tests in 28 youths (15.9±2.4y, 14F, 13 NGT, 15 IGT). The NGT and IGT groups did not differ with respect to age, ethnicity, BMI, fasting glucose. No significant differences were observed between the two groups in either measure of β-cell function [ACPRg, steady- state C-peptide, ACPRmax, (p=0.372, p=0.478 and p=0.230)] or in insulin sensitivity [M/I] (p=0.106). The incretin effect was higher in the NGT than IGT group (+28.3%[-4, 62] and -10.3%[-34.3, 14.2], p=0.022), in spite of a lower GLP-1 secretion rate during the OGTT in the NGT group (p<0.001). Conclusion. Impairment of glucose tolerance in youths is associated with a reduced incretin effect in the absence of a significant impairment of β-cell function. The higher secretion rate of GLP-1 is suggestive for a primary incretin resistance. The incretin pathway could represent potential target for therapeutic interventions in youth onset prediabetes.
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18

Kondo, Yaeko. "The study of plasma glucose level and insulin secretion capacity after glucose load in Japanese." Kyoto University, 2016. http://hdl.handle.net/2433/215958.

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19

Venter, Teneille. "The effects of three carbohydrate supplementation protocols on the blood glucose levels in type I diabetic subjects during a 60 minute bout on the treadmill." Thesis, Nelson Mandela Metropolitan University, 2014. http://hdl.handle.net/10948/4157.

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Diabetes associated complications make management during exercise complex (Brugnara, Vinaixa, Murillo, Samino, Rodriguez, Beltran, Lerin, Davison, Correig & Novials, 2012). Research on the prevention of such challenges is of paramount importance. The aim of this study was to determine the effects of three different carbohydrate supplementation protocols on blood glucose levels after every 10 minutes of a 60 minute exercise bout at 65 to 75 % HRR on the treadmill as well as every half hour during a two hour post exercise recovery period. The three protocols implemented after a standardized pre-exercise meal were: control protocol (no carbohydrate supplementation), protocol 1 (one carbohydrate supplementation of 15 grams given at 30 minutes) and protocol 2 (two carbohydrate supplementation of 15 grams given at 30 minutes and 45 minutes). A total of 32 participants took part in the study (Mean age: 32.84 ±12.12). All participants were submitted to all three protocols. Statistical and practical significant differences were found between blood glucose levels of protocol 0 and protocol 1 (MDIF = 2.62 ± 3.99 mmol.L--‐1) at 20 minutes of the exercise duration (p=.024;d=0.42). Statistical and practical significant differences in blood glucose levels with protocol 0 rendering the higher glucose values were also found between protocols 0 and 2 at 10 minutes (MDIF = 3.44 ± 5.54 mmol.L--‐1; p=.001;d=0.62), 20 minutes (MDIF = 3.32 ± 5.23 mmol.L--‐1; p=.001;d=0.63) and 30 minutes of exercise (MDIF = 2.81 ± 5.40 mmol.L--‐1; p=.006;d=0.52) as well as between the mean minimum (M0 = 9.49 ± 4.51 mmol.L--‐1 and M2 = 7.28 ± 4.07 mmol.L--‐1; p=.013;d=0.46), mean maximum (M0 = 12.73 ± 5.51 mmol.L--‐1 and M2 = 10.07 ± 4.63 mmol.L--‐1; p=.015;d=0.46) and overall mean (M0 = 9.07 ± 4.88 mmol.L--‐1 and M2 = 8.53 ± 4.25 mmol.L--‐1; p=.011;d=0.48) with protocol 0 rendering the higher glucose values in all these comparisons. It was concluded that carbohydrate supplementation during exercise affects blood glucose levels positively particularly considering the significant difference found between protocol 0 and 2. Whilst protocol 2 also resulted in less fluctuations in the blood glucose levels during exercise and minimum, overall mean and maximum blood glucose values were closer to “normal/safe” range, there was no conclusive evidence that protocol 2 was better than protocol 1.
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20

Crimmins, Nancy. "Prevalence and Predictors of Abnormalities in Carbohydrate Metabolism in a Cohort of Obese Youth." University of Cincinnati / OhioLINK, 2009. http://rave.ohiolink.edu/etdc/view?acc_num=ucin1258490989.

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21

Corpeleijn, Eva. "Fatty acid metabolism, impaired glucose tolerance and the effects of lifestyle." [Maastricht] : Maastricht : [Maastricht University] ; University Library, Universiteit Maastricht [host], 2006. http://arno.unimaas.nl/show.cgi?fid=10536.

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22

Abtahi, Zohreh. "Ethanol and glucose tolerance of M.indicus in aerobic and anaerobic conditions." Thesis, Högskolan i Borås, Institutionen Ingenjörshögskolan, 2008. http://urn.kb.se/resolve?urn=urn:nbn:se:hb:diva-19029.

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Over the last few decades, ethanol production from renewable resources has been of interest as an alternative fuel to the current fossil fuel, due to the unstable oil market and in order to decrease net emission of carbon dioxide which leads to global warming. According to analyses of DG Transport and Energy (TREN), it is not possible to reach the current biofuels directive promoting 5,75 % biofuel by the year 2010, due to the markets and technologies, but by the year 2020 achievement of 6.9% is expected. This new law will increase biofuel demand by 3,1 %.Lignocelluloses materials, which are relatively cheap and plentiful, are considered to be the main source of feedstock’s for low-cost bio-ethanol production. The general procedure to convert lignocelluloses material to bioethanol is hydrolysis of the hemicelluloses and the cellulose to its monomer sugars, fermentation and distillation.Bacteria, yeasts and filamentous fungi are able to ferment hydrolysates from different plants and convert it to bioethanol.Mucor indicus is a filamentous fungus; it is able to utilize a wide range of hexoses, phentoses and disaccharides (cellobiose) in order to produce ethanol. The Ethanol yield and productivity of this microorganism from hexoses are as same as Saccharomyces cerevisiae. But the reason that it is one of the candidates for ethanol production is the fungus ability to utilize xylose. The cell wall of M.indicus contains significant quantity of chitosan/chitin which can be easily extracted. Chitosan is the deacetylated products of chitin. They have many applications in chemistry, biotechnology, medicine, veterinary, dentistry, agriculture, food processing, environmental protection, water purification, cosmetic and textile industries.The results of the current work show that the glucose concentration in the medium had a great impact on the lag phase, glucose consumption and ethanol production in both aerobic and anaerobic conditions. The lag phase increased as the initial concentration of glucose increased. While the glucose concentration increased above 190 g/l in the medium the glucose consumption and ethanol production decreased in both aerobic and anaerobic conditions. The glucose tolerance of M.indicus in both aerobic and anaerobic condition is about 190 g/l and in the anaerobic condition the ethanol tolerance of this fungus is around 70 g/.
Uppsatsnivå: D
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23

Suzuki, Haruhiko. "Factors responsible for development from normal glucose tolerance to isolated postchallenge hyperglycemia." Kyoto University, 2008. http://hdl.handle.net/2433/135917.

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24

Macklin, Lauren Nicole. "EXAMINING PERIPHERAL GLUCOSE TOLERANCE IN THE 3xTg MOUSE MODEL OF ALZHEIMER'S DISEASE." OpenSIUC, 2011. https://opensiuc.lib.siu.edu/theses/599.

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Alzheimer's disease (AD) is a progressive neurodegenerative disease characterized by beta-amyloid (Abeta) deposition, neurofibrillary tangles and cognitive decline. Clinical data suggest that diabetes may be a risk factor for AD and several studies have linked pro-diabetic diets with an acceleration of AD pathology. Consequently, we hypothesized that the 3xTg AD-like mouse model may show impaired glucose tolerance, therefore; we examined whether glucose tolerance was altered in the 3xTg mouse model of AD early in the pathogenesis (prior to Abeta plaques, neurofibrillary tangle sand cognitive decline) and if so, did it persist throughout. Specifically, 1, 2-3, 4-6, 8-10 and 17 month old male 3xTg mice and wild-type counterparts were assessed for fasting glucose levels, glucose tolerance, plasma insulin levels, insulin sensitivity and the neural and behavioral pathological characteristics of AD. At 1 month, 3xTg mice compared to wild-type controls exhibited impaired glucose tolerance during an intraperitoneal glucose tolerance test (ipGTT), a trend for reduced fasting plasma insulin levels at time 0 and significantly reduced fasting plasma insulin levels 15 minutes post glucose bolus suggesting a possible defect in beta cell function. Interestingly, the glucose intolerance was not a consequence of altered food intake or body weight since these parameters were similar between the 3xTg mice and wild-type controls. Moreover, responsiveness to exogenous insulin during the intraperitoneal insulin tolerance test was not significantly different suggesting equivalent insulin sensitivity. During aging both 3xTg mice and controls exhibited exacerbated changes in fasting glucose levels and glucose tolerance. Interestingly, while control animals show an increase in fasting insulin levels with age, 3xTg mice do not. Immunohistochemical staining for 6E10 and Abeta 1-42 revealed only intraneuronal deposition of reaction product in 3xTg mice with no extracellular depositions noted until 14 months of age. Immunoreactivity of p-tau was observed at 1 month in the hippocampus and cortex and worsened throughout the time period examined. Behavioral deficits began to be detected in 3xTg mice relative to wild-type controls at 21 months of age. The islets in the pancreas suggest that at 2-3 months of age 3xTg mice compared to wild-type controls have a significantly lower amount of immunoreactivity for insulin within their islets although islet size did not differ between groups and this persisted throughout all the time points examined (4-6 and 8-10 months). Taken together, these data reveal that the AD-like 3xTg mouse model exhibits a pro-diabetic phenotype early in the development of AD-like pathology and that this metabolic deficit persists throughout their lifespan raising the question of whether altered glucose regulation and insulin production/secretion could contribute to AD pathogenesis.
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25

Price, Sally Ann. "Continuous Subcutaneous Glucose Monitoring (CGM) to predict progression from abnormal glucose tolerance (Pre-diabetes) to Type 2 Diabetes Mellitus." Thesis, Cardiff University, 2016. http://orca.cf.ac.uk/95959/.

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The global incidence of Type 2 Diabetes Mellitus (T2DM) is increasing rapidly. Many people with impaired fasting glucose (IFG) or impaired glucose tolerance (IGT) will however not progress to T2DM but appear to spontaneous revert to normal glucose homeostasis, others however will progress slowly and in some cases rapidly progress towards diabetes. Therapeutic interventions will reduce the risk, or at least the pace, of deterioration from IFG and IGT to T2DM. However, in order to target interventions appropriately, to prevent progression in those at greatest risk further information as to which individuals are most likely to progress is needed. There is a variable rate of progression from either IFG, IGT or combined IFG and IGT to T2DM and in general, progression rates are lowest in the general population and highest in target “at-risk” group. Age, body mass index (BMI), fasting and 2 hour plasma glucose concentrations, elevated fasting pro-insulin, low 2-hour insulin and fasting triglyceride levels are known to be associated with a greater risk of progression and in order to maintain normoglycemia, adequate quantitative and qualitative moment-by-moment pancreatic beta-cell secretion and action is essential. A marker of deteriorating carbohydrate homeostasis would be increased fluctuations in blood glucose levels and continuous glucose monitoring (CGM) is an ideal method to look at just this. The use of CGM to quantify the fluctuations was proposed to assess whether CGM can help identify people with abnormal glucose tolerance that progress to T2DM. In this study, CGM profiles inspected by eye for variability appeared to correlate well with mathematically devised CGM parameters based on CGM data, both at baseline and at Year 1. However, neither the subject CGM profiles nor the CGM parameters at baseline were significant in predicting progression to diabetes (T2DM) at Year 1 or Year 3 from a pre diabetic state at baseline. However, when one looked at progression from pre diabetes to diabetes, with regard to CGM profiles and CGM parameters, the interval period between study baseline and Year 1 appeared to be when most variation in glucose levels occurred; this was especially the case for those subjects with IFG, compared to subjects with IGT or IFG+IGT mix, respectively. This effect was diluted at Year 3 and not observed. In conclusion, this study demonstrated that CGM did not predict progression from pre diabetes to diabetes (T2DM), but did however, correlate well by eye with mathematical assessments models of the same CGM data and identify an at risk IFG group that could be targeted at baseline with more intensive therapy.
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26

Dietz, Richard E. "Effects of feeding supplemental fat to cows in late gestation on cold tolerance in newborn calves." Thesis, Virginia Tech, 2000. http://hdl.handle.net/10919/34572.

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Two experiments were conducted to investigate the effects of added fat in late gestation cow and heifer diets on thermogenic and neonatal metabolic responses. In Experiment 1, the effects of source of fat in late gestation diets on serum glucose and thermogenic response during short-term cold stress were examined in fall-born neonatal beef calves. Pregnant fall-calving heifers (n = 15) were randomly assigned to three dietary treatments: Control (CON, n=5), Safflower seed (SAF, n=5), or Cottonseed (COT, n=5) supplement. Hay-based isonitrogenous and isocaloric diets met NRC requirements while containing 1.53%, 4.0% and 5.0% fat for CON, SAF and COT diets, respectively. Diets were fed for 47.5 ( 5.4 d before calving. Heifers were weighed weekly and at parturition. At parturition, colostrum samples were taken from the dam, calves weighed, and vigor scores recorded. Calves remained with their dams for 5 h to nurse. At 5.5 h of age, calves were fitted with an indwelling jugular catheter. At 6.5 h of age, calves were placed in a 5(C cold room for 90 min. Shivering scores (1= no shivering, 2 = slight shivering 3 = muscle shivering, 4 = severe muscle shivering), rectal temperatures and blood samples were taken every 15 min. Colostrum samples were analyzed for fat, solids, protein, lactose and IgG concentrations. BW and BCS of heifers at calving, and birth weights and vigor scores of calves were unaffected by diet (P > .5). Mean fat, lactose and IgG concentrations in colostrum were not different (P > .3) among treatments. SAF tended to increase colostral solids (P = .11) and protein (P = .13) compared to COT or CON. During cold stress, calf body temperature increased in a quadratic fashion (P < .03). Mean glucose levels tended (P = .12) to be greater and shivering scores were non-significantly increased in CON compared to SAF or COT calves. Glucose concentrations averaged 74.4, 51.9, and 60.0 ( 7.3 mg/dl, whereas shivering score averaged 2.14, 1.69, and 1.68 ( .24 in CON, SAF and COT calves, respectively. Shivering scores increased in all groups during cold exposure in a linear fashion (P < .001). Vigor scores increased in a linear fashion throughout cold exposure for all groups (P < .04). Cortisol concentrations decreased in a cubic fashion throughout cold exposure for all groups (P < .02). Cortisol concentrations averaged 28.62, 37.7, and 35.65 + 3.58 ng/ml in CON, SAF and COT calves, respectively. We conclude that calves from dams fed high fat diets containing safflower seeds or cottonseed respond similarly to cold stress, but these responses are not necessarily consistent with greater cold resistance. In Experiment two, pregnant spring-calving cows (n = 75) were randomly assigned to two dietary treatments: Control (CON, n=35) and Cottonseed (COT, n=40). Hay-based isonitrogenous and isocaloric diets met NRC requirements while containing 2.0% and 5.0% fat for CON and COT diets, respectively. Diets were fed for 60 ( 5 d before calving. At parturition, calves were weighed, ambient temperature was recorded and dystocia score was recorded. At 30 min of age, rectal temperature one was recorded and shivering scores (1= no shivering, 2 = slight shivering 3 = muscle shivering, 4 = severe muscle shivering) were recorded. At 180 min postpartum, two blood samples were drawn from each calf to determine blood glucose and cortisol concentrations. At 36 + 4 h postpartum, two blood samples were again drawn from each calf to determine blood glucose and IgG concentrations. Calf birth weight, calf sex, vigor score, shivering score, time to stand, dystocia score, and serum IgG concentrations were unaffected (P > .5) by diet. Shivering score was affected by ambient temperature (P < .003) and time of calving (P < .006). Calf birth weights were unaffected by diet, calf sex, and the diet x calf sex interaction (P > .2). Mean time to nurse was non-significantly longer (101.2 vs 70.1 min), respectively, for COT calves compared to CON calves. At 30 min (P < .05) rectal temperatures were higher in male than female calves from dams on the COT diet (39.3 vs 39.1(C). Whereas rectal temperatures were lower in male calves than female calves from dams on the CON diet (39.1 vs 39.3(C; diet x calf/sex, P < .05). The same relationship among rectal temperatures was observed at 180 min (diet x calf/sex, P < .05). Changes in body temperature between 30 and 180 min were affected by diet (P < .05) as body temperatures for COT calves increased more from 30 min to 180 min than CON calves. Body temperature at 30 min was affected by time of calving (P < .01). Body temperature at 180 min was affected by ambient temperature at calving (P < .03) and there was a tendency for body temperature at 180 min to be affected by time of calving (P < .09). Serum glucose concentrations at time 180 min were unaffected by diet (P > .3). Serum glucose concentrations at time 36 + 4 h tended to be affected by sex (P < .07). With glucose levels higher in females (127 mg/dl) than in males (119 mg/dl). Differences in serum glucose at time 180 min and 36 + 4 h were not affected by diet, sex, or diet x sex interaction (P > .7). Serum glucose at 36 + 4 h was affected by ambient temperature at calving (P < .04). Mean serum cortisol concentrations tended to be higher (47.4 ng/ml vs 36.5 ng/ml) for COT calves compared to CON calves (P < .09). Differences in serum cortisol levels were unaffected by sex or diet x sex interaction (P > .5). When ambient temperature or time of calving were included as covariates, calf weight, calf vigor and serum IgG were unaffected by ambient temperature or time of calving (P > .05).
Master of Science
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27

Mbu, Desiree Lem. "Expression of circulating Microrna’s (Mirnas) in blood of mixed ancestry subjects with glucose intolerance." Thesis, Cape Peninsula University of Technology, 2018. http://hdl.handle.net/20.500.11838/2816.

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Thesis (MSc (Biomedical Sciences))--Cape Peninsula University of Technology, 2018.
Background: Early detection of individuals who are at risk of developing Glucose Intolerance would decrease the morbidity and mortality associated with this disease. MicroRNA is one of the most widely studied biomolecules involved in epigenetic mechanisms, hence it offers unique opportunities in this regard. Circulating microRNAs are associated with disease pathogenesis during the asymptomatic stage of disease. This has therefore attracted a lot of attention as a potential biomarker for identifying individuals who have an increased risk of developing Glucose Intolerance. The identification of high risk biomarkers for Glucose Intolerance will go a long way to eliminate the possible complications that arise due to late diagnosis and treatment of Glucose Intolerance. This could ultimately lead to better ways to prevent, manage and control the Glucose Intolerance epidemic that is rampant worldwide. The aim of the study is to investigate expression of circulating microRNA’s in blood of mixed ancestry subjects with glucose intolerance. Methods: A quantitative cross-sectional study design involving 36 individuals [who were age, gender and BMI (Body Mass Index) matched] from a total population of 1989 participants of mixed ancestry descent, residing in Bellville South, South Africa was used. Participants were classified as controls (normoglycemic), pre-diabetic (preDM) and diabetic (DM) (screen detected diabetic) according to WHO criteria of 1998. MicroRNAs were extracted from serum using the Qiagen miRNeasy Serum/Plasma Kit (ThermoFisher). The purified micro RNAs were reverse-transcribed to cDNA (complementary deoxyribonucleic acid) using the Qiagen RT2 First Strand Kit. Then, using Qiagen miScript SYBR Green PCR kit and miScript miRNA PCR arrays (ThermoFisher), the real time polymerase chain reaction was done to determine the expression profile the circulating micro RNAs present in the serum of the participants. Results: The 36 participants were evenly divided into 3 groups of 12 participants each as mentioned earlier. There were significant differences between groups in the waist (cm) (p=0.0415) and waist/hip ratio (p=0.0011) with highest values in the DM group and lowest in the normal group. Clinical parameters varied significantly according to glycemic status. As expected, the FBG (mmol/L) (p<0.0001), 2 HRs Post Glucose (mmol/L) (p<0.0001), HbA1c (%) (p=0.0009), Fasting Insulin (mIU/L) (p=0.0039), were all highest in the DM and lowest in the control group. In contrast, the 2 HRs Post Insulin (mIU/L) (p = 0.0027) was highest in the preDM group and lowest in the normal group, while the Glucose/Insulin ratio (p=0.0477) was highest in the normal group and lowest in the preDM group. Triglycerides (mmol/L) (p=0.0043) and Total Chol (mmol/L) (p=0.0429) were significantly increased through the three groups, with highest values in the DM group and lowest in the normal group. Furthermore, 12 of the 84 miRNAs studied were expressed through all the 3 groups and they exhibited both inverse and positive correlations between the clinical parameters, especially the glucose parameters (Fasting blood glucose, 2 hours post glucose, Fasting blood insulin, 2 hours post insulin and Glycated Hemoglobin).
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28

Norhammar, Anna. "Diabetes mellitus, glucose abnormalities and acute coronary syndromes : studies on prevalence, risk and impact of treatment /." Stockholm, 2003. http://diss.kib.ki.se/2003/91-7349-561-1.

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29

Marchionne, Elizabeth Marie, M. K. Diamond-Stanic, and E. J. Henriksen. "Chronic Renin Inhibition with Aliskiren Improves Glucose Tolerance, Insulin Sensitivity, and Skeletal Muscle Glucose Transport Activity in Obese Zucker Rats." Thesis, The University of Arizona, 2011. http://hdl.handle.net/10150/144566.

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30

Guan, Jiayan. "Glucose tolerance and turnover, and insulin sensitivity, in rats with pancreas islet transplants." Thesis, National Library of Canada = Bibliothèque nationale du Canada, 1998. http://www.collectionscanada.ca/obj/s4/f2/dsk2/ftp02/NQ31137.pdf.

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31

Fluckey, James D. "The effects of progressive resistance exercises on glucose tolerance in individuals with NIDDM." Virtual Press, 1992. http://liblink.bsu.edu/uhtbin/catkey/834626.

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This study was conducted to determine if improvements in glucose tolerance could be demonstrated following an acute bout of progressive resistance exercises. Fourteen individuals, not currently weight training, were assigned to two groups using the guidelines established by the WHO for NIDDM and normal (CON), based on the results of a three hour 75 g (-1.2M) load oral glucose tolerance test (OGTT). Eight blood samples were collected during the OGTT and assayed for glucose, insulin, and C-peptide. Each subject from the NIDDM (n=7) and CON (n=7) groups participated in a familiarization period, including a IRM, with eight different Nautilus selectorized exercise machines utilizing both the upper and lower body. A 3 set x 10 repetition exercise protocol based on the IRM was conducted and followed 18 hours later by another OGTT. Two day diets were replicated from the prior OGTT. Analysis of variance failed to demonstrate significant differences in the total responses or at any specific sampling points from pre to postprotocol for glucose (p=0.53), C-peptide (p=0.07) or the C-peptide:insulin ratio (p=0.16) in either group. Blood insulin levels from pre to postprotocol were significantly reduced (p=0.001) by 24% and 22% for the NIDDM and CON groups, respectively. These data suggest that a single series of progressive resistance exercises improve insulin uptake by the tissues without augmenting glucose disposal.
School of Physical Education
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32

Sinsigalli, Nancy A. "Glucose tolerance, plasma insulin, and plasma glucagon in relation to obesity in chickens." Thesis, Virginia Tech, 1985. http://hdl.handle.net/10919/45737.

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Relationships among glucose tolerance, plasma insulin, and plasma glucagon were examined in chicks developed through selection for high (HW) and low (LW) body weight, and in F, crosses (HL) between HW males and LW females. At 21, 42, 63, and 84 days of age, chicks from each population were intubated with glucose (2 g/kg body weight) following a 24-hr fast. Blood was collected at 20-minute intervals up to 100 minutes postadministration. At all ages, the LW chicks were better able to metabolize glucose than their HW counterparts, while the HLs exhibited intermediate responses. Impaired glucose tolerance in the HWs and HLs was not associated with insulin insufficiency; the HWs and HLs, in comparison to the LWs, were hyperinsulinemic at 42 and 63 days of age and plasma insulin levels did not differ among populations at 21 or 84 days of age. Plasma glucagon responses to glucose administration were inconsistent, but plasma glucagon levels were consistently higher in the HWs and HLs than in the LWs. It was concluded that excessive fat deposition in chickens selected for rapid growth is associated with hyperinsulinemia and insulin resistance.
Master of Science
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33

van, Eyk Gregory Ryan. "Dietary Fat and Sugar Induce Obesity and Impair Glucose Tolerance in Prepubertal Pigs." Thesis, Virginia Tech, 2012. http://hdl.handle.net/10919/32892.

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A pig model of childhood obesity was used to study the effects of dietary energy on body adiposity, and blood parameters associated with impaired glucose clearance. Prepubertal female pigs weaned at 21 d of age were fed control (CON), refined sugar (SUG), fat (FAT), and sugar-fat (SUGFAT) diets in a completely randomized arrangement for 16 wk. Calories from fat were 8.9% for CON, 5.6% for SUG, 35.5% for FAT and 32.3% for SUGFAT. Calories from sugar were 36.0% for SUG and 30.7% for SUGFAT. Adding fat, sugar or both to diets increased (P < 0.003) calorie intake. Percentage body fat was higher (P < 0.0001) in all treatments compared to CON, and in SUGFAT and FAT compared to SUG. Ultrasound back fat depth was positively correlated (r2 = 0.909; P < 0.001) with percentage body fat and negatively (r = 0.912; P-value ) with percentage body protein. Area under the curve (AUC) in response to oral glucose tolerance at 14 wk was higher (P < 0.03) in FAT (+14.6%) and SUGFAT (+25.5%) pigs compared to CON. Glucose AUC from sugar-fed pigs was not different (P = 0.2) from fat alone-fed pigs. Adding sugar, fat, or their combination to diets increased (P < 0.008) blood glucose and decreased (P < 0.0009) plasma insulin AUC. These data show that inclusion of fat and refined sugar in pig diets increases body adiposity and impairs glucose homeostasis and suggests that the composition of calories consumed may have different effects than simply consumption of excess of calories.
Master of Science
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34

Baker-Kuhn, Allison E. "Infant Adiposity at Birth in Relation to Maternal Glucose Tolerance and Cytokine Levels." University of Cincinnati / OhioLINK, 2015. http://rave.ohiolink.edu/etdc/view?acc_num=ucin1439281187.

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35

Strat, Karen M. "The Effects of Acute Consumption and Chronic Supplementation of Cocoa on Overweight and Obese Adults at Risk of Developing Diabetes." Diss., Virginia Tech, 2016. http://hdl.handle.net/10919/82433.

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The prevalence of obesity and diabetes is increasing in the United States and abroad and strategies are needed to prevent the progression from an at-risk state to the clinically diagnosed diseases. Flavanols in cocoa powder have been shown to reduce blood glucose concentrations, improve insulin sensitivity, and decrease gut permeability in animals and humans, but it is unknown if this occurs in adults with prediabetes. Therefore, we first hypothesized that an acute dose of cocoa would reduce postprandial glucose and enhance insulin and incretin hormone responses to a mixed meal challenge compared to a placebo. Second, we hypothesized that 15 g cocoa/day for 4-weeks would reduce gut permeability, attenuate endotoxin response to a high fat meal, improve insulin sensitivity, and improve measures of skeletal muscle substrate flexibility in a randomized, double blinded, placebo controlled parallel group design. To test the first hypothesis, 30 overweight or obese volunteers who were at-risk for diabetes completed two meal challenges using a randomized crossover design. Blood samples were collected hourly for 4 hours and were analyzed for glucose, insulin, C-peptide, glucagon-like peptide 1 (GLP-1), and gastric inhibitory peptide (GIP). Cocoa did not influence these measures. However, participants with the lowest fasting blood glucose concentrations were more likely to respond to the cocoa as hypothesized. To test our second hypothesis, 15 overweight or obese adults at risk for developing diabetes consumed either the cocoa or placebo treatments along with a controlled diet for one month. Overall, cocoa did not seem to influence insulin sensitivity, gut permeability, or endotoxin levels, although cocoa may influence skeletal muscle substrate metabolism. In conclusion, the data for both studies suggests that cocoa did not exert substantial effects on the evaluated outcomes. However, the experiments did provide valuable information about incretin hormone levels in adults with impaired glucose tolerance. More research is needed to understand how cocoa can affect glucose homeostasis for overweight or obese adults.
Ph. D.
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36

Soita, David Jonah. "The prevalence of impaired glucose tolerance and diabetes amongst the middle aged population of Bellville South community, Cape Town, South Africa." Thesis, [S.l. : s.n.], 2009. http://dk.cput.ac.za/cgi/viewcontent.cgi?article=1060&context=td_cput.

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37

Armaghanian, Natasha. "Abnormal Glucose Tolerance in Cystic Fibrosis and the Role of Low Glycaemic Index Diets." Thesis, The University of Sydney, 2018. http://hdl.handle.net/2123/20456.

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Abnormal glucose metabolism states have increased in prevalence in cystic fibrosis (CF). Hypoglycaemia without glucose lowering therapies is a novel complication, with no unifying definition or hypothesis for its aetiology. Thus optimal management strategies for discomforting symptoms remain unclear. Furthermore, there is little evidence for what might prevent progression of impaired glucose tolerance in CF and modifiable factors such as dietary intake in abnormal glucose tolerance may be useful. Five studies were conducted in this thesis: 1) a systematic review of hypoglycaemia in CF in the absence of glucose lowering therapies; 2) a review of an adult CF clinic describing the prevalence of hypoglycaemia on an oral glucose tolerance test (OGTT) and in free-living situations; 3) an extended OGTT study exploring hormonal responses to and the prevalence of post-prandial hypoglycaemia; 4) a study utilising a semi-structured questionnaire and continuous glucose monitoring (CGM) to report on the prevalence of hypoglycaemia in free-living states; 5) a study describing diet quality and the relationship between dietary intake, including dietary glycaemic index (GI) and glucose load (GL), and glucose dysmetabolism using CGM. The systematic review found hypoglycaemia in the absence of glucose lowering therapies occurred during OGTT and CGM. Hypoglycaemia was confirmed on OGTTs and a sub-group of participants reported symptoms suggestive of hypoglycaemia in free-living states. The prevalence of hypoglycaemia may be unmasked by extension of the OGTT out to 3 hours. Abnormal insulin release appears to have a role in its aetiology. The semi-structured questionnaire and CGM confirmed episodes of hypoglycaemia in free-living situations. A detailed food record and formal dietary analysis provided some support for a correlation between dietary GI, GL and glycaemic response variables on CGM. These studies provide empirical support for randomised controlled trials of dietary intervention in CF related glucose dysmetabolism.
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38

Massimino, Stefan Patrick. "The effect of fermentable dietary fiber on glucose tolerance and immune function in dogs." Thesis, National Library of Canada = Bibliothèque nationale du Canada, 1997. http://www.collectionscanada.ca/obj/s4/f2/dsk3/ftp05/mq22635.pdf.

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39

Brambrink, Jill K. "Glucose tolerance and insulin sensitivity following exercise : influence of muscle mass and absolute work." Virtual Press, 1992. http://liblink.bsu.edu/uhtbin/catkey/834516.

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To determine the influence of muscle mass and absolute work on glucose tolerance and insulin sensitivity following exercise, glucose and insulin responses to an oral glucose tolerance test (OGTT) were analyzed in twelve subjects at baseline and 16 to 18 hrs following three different exercise trials performed on a cycle ergometer: 1) two-legged exercise at 60% of two-leg maximal oxygen uptake (VO2max), 2) one-legged exercise at 60% of the oneleg VO2max, and 3) a second one-leg trial at 60% of one-leg VO2max with work matched to the work obtained during the two-leg trial. Each trial was preceeded by two days of inactivity and a three day diet replication. Analysis of serum glucose concentrations during the post-exercise OGTTs demonstrated that glucose tolerance was unaffected by either the amount of active tissue incorporated in the exercise and/or the amount of work completed by the active tissue. On the other hand, serum insulin concentrations following the two-leg trial decreased 23.5% from 347.62 ±37.98 to 266.05 :L41.62 gU/ml in comparison to the one-leg trial (p < 0.05). The incorporation of a smaller muscle mass which completed an equal amount of absolute work as the larger muscle mass (i.e. one-leg work matched trial) resulted in a large (19%), but nonsignificant reduction in the total insulin compared to the one-leg relative work trial. In addition, total insulin following the two-leg and the one-leg work matched trials were reduced by 19% and 14%, respectively, in comparison to baseline. However, they did not reach statistical significance. The results of this study indicate that the incorporation of a larger muscle mass during an acute bout of aerobic exercise results in a reduction in serum insulin in response to a post-exercise oral glucose challenge. In addition, increasing the absolute work of a muscle mass results in similar reductions in serum insulin regardless of the amount of muscle mass involved in the exercise. While glucose tolerance was unaltered by either the amount of active tissue and/or the amount of work completed by the active tissue.
School of Physical Education
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40

Baird, Janis. "Birth size, blood pressure and glucose tolerance in twins : testing the fetal origins hypothesis." Thesis, University of Southampton, 2000. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.341624.

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41

Schneider, Barbara Anne. "Resistive exercise : strength, body composition, glucose tolerance and insulin action in african american women /." The Ohio State University, 1996. http://rave.ohiolink.edu/etdc/view?acc_num=osu148793512587949.

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42

Kuroe, Akira. "Impaired β-cell function and insulin sensitivity in Japanese subjects with normal glucose tolerance." Kyoto University, 2003. http://hdl.handle.net/2433/148666.

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43

OKUMURA, NOBUYOSHI, TAKAHARU KONDO, AIJI NODA, and TETUO HAYAKAWA. "Effects of Acarbose, an α-Glucosidase Inhibitor (BAY G 5421), on Orally Loaded Glucose, Maltose and Sucrose and on Blood Glucose Control in Non-Insulin-Dependent Diabetics." Nagoya University School of Medicine, 1985. http://hdl.handle.net/2237/17475.

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44

Bartnik, Małgorzata Zofia. "Glucose regulation and coronary artery disease : studies on prevalence, recognition and prognostic implications /." Stockholm, 2005. http://diss.kib.ki.se/2005/91-7140-401-5/.

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45

Glynn, A. Elizabeth. "Glycemic response to a peanut butter and cracker snack in noninsulin dependent diabetics and nondiabetics." Thesis, This resource online, 1993. http://scholar.lib.vt.edu/theses/available/etd-09292009-020319/.

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46

Malik, Amirmuslim, and mikewood@deakin edu au. "Studies on dietary fibre: Analysis, epidemiological and physiological aspects." Deakin University. School of Sciences, 1986. http://tux.lib.deakin.edu.au./adt-VDU/public/adt-VDU20050902.142103.

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This thesis involves an investigation in three areas; first, a study of an enzymatic-gravimetric method for the analysis of dietary fibre; second, a survey of dietary fibre intake in an area of a developing country, and finally, some observations on the functional aspects of gel-forming dietary fibre in the rat. A simple and rapid enzymatic-gravimetric assay for both soluble and insoluble dietary fibre has been critically investigated. Reference samples were also analysed by a more comprehensive, enzymatic gas chromatographic method to allow testing of the relative accuracy of the enzymatic-gravimetric method. The enzymatic-gravimetric method was found to be highly reproducible but gave a slightly higher value for total dietary fibre than the more comprehensive method. This discrepancy is probably due to the presence of small quantities of resistant starch and protein residue which are recovered in the enzymatic-gravimetric method. In the enzymatic-gas chromatographic method, protein residue is not measured, and resistant starch is estimated, but not counted as dietary fibre. The enzymatic-gravimetric method was applied to the analysis of foods commonly consumed in the Padang region of West Sumatra in Indonesia, in order to estimate dietary fibre intake in the region. Daily intakes of usual foods were estimated by use of a 24-hour recall procedure aided by food photographs to assist in the estimation of portion size. Samples of approximately 60 of the most commonly consumed foods were collected and analysed for dietary fibre. These appear to be the first data which report values for dietary fibre in Indonesion foods and they represent a significant improvement upon the existing data on crude fibre content. Knowledge of the amounts of foods usually consumed and their dietary fibre content allowed an estimation of usual intakes of dietary fibre. Fibre intake was found to be lower than in the developing countries of Africa and was comparable to intakes measured in the U.K. This is the first study to show that in this part of South East Asia, a developing country area using polished rice as a staple food, dietary fibre intakes are as low as in Western countries. Low intakes of fibre are believed to be related to the prevalence of a range of diseases and, in this study, preliminary data on the rates of non-infective, chronic diseases were collected from the two main hospitals in West Sumatra. Chronic, non-infectious diseases such as inguinal hernia, appendicitis, haemorrhoids, diabetes mellitus, hypertension and malignant neoplasms of the rectum are relatively frequent in West Sumatra. While no firm conclusions can be drawn from these data, they do show the possibility of a relationship between low intakes of dietary fibre and the prevalence of these diseases, and suggest that further investigation is necessary. Some observations were made of the effect of gel-forming dietary fibre on stomach emptying and intestinal transit rate in the rat. Xanthan gum was added to iso-osmotic solutions to produce increased viscosity and phenol sulphonphthalein (phenol red) was used as a non-absorbable marker. Gavage feeding of solutions with a range of viscosities was used to study the effect of viscosity on the rate of stomach emptying and intestinal transit. Increased viscosity was observed to slow gastro-intestinal transit and this provides one mechanism by which dietary fibre of the gel-forming type ray improve glucose tolerance.
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47

Broughton, David L. "Peripheral and hepatic insulin sensitivity in the elderly." Thesis, University of Newcastle Upon Tyne, 1992. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.309064.

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48

Lamport, David Joseph. "The impact of impaired glucose tolerance, Type 2 diabetes, and glycaemic index on cognitive performance." Thesis, University of Leeds, 2010. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.555867.

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Abnormalities in glucose tolerance such as Type 2 diabetes (T2DM) are associated with cognitive impairment. However, there is an absence of research which investigates whether impaired glucose tolerance (IGT), a precursor of T2DM, is also associated with cognitive impairment. It can be hypothesised that progressively poorer glucose tolerance is associated with a trajectory of increasing cognitive impairment. Low glycaemic index (LGI) and low glycaemic load (LGL) foods are recommended as a method for managing T2DM and IGT. They have also been associated with effects on cognitive function. The potential for LGI and LGL foods to attenuate cognitive impairment associated with abnormalities in glucose tolerance remains unexplored. The main aim of this thesis was to investigate the relationship between glucose tolerance and cognitive performance, across the range of normal glucose tolerance through to seriously impaired glucose tolerance. Study 1, in 23 healthy young adults, demonstrated that the GI of an evening meal can affect objective and subjective cognitive performance the next morning. These findings indicate that an overnight fast is not sufficient to control for the effects of previous nutritional intake, and guided the, design of studies 2 and 3. Study 2 examined cognitive performance and subjective ratings of appetite, mood and alertness in middle-aged females with IGT (n=18) and NGT (n=47) over the morning following the consumption of LGL, HGL, and water breakfasts in a repeated measures design. Study 3 used an identical design to examine cognitive performance in older adults with T2DM (n=24) and age matched non-diabetic adults (n=10). Adults with T2DM showed cognitive impairment on a wide range of cognitive domains, whereas, in those with IGT primarily memory was impaired. Subclinical abnormalities in glucose tolerance can therefore have demonstrable negative effects on cognitive performance, even in ostensibly healthy middle-aged females. As hypothesised, worsening glucose tolerance was associated with a trajectory of cognitive decline. Manipulating the GL of breakfast did not acutely attenuate cognitive impairment in IGT or T2DM. Taken together, these findings suggest that maintaining a state of good health, by preventing the onset of glucose tolerance abnormalities is important for protecting and maintaining cognitive function.
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49

McNeilly, Andrea Margaret. "Exercise and a-lipoic acid in the prevention of metabolic disturbances in impaired glucose tolerance." Thesis, University of Ulster, 2010. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.523108.

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50

Wat, Ming-sun Nelson, and 屈銘伸. "Genetic and environmental determinants of impaired glucose tolerance in Hong Kong: implications on health caremanagement." Thesis, The University of Hong Kong (Pokfulam, Hong Kong), 2006. http://hub.hku.hk/bib/B37217677.

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