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Showing 61 to 68 of 68 (0.024 seconds)Spelling suggestions: "subject:"glycemic""
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Inpatient diabetes care : evaluation and interventionVan Zyl, Danie G. 28 April 2012 (has links)
The management of patients hospitalised with diabetes mellitus is neglected in South Africa. The research on which this thesis is based assessed factors contributing to glycaemic control as well as evaluated an intervention aimed at improving of such control in diabetic inpatients. A survey of doctors and nurses measuring their perceptions, knowledge and attitudes regarding care of diabetic inpatients was done. This indicated a need for special training in inpatient diabetes care, where 90.5% of respondents realised that diabetes is a serious condition and 92.2% valued the importance of tight glycaemic control. Despite these perceptions, the knowledge of doctors and nurses caring for diabetic inpatients was suboptimal. A before and after study regarding an intervention to improve glycaemic control of diabetic inpatients consisted of a training programme and the introduction of an inpatient management protocol. The mean blood glucose on day one of admission after the intervention was significantly higher than before the intervention (p < 0.001). A significant improvement in mean blood glucose from day 1 to day 7 of hospitalisation was seen after the intervention (p < 0.001), which was not significant before (p = 0.33). The proportion of patients achieving glycaemic control did not significantly differ before and after the intervention (43.0% versus 43.7%, p = 0.97). A double blind randomised controlled trial to assess superiority of Ringer’s lactate solution compared to 0.9% Sodium chloride solution in the normalisation of pH in patients with diabetic ketoacidosis was done. The outcome of this study indicated that the time to normalisation of venous pH (pH > 7.32) (HR: 1.863, CI: 0.937 to 3.705, p = 0.758) was not significantly different between the two resuscitation fluid groups The time to reach a blood glucose of 14 mmol/L was significantly longer in the Ringer’s lactate group (p = 0.044) and patients needed significantly more insulin (p = 0.02). The overall conclusion of this study is that there is no significant benefit in using Ringer’s lactate solution as initial resuscitation fluid compared to the currently advised 0.9% Sodium chloride solution. / Thesis (PhD)--University of Pretoria, 2012. / Internal Medicine / unrestricted
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Vztah oxidačního stresu k parametrům kompenzace diabetu při rozvoji cévních komplikací. / Relationship of oxidative stress to parameters of diabetes control in development of vascular complications.Pelcl, Tomáš January 2020 (has links)
The aim of this thesis is to contribute to the clarification of the pathogenesis of chronic complications of diabetes mellitus. The main goal of the research was glycaemic variability, its contribution to the activation of oxidative stress and its possible role in the process of advanced glycation, all beyond the scope of persistent hyperglycaemia itself. Another aim of the work is to contribute to the clarification of a possible relationship between glycaemic variability and vascular complications of diabetes. We were the first to describe the association between the concentrations of reactive aldehydes formed during lipid peroxidation and disorders of skin microvascular reactivity in patients with type 1 diabetes (DM1). Elevated markers of oxidative stress were found in this group, furthermore during the 3 years of follow-up higher plasma antioxidant activity was observed. These findings were not dependent of the method of glucose monitoring and glucose variability, which was lower in a subgroup of patients using real-time continuous glucose monitoring (rt-CGM), compared to a subgroup using conventional glucometers. However, it is clear, that hyperglycaemia alone induces increased oxidative stress in patients with diabetes. Simultaneously we observed the opposite process of oxidative stress...
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Analysis of non-steady state physiological and pathological processesHill, Nathan R. January 2008 (has links)
The analysis of non steady state physiological and pathological processes concerns the abstraction, extraction, formalisation and analysis of information from physiological systems that is obscured, hidden or unable to be assessed using traditional methods. Time Series Analysis (TSA) techniques were developed and built into a software program, Easy TSA, with the aim of examining the oscillations of hormonal concentrations in respect to their temporal aspects – periodicity, phase, pulsatility. The Easy TSA program was validated using constructed data sets and used in a clinical study to examine the relationship between insulin and obesity in people without diabetes. In this study fifty-six non-diabetic subjects (28M, 28F) were examined using data from a number of protocols. Fourier Transform and Autocorrelation techniques determined that there was a critical effect of the level of BMI on the frequency, amplitude and regularity of insulin oscillations. Second, information systems formed the background to the development of an algorithm to examine glycaemic variability and a new methodology termed the Glycaemic Risk in Diabetes Equation (GRADE) was developed. The aim was to report an integrated glycaemic risk score from glucose profiles that would complement summary measures of glycaemia, such as the HbA1c. GRADE was applied retrospectively to blood glucose data sets to determine if it was clinically relevant. Subjects with type 1 and type 2 diabetes had higher GRADE scores than the non-diabetic population and the contribution of hypo- and hyperglycaemic episodes to risk was demonstrated. A prospective study was then designed with the aim to apply GRADE in a clinical context and to measure the statistical reproducibility of using GRADE. Fifty-three (Male 26, Female 27) subjects measured their blood glucose 4 times daily for twenty-one days. The results were that lower HbA1c’s correlated with an increased risk of hypoglycaemia and higher HbA1c’s correlated with an increased risk of hyperglycaemia. Some subjects had HbA1c of 7.0 but had median GRADE values ranging from 2.2 to 10.5. The GRADE score summarized diverse glycaemic profiles into a single assessment of risk. Well-controlled glucose profiles yielded GRADE scores <= 5 and higher GRADE scores represented increased clinical risk from hypo or hyperglycaemia. Third, an information system was developed to analyse data-rich multi-variable retinal images using the concept of assessment of change rather than specific lesion recognition. A fully Automated Retinal Image Differencing (ARID) computer system was developed to highlight change between retinal images over time. ARID was validated using a study and then a retrospective study sought to determine if the use of the ARID software was an aid to the retinal screener. One hundred and sixty images (80 image pairs) were obtained from Gloucestershire Diabetic Eye Screening Programme. Images pairs were graded manually and categorised according to how each type of lesion had progressed, regressed, or not changed between image A and image B. After a 30 day washout period image pairs were graded using ARID and the results compared. The comparison of manual grading to grading using ARID (Table 4.3) demonstrated an increased sensitivity and specificity. The mean sensitivity of ARID (87.9%) was increased significantly in comparison to manually grading sensitivity (84.1%) (p<0.05). The specificity of the automated analysis (87.5%) increased significantly from the specificity (56.3%) achieved by manually grading (p<0.05). The conclusion was that automatic display of an ARID differenced image where sequential photographs are available would allow rapid assessment and appropriate triage. Forth, non-linear dynamic systems analysis methods were utilised to build a system to assess the extent of chaos characteristics within the insulin-glucose feedback domain. Biological systems exist that are deterministic yet are neither predictable nor repeatable. Instead they exhibit chaos, where a small change in the initial conditions produces a wholly different outcome. The glucose regulatory system is a dynamic system that maintains glucose homeostasis through the feedback mechanism of glucose, insulin, and contributory hormones and was ideally suited to chaos analysis. To investigate this system a new algorithm was created to assess the Normalised Area of Attraction (NAA). The NAA was calculated by defining an oval using the 95% CI of glucose & Insulin (the limit cycle) on a phasic plot. Thirty non-diabetic subjects and four subjects with type 2 diabetes were analysed. The NAA indicated a smaller range for glucose and insulin excursions with the non-diabetics subjects (p<0.05). The conclusion was that the evaluation of glucose metabolism in terms of homeostatic integrity and not in term of cut-off values may enable a more realistic approach to the effective treatment and prevention of diabetes and its complications.
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Effects of kolaviron–a Garcinia kola biflavonoid on biochemical and histological parameters in streptozotocin - induced diabetes and diabetic complications (nephrotoxicity and hepatotoxicity) in male Wistar ratsAyepola, Omolola Rebecca January 2014 (has links)
Thesis submitted in fulfillment of the requirements for the
Doctor of Technology: Biomedical Technology
In the Faculty of Health and Wellness
At the
CAPE PENINSULA UNIVERSITY OF TECHNOLOGY
2014 / Diabetes mellitus (DM) results in severe metabolic imbalances and pathological changes in many
tissues. Chronic inflammation and oxidative stress have been implicated in the pathophysiology
of diabetes mellitus. Garcinia kola (Family: Guttiferae) is a plant well known for its ample
medicinal values. The seed of the plant also known as ‘bitter kola’ due to its bitter taste is used as
a masticatory agent in traditional hospitality, cultural and social ceremonies in Africa. Kolaviron
(KV) is a defatted ethanol extract from the seeds of Garcinia kola (GK). Kolaviron has been
shown in experimental models of diseases to have numerous beneficial effects due to the
presence of flavonoids (mainly Garcinia biflavonoid (GB)-1, GB-2 and kolaflavanone).
However, there is paucity of information regarding the possible effect of kolaviron on
inflammatory mediators and oxidative stress in diabetes mellitus. Therefore, this study was
carried out to investigate the potential beneficial effects of kolaviron on antioxidant status,
inflammatory mediators and apoptosis. Other biochemical and histological alterations in the
blood, liver and kidney of streptozotocin-induced diabetic rats were also evaluated.
A single intraperitoneal injection of freshly prepared solution of streptozotocin (50 mg/kg.b.wt.)
in citrate buffer (0.1M, pH 4.5) was administered to overnight fasted rats for diabetes induction.
Diabetes was confirmed by stable hyperglycemia (>18 mmol/l) in the tail blood glucose after 5
days of streptozotocin injection. Kolaviron (100 mg/kg b.wt.) was administered to diabetic rats
(by gastric gavage) on the 6th day after the induction of diabetes and treatment continued for 6
weeks (5 times weekly). The effects on blood glucose, body weight, organ (liver and kidney)
weight, serum biochemical parameters, oxidative status, inflammatory mediators and histology
of the liver, kidney and pancreas were assessed.
Kolaviron (KV) treatment lowered blood glucose in diabetic and normoglycemic rats and
reduced glycated haemoglobin [HbA1C (%)]. Plasma insulin level was raised in diabetic rats
treated with KV. Histomorphometric analysis of the pancreas revealed increased β-cell area of
pancreatic islets of kolaviron-treated diabetic group. The indices of organ (liver and kidney)
damage were increased in diabetic rats. However, KV treatment protected against liver and
kidney damage. The characteristic features of diabetic dyslipidemia such as elevated serum
triglyceride and cholesterol concentration which are major risk factors for cardiovascular disease
were also significantly reduced in KV-treated diabetic rats.
Alteration in antioxidant enzymes status was observed in the liver, kidney and blood
(erythrocyte, plasma and serum) of diabetic rats. Lowered catalase (CAT) activity was observed
in the liver and kidney of diabetic rats while KV treatment significantly (p < 0.05) elevated
catalase activity in the liver and kidney. There was no significant change (p > 0.05) in
erythrocyte catalase activity among all treatment groups. Erythrocyte of diabetic rats showed a
marked reduction in the activity of superoxide dismutase (SOD) with no significant changes in
liver and kidney SOD activity of diabetic rats compared to control whereas KV administration to
rats markedly increased SOD activity. Glutathione peroxidase (GPX) activity was elevated in the
erythrocyte and kidney of STZ-induced diabetic rats with no significant effect on liver GPX
activity. KV treatment reversed the alteration in GPX activity in the kidney and erythrocyte.
Level of reduced glutathione (GSH), a non-enzymatic antioxidant was decreased in the both liver
and kidney of diabetic rats and treatment of diabetic rats with KV elevated GSH concentration in
both tissues. Also, malondialdehyde (MDA), a marker of lipid peroxidation was elevated in the
liver, kidney and plasma of diabetic rats and significantly (p < 0.05) lowered following KV
treatment. Diabetes induction reduced the capacity of liver and kidney to absorb oxygen radicals
as demonstrated by lowered oxygen radical absorbance capacity (ORAC) values. KV
administration to normal and diabetic rats significantly increased ORAC values.
Increased rate of apoptosis, a major cellular response to high glucose induced stress was
observed in the renal and hepatic tissues of diabetic control rats. Kolaviron treatment of diabetic
rats protected the liver and kidney against hyperglycemia-induced apoptosis and decreased the
number of TUNEL positive cells
A significant (p < 0.05) elevation of pro-inflammatory cytokines; monocyte chemoattractant
protein (MCP-1), Interleukin-1β (IL-1β), IL-6 and tumor necrosis factor (TNF)-𝛂 was observed
in the liver of diabetes rats. KV treatment lowered these inflammatory biomarkers. On the other
hand, the kidney of diabetic rats showed elevated concentration of pro-inflammatory IL-1β with
no significant effect on kidney TNF-𝛂. An increase in the serum concentration of MCP-1 and
IL-1β was observed in the untreated diabetic rats while kolaviron treatment normalized the
alteration in serum concentration of MCP-1, IL-1β and vascular endothelial growth factor
(VEGF).
In conclusion, persistent and chronic hyperglycemia promotes the generation of free radicals and
inflammatory molecules which contributes to progressive development of micro- and macro
vascular complications and multi-organ damage. Kolaviron demonstrated beneficial effects on
markers of oxidative stress and inflammation in the diabetic rats and also promoted the survival
and functional integrity of the liver and kidney.
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Effekte einer Chromhefezugabe auf die glycämischen und insulinämischen Reaktionen bei insulinresistenten Ponies und Pferden: Effekte einer Chromhefezugabe auf die glycämischenund insulinämischen Reaktionen bei insulinresistentenPonies und PferdenOßwald, Barbara 08 February 2011 (has links)
Dem Spurenelement Chrom wird seit mehreren Jahrzehnten eine maßgebliche Funktion im Glucosestoffwechsel zugeschrieben. In der vorliegenden placebokontrollierten Studie wurden die Effekte einer Chromhefezulage bei insulinresistenten Ponies und Pferden untersucht.
Aus dem Patientenklientel der Pferdeklinik an der Rennbahn wurden mittels eines Stärketoleranztest 27 Ponies und Pferde ausgewählt, welche einen veränderten Glucosestoffwechsel aufwiesen.
Die Versuchsprobanden waren 13,9 ± 4,8 Jahre alt, wiesen eine mittlere Körpermasse von 422 ± 138 kg und einen mittleren Body Condition Score von 7,6 ± 0,8 (Skala 1-9) auf. Die 27 Ponies und Pferde wurden nach dem Zufallsprinzip in 2 Gruppen unterteilt. Die Chromgruppe (N=15) erhielt über einen Zeitraum von 28 ± 7 Tagen eine Chromhefezulage in einer täglichen Dosierung von 25 μg/kg KM, die Placebogruppe (N=12) erhielt eine Hefezulage ohne Chrom in derselben Hefemenge wie die Chromgruppe.
Während des Versuchszeitraumes wurden alle Probanden mit Heu 1,5 kg /100 kg KM gefüttert.
Zu Beginn und am Ende des Versuchszeitraumes wurde jeweils ein Stärketoleranztest (1,5 g Stärke/kg KM) über eine Dauer von 420 min durchgeführt. Die Blutproben wurden postprandial in definierten Intervallen entnommen.
In beiden Gruppen konnte ein deutlicher Gewichtsverlust über die vierwöchige Versuchszeit beobachtet werden. Dabei wurde ein signifikanter Gewichtsverlust bei der chromsupplementierten
Gruppe von 3,8 ± 4,3 % (p < 0,05) und ein ebenfalls signifikanter Gewichtsverlust bei der Placebogruppe von 2,1 ± 3,2 % (p < 0,05) verzeichnet. Unterschiede zwischen den Behandlungsgruppen konnten aber nicht mit p < 0,05 abgesichert werden.
Die Ruheglucosekonzentrationen bewegten sich bei den chromsupplementierten Tieren im Mittel bei 6,3 ± 2,1 mmol/l, die placebosupplementierte Gruppe wies mittlere Werte von 5,5 ± 0,9
mmol/l auf. Nach der Behandlung konnten Ruheglucosekonzentrationen von 6,0 ± 2,0 mmol/l für die chromsupplementierten Tiere und Ruheglucosekonzentrationen von 5,6 ± 0,5 mmol/l für die placebosupplementierten Probanden gemessen werden. Die Nüchterninsulinkonzentrationen im Plasma lagen vor der Supplementierung bei 63,7 ± 81,9 μU/ml für die Chromgruppe und
bei 42,9 ± 47,8 μU/ml für die Placebogruppe. Nach der Behandlung konnten Nüchterinsulinkonzentrationen bei den chromsupplementierten Pferden und Ponies von 33,2 ± 35,7 μU/ml sowie bei den placebosupplementierten Tieren von 14,4 ± 8,7 μU/ml verzeichnet werden. Diese Veränderung der Nüchterninsulinwerte innerhalb der beiden Behandlungsgruppen war jedoch nicht signifikant.
Beim 1. Stärketoleranztest erreichte die Chromgruppe eine mittlere maximale Plasmaglucosekonzentration von 12,4 ± 2,6 mmol/l mit Einzelwerten bis zu 19,3 mmol/l, die Placebogruppe wies eine mittlere maximale Plasmaglucosekonzentration von 11,8 ± 2,0 mmol/l mit Einzelwerten bis 16,3 mmol/l auf. Die Plasmainsulinkonzentrationen stiegen im 1. Stärketoleranztest bei der Chromgruppe auf mittlere maximale Werte von 1902 ± 1393 μU /ml sowie in der Placebogruppe
auf 1158 ± 753 μU/ml.
Im 2. Stärketoleranztest erreichte die Chromgruppe eine mittlere maximale Plasmaglucosekonzentration von 11,0 ± 3,0 mmol/l und die Placebogruppe wies eine mittlere maximale Plasmaglucosekonzentration
von 10,7 ± 2,6 mmol/l auf (Behandlung und Zeit: nicht signifikant).
Die Plasmainsulinkonzentrationen der Chromgruppe stiegen im 2. Stärketoleranztest auf mittlere maximale Plasamainsulinkonzentrationen von 1277 ± 856 μU/ml, für die placebosupplementierte Gruppe wurden mittlere Maximalwerte von 883 ± 725 μU/ml ermittelt; diese Unterschiede waren jedoch nicht signifikant.
Der beobachtete Körpergewichtsverlust scheint für beide Gruppen von Bedeutung für die Verbesserung der Insulinresistenz zu sein. Nach der vierwöchigen Supplementierungsphase konnte allerdings bei den Tieren die Cr erhielten, eine deutlichere Reduktion bei der Insulinreaktion im Verlaufe des 2. STT beobachtet werden, wohingegen die Placebopferde nur eine moderate Veränderung
in der Insulinreaktion aufwiesen.:Inhaltsverzeichnis
Tabellenverzeichnis
Abbildungsverzeichnis
Abkürzungen
1 Einleitung 1
2 Schrifttum 2
2.1 Definition des Equinen Metabolischen Syndroms 2
2.2 Vorkommen und klinisches Erscheinungsbild des EMS 2
2.3 Pathogenese des equinen metabolischen Syndroms in Anlehnung an das
metabolische Syndrom beim Menschen 4
2.3.1 Insulinresistenz 4
2.3.2 Ursachen der Insulinresistenz auf zellulärer Ebene 5
2.4 Folgen der Insulinresistenz für den Organismus 12
2.4.1 Glucotoxizität 13
2.4.2 Insulintoxizität 14
2.5 Risikofaktoren für die Entstehung von EMS 16
2.5.1 Bewegungsmangel 16
2.5.2 Quantität der Energiezufuhr 16
2.5.3 Qualität der Energiezufuhr 17
2.6 Einsatz von Chrom zur Behandlung des metabolischen Syndroms 18
2.6.1 Wertigkeit 18
2.6.2 Chrom, Absorption und Transport 19
2.6.3 Serumgehalt und Organspeicherung 19
2.6.4 Bindung von Chrom an den Insulinrezeptor 20
2.6.5 Chromausscheidung 20
2.6.6 Weitere Chromverluste 20
2.6.7 Toxizität 20
2.6.8 Chromgehalt in Futtermitteln 21
2.6.9 Biologische Wirksamkeit 21
2.6.10 Chrombedarf 23
2.6.11 Studien über die Wirkung von Chrom im Organismus bei Mensch und
Pferd 23
3 Tiere, Material und Methoden 27
3.1 Versuchsziel 27
3.2 Versuchsübersicht 27
3.3 Vorversuch 27
3.3.1 Durchführung Vorversuch 27
3.4 Hauptversuch 29
3.4.1 Pferde / Ponies 29
3.4.2 Haltung der Pferde und Ponies 29
3.4.3 Fütterung der Versuchspferde und -ponies 29
3.4.4 Chromsupplementation 31
3.4.5 Stärketoleranztest 32
4 Untersuchungsmethoden 33
4.1 Körpergewicht vor und nach Supplementierung 33
4.2 Erhebung des BCS HENNEKE et al. (1983) 33
4.3 Untersuchungsmethoden der Blutproben im Vorversuch 33
4.4 Untersuchungsmethode zur Glucosebestimmung im Hauptversuch 34
4.5 Untersuchungsmethode zur Bestimmung von Insulin im Hauptversuch 35
4.6 Statistische Auswertung 35
5 Ergebnisse 36
5.1 Vorversuch 36
5.1.1 Glucosekonzentration im Plasma 36
5.2 Hauptversuch 38
5.2.1 Körpergewichtsentwicklung 38
5.2.2 Body Condition Score (BCS) 38
5.2.3 Glucosekonzentration im Plasma vor Behandlungsbeginn 39
5.2.4 Glucosekonzentration im Plasma nach Behandlungsende 40
5.2.5 Insulinkonzentration im Plasma vor Behandlungsbeginn 42
5.2.6 Insulinkonzentration im Plasma nach Behandlungsende 44
5.2.7 Beziehung zwischen Plasmaglucosekonzentration und Plasmainsulinkonzentration 47
5.2.8 Beziehung zwischen den Veränderungen der Plasmaglucosekonzentration
bzw. Plasmainsulinkonzentration und den Veränderungen in der KM 49
5.3 Zusammenfassung der Ergebnisse 51
6 Diskussion 52
6.1 Kritik der Methoden 52
6.1.1 Auswahl der Versuchstiere 52
6.1.2 Haltung und Fütterung 52
6.1.3 Auswahl der Chromhefe und Dosierung 53
6.1.4 Supplementationsdauer 54
6.1.5 Rechtsgrundlage 55
6.1.6 Stärkedosierung im Stärketoleranztest 57
6.1.7 Durchführung des Stärketoleranztest 57
6.1.8 Diagnostik der Insulinresistenz 58
6.1.9 KM - Entwicklung 60
6.2 Nüchternwerte von Glucose und Insulin beim Pferd und ihre Bedeutung
beim equinen metabolischen Syndrom 63
6.3 Veränderungen im Glucosestoffwechsel- und Insulinreaktion vor und
nach Chromsupplementation 65
7 Schlussfolgerung 70
8 Zusammenfassung 71
9 Summary 73
10 Literaturverzeichnis 75
11 Anhang 96
Danke
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BIRTHWEIGHT AND SUSCEPTIBILITY TO CHRONIC DISEASEIssa Al Salmi Unknown Date (has links)
The thesis examines the relationship of birthweight to risk factors and markers, such as proteinuria and glomerular filtration rate, for chronic disease in postnatal life. It made use of the Australian Diabetes, Obesity and Lifestyle Study (AusDiab). The AusDiab study is a cross sectional study where baseline data on 11,247 participants were collected in 1999-2000. Participants were recruited from a stratified sample of Australians aged ≥ 25 years, residing in 42 randomly selected urban and non-urban areas (Census Collector Districts) of the six states of Australia and the Northern Territory. The AusDiab study collected an enormous amount of clinical and laboratory data. During the 2004-05 follow-up AusDiab survey, questions about birthweight were included. Participants were asked to state their birthweight, the likely accuracy of the stated birthweight and the source of their stated birthweight. Four hundred and twelve chronic kidney disease (CKD) patients were approached, and 339 agreed to participate in the study. The patients completed the same questionnaire. Medical records were reviewed to check the diagnoses, causes of kidney trouble and SCr levels. Two control subjects, matched for gender and age, were selected for each CKD patient from participants in the AusDiab study who reported their birthweight. Among 7,157 AusDiab participants who responded to the questionnaire, 4,502 reported their birthweights, with a mean (standard deviation) of 3.4 (0.7) kg. The benefit and disadvantages of these data are discussed in chapter three. The data were analysed for the relationship between birthweight and adult body size and composition, disorders of glucose regulation, blood pressure, lipid abnormalities, cardiovascular diseases and glomerular filtration rate. Low birthweight was associated with smaller body build and lower lean mass and total body water in both females and males. In addition low birthweight was associated with central obesity and higher body fat percentage in females, even after taking into account current physical activity and socioeconomic status. Fasting plasma glucose, post load glucose and glycosylated haemoglobin were strongly and inversely correlated with birthweight. In those with low birthweight (< 2.5 kg), the risks for having impaired fasting glucose, impaired glucose tolerance, diabetes and all abnormalities combined were increased by 1.75, 2.22, 2.76 and 2.28 for females and by 1.40, 1.32, 1.98 and 1.49 for males compared to those with normal birthweight (≥ 2.5 kg), respectively. Low birthweight individuals were at higher risk for having high blood pressure ≥ 140/90 mmHg and ≥ 130/85 mmHg compared to those with normal birthweight. People with low birthweight showed a trend towards increased risk for high cholesterol (≥ 5.5 mmol/l) compared to those of normal birthweight. Females with low birthweight had increased risk for high low density lipoprotein cholesterol (≥ 3.5 mmol/l) and triglyceride levels (≥ 1.7 mmol/l) when compared to those with normal birthweight. Males with low birthweight exhibited increased risk for low levels of high density lipoprotein cholesterol (<0.9 mmol/l) than those with normal birthweight. Females with low birthweight were at least 1.39, 1.40, 2.30 and 1.47 times more likely to have angina, coronary artery disease, stroke and overall cardiovascular diseases respectively, compared to those ≥ 2.5 kg. Similarly, males with low birthweight were 1.76, 1.48, 3.34 and 1.70 times more likely to have angina, coronary artery disease, stroke and overall cardiovascular diseases compared to those ≥ 2.5 kg, respectively. The estimated glomerular filtration rate was strongly and positively associated with birthweight, with a predicted increase of 2.6 ml/min (CI 2.1, 3.2) and 3.8 (3.0, 4.5) for each kg of birthweight for females and males, respectively. The odd ratio (95% confidence interval) for low glomerular filtration rate (<61.0 ml/min for female and < 87.4 male) in people of low birthweight compared with those of normal birthweight was 2.04 (1.45, 2.88) for female and 3.4 (2.11, 5.36) for male. One hundred and eighty-nineCKD patients reported their birthweight; 106 were male. Their age was 60.3(15) years. Their birthweight was 3.27 (0.62) kg, vs 3.46 (0.6) kg for their AusDiab controls, p<0.001 and the proportions with birthweight<2.5 kg were 12.17% and 4.44%, p<0.001. Among CKD patients, 22.8%, 21.7%, 18% and 37.6% were in CKD stages 2, 3, 4 and 5 respectively. Birthweights by CKD stage and their AusDiab controls were as follows: 3.38 (0.52) vs 3.49 (0.52), p=0.251 for CKD2; 3.28 (0.54) vs 3.44 (0.54), p=0.121 for CKD3; 3.19 (0.72) vs 3.43 (0.56), p= 0.112 for CKD4 and 3.09 (0.65) vs 3.47 (0.67), p<0.001 for CKD5. The results demonstrate that in an affluent Western country with a good adult health profile, low birthweight people were predisposed to higher rates of glycaemic dysregulation, high blood pressure, dyslipidaemia, cardiovascular diseases and lower glomerular filtration rate in adult life. In all instances it would be prudent to adopt policies of intensified whole of life surveillance of lower birthweight people, anticipating this risk. The general public awareness of the effect of low birthweight on development of chronic diseases in later life is of vital importance. The general public, in addition to the awareness of people in medical practice of the role of low birthweight, will lead to a better management of this group of our population that is increasingly surviving into adulthood.
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BIRTHWEIGHT AND SUSCEPTIBILITY TO CHRONIC DISEASEIssa Al Salmi Unknown Date (has links)
The thesis examines the relationship of birthweight to risk factors and markers, such as proteinuria and glomerular filtration rate, for chronic disease in postnatal life. It made use of the Australian Diabetes, Obesity and Lifestyle Study (AusDiab). The AusDiab study is a cross sectional study where baseline data on 11,247 participants were collected in 1999-2000. Participants were recruited from a stratified sample of Australians aged ≥ 25 years, residing in 42 randomly selected urban and non-urban areas (Census Collector Districts) of the six states of Australia and the Northern Territory. The AusDiab study collected an enormous amount of clinical and laboratory data. During the 2004-05 follow-up AusDiab survey, questions about birthweight were included. Participants were asked to state their birthweight, the likely accuracy of the stated birthweight and the source of their stated birthweight. Four hundred and twelve chronic kidney disease (CKD) patients were approached, and 339 agreed to participate in the study. The patients completed the same questionnaire. Medical records were reviewed to check the diagnoses, causes of kidney trouble and SCr levels. Two control subjects, matched for gender and age, were selected for each CKD patient from participants in the AusDiab study who reported their birthweight. Among 7,157 AusDiab participants who responded to the questionnaire, 4,502 reported their birthweights, with a mean (standard deviation) of 3.4 (0.7) kg. The benefit and disadvantages of these data are discussed in chapter three. The data were analysed for the relationship between birthweight and adult body size and composition, disorders of glucose regulation, blood pressure, lipid abnormalities, cardiovascular diseases and glomerular filtration rate. Low birthweight was associated with smaller body build and lower lean mass and total body water in both females and males. In addition low birthweight was associated with central obesity and higher body fat percentage in females, even after taking into account current physical activity and socioeconomic status. Fasting plasma glucose, post load glucose and glycosylated haemoglobin were strongly and inversely correlated with birthweight. In those with low birthweight (< 2.5 kg), the risks for having impaired fasting glucose, impaired glucose tolerance, diabetes and all abnormalities combined were increased by 1.75, 2.22, 2.76 and 2.28 for females and by 1.40, 1.32, 1.98 and 1.49 for males compared to those with normal birthweight (≥ 2.5 kg), respectively. Low birthweight individuals were at higher risk for having high blood pressure ≥ 140/90 mmHg and ≥ 130/85 mmHg compared to those with normal birthweight. People with low birthweight showed a trend towards increased risk for high cholesterol (≥ 5.5 mmol/l) compared to those of normal birthweight. Females with low birthweight had increased risk for high low density lipoprotein cholesterol (≥ 3.5 mmol/l) and triglyceride levels (≥ 1.7 mmol/l) when compared to those with normal birthweight. Males with low birthweight exhibited increased risk for low levels of high density lipoprotein cholesterol (<0.9 mmol/l) than those with normal birthweight. Females with low birthweight were at least 1.39, 1.40, 2.30 and 1.47 times more likely to have angina, coronary artery disease, stroke and overall cardiovascular diseases respectively, compared to those ≥ 2.5 kg. Similarly, males with low birthweight were 1.76, 1.48, 3.34 and 1.70 times more likely to have angina, coronary artery disease, stroke and overall cardiovascular diseases compared to those ≥ 2.5 kg, respectively. The estimated glomerular filtration rate was strongly and positively associated with birthweight, with a predicted increase of 2.6 ml/min (CI 2.1, 3.2) and 3.8 (3.0, 4.5) for each kg of birthweight for females and males, respectively. The odd ratio (95% confidence interval) for low glomerular filtration rate (<61.0 ml/min for female and < 87.4 male) in people of low birthweight compared with those of normal birthweight was 2.04 (1.45, 2.88) for female and 3.4 (2.11, 5.36) for male. One hundred and eighty-nineCKD patients reported their birthweight; 106 were male. Their age was 60.3(15) years. Their birthweight was 3.27 (0.62) kg, vs 3.46 (0.6) kg for their AusDiab controls, p<0.001 and the proportions with birthweight<2.5 kg were 12.17% and 4.44%, p<0.001. Among CKD patients, 22.8%, 21.7%, 18% and 37.6% were in CKD stages 2, 3, 4 and 5 respectively. Birthweights by CKD stage and their AusDiab controls were as follows: 3.38 (0.52) vs 3.49 (0.52), p=0.251 for CKD2; 3.28 (0.54) vs 3.44 (0.54), p=0.121 for CKD3; 3.19 (0.72) vs 3.43 (0.56), p= 0.112 for CKD4 and 3.09 (0.65) vs 3.47 (0.67), p<0.001 for CKD5. The results demonstrate that in an affluent Western country with a good adult health profile, low birthweight people were predisposed to higher rates of glycaemic dysregulation, high blood pressure, dyslipidaemia, cardiovascular diseases and lower glomerular filtration rate in adult life. In all instances it would be prudent to adopt policies of intensified whole of life surveillance of lower birthweight people, anticipating this risk. The general public awareness of the effect of low birthweight on development of chronic diseases in later life is of vital importance. The general public, in addition to the awareness of people in medical practice of the role of low birthweight, will lead to a better management of this group of our population that is increasingly surviving into adulthood.
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BIRTHWEIGHT AND SUSCEPTIBILITY TO CHRONIC DISEASEIssa Al Salmi Unknown Date (has links)
The thesis examines the relationship of birthweight to risk factors and markers, such as proteinuria and glomerular filtration rate, for chronic disease in postnatal life. It made use of the Australian Diabetes, Obesity and Lifestyle Study (AusDiab). The AusDiab study is a cross sectional study where baseline data on 11,247 participants were collected in 1999-2000. Participants were recruited from a stratified sample of Australians aged ≥ 25 years, residing in 42 randomly selected urban and non-urban areas (Census Collector Districts) of the six states of Australia and the Northern Territory. The AusDiab study collected an enormous amount of clinical and laboratory data. During the 2004-05 follow-up AusDiab survey, questions about birthweight were included. Participants were asked to state their birthweight, the likely accuracy of the stated birthweight and the source of their stated birthweight. Four hundred and twelve chronic kidney disease (CKD) patients were approached, and 339 agreed to participate in the study. The patients completed the same questionnaire. Medical records were reviewed to check the diagnoses, causes of kidney trouble and SCr levels. Two control subjects, matched for gender and age, were selected for each CKD patient from participants in the AusDiab study who reported their birthweight. Among 7,157 AusDiab participants who responded to the questionnaire, 4,502 reported their birthweights, with a mean (standard deviation) of 3.4 (0.7) kg. The benefit and disadvantages of these data are discussed in chapter three. The data were analysed for the relationship between birthweight and adult body size and composition, disorders of glucose regulation, blood pressure, lipid abnormalities, cardiovascular diseases and glomerular filtration rate. Low birthweight was associated with smaller body build and lower lean mass and total body water in both females and males. In addition low birthweight was associated with central obesity and higher body fat percentage in females, even after taking into account current physical activity and socioeconomic status. Fasting plasma glucose, post load glucose and glycosylated haemoglobin were strongly and inversely correlated with birthweight. In those with low birthweight (< 2.5 kg), the risks for having impaired fasting glucose, impaired glucose tolerance, diabetes and all abnormalities combined were increased by 1.75, 2.22, 2.76 and 2.28 for females and by 1.40, 1.32, 1.98 and 1.49 for males compared to those with normal birthweight (≥ 2.5 kg), respectively. Low birthweight individuals were at higher risk for having high blood pressure ≥ 140/90 mmHg and ≥ 130/85 mmHg compared to those with normal birthweight. People with low birthweight showed a trend towards increased risk for high cholesterol (≥ 5.5 mmol/l) compared to those of normal birthweight. Females with low birthweight had increased risk for high low density lipoprotein cholesterol (≥ 3.5 mmol/l) and triglyceride levels (≥ 1.7 mmol/l) when compared to those with normal birthweight. Males with low birthweight exhibited increased risk for low levels of high density lipoprotein cholesterol (<0.9 mmol/l) than those with normal birthweight. Females with low birthweight were at least 1.39, 1.40, 2.30 and 1.47 times more likely to have angina, coronary artery disease, stroke and overall cardiovascular diseases respectively, compared to those ≥ 2.5 kg. Similarly, males with low birthweight were 1.76, 1.48, 3.34 and 1.70 times more likely to have angina, coronary artery disease, stroke and overall cardiovascular diseases compared to those ≥ 2.5 kg, respectively. The estimated glomerular filtration rate was strongly and positively associated with birthweight, with a predicted increase of 2.6 ml/min (CI 2.1, 3.2) and 3.8 (3.0, 4.5) for each kg of birthweight for females and males, respectively. The odd ratio (95% confidence interval) for low glomerular filtration rate (<61.0 ml/min for female and < 87.4 male) in people of low birthweight compared with those of normal birthweight was 2.04 (1.45, 2.88) for female and 3.4 (2.11, 5.36) for male. One hundred and eighty-nineCKD patients reported their birthweight; 106 were male. Their age was 60.3(15) years. Their birthweight was 3.27 (0.62) kg, vs 3.46 (0.6) kg for their AusDiab controls, p<0.001 and the proportions with birthweight<2.5 kg were 12.17% and 4.44%, p<0.001. Among CKD patients, 22.8%, 21.7%, 18% and 37.6% were in CKD stages 2, 3, 4 and 5 respectively. Birthweights by CKD stage and their AusDiab controls were as follows: 3.38 (0.52) vs 3.49 (0.52), p=0.251 for CKD2; 3.28 (0.54) vs 3.44 (0.54), p=0.121 for CKD3; 3.19 (0.72) vs 3.43 (0.56), p= 0.112 for CKD4 and 3.09 (0.65) vs 3.47 (0.67), p<0.001 for CKD5. The results demonstrate that in an affluent Western country with a good adult health profile, low birthweight people were predisposed to higher rates of glycaemic dysregulation, high blood pressure, dyslipidaemia, cardiovascular diseases and lower glomerular filtration rate in adult life. In all instances it would be prudent to adopt policies of intensified whole of life surveillance of lower birthweight people, anticipating this risk. The general public awareness of the effect of low birthweight on development of chronic diseases in later life is of vital importance. The general public, in addition to the awareness of people in medical practice of the role of low birthweight, will lead to a better management of this group of our population that is increasingly surviving into adulthood.
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