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21	Μελέτη της σχέσης λεπτίνης και αυξητικής ορμόνης κατά τη διάρκεια του εικοσιτετραώρου και μετά φαρμακολογική πρόκληση σε παχύσαρκα παιδιά Νικολακοπούλου, Νικολέτα 24 January 2011 (has links) Σκοπός της μελέτης ήταν: (1) να προσδιοριστεί η συχνότητα της διαταραχής ανοχής στη γλυκόζη (IGT) και του σακχαρώδη διαβήτη τύπου II (ΣΔII) σε παχύσαρκα παιδιά και εφήβους στην Ελλάδα και (2) να καθοριστεί εάν οι συγκεντρώσεις γλυκόζης και ινσουλίνης νηστείας μπορούν να προβλέψουν τη διαταραχή ανοχής στη γλυκόζη (IGT)) στα παιδιά αυτά σε σχέση με τα επίπεδα της λεπτίνης, της γκρελίνης, της αδιπονεκτίνης και της σωματομεδίνης, και την έκκριση της αυξητικής ορμόνης (GH) και της θυρεοειδοτρόπου ορμόνης (TSH) κατά τη διάρκεια του 24ωρου μαζί με την ημερήσια έκκριση της κορτιζόλης. Έγινε καμπύλη σακχάρου (OGTT) μαζί με επίπεδα ινσουλίνης σε 117 παχύσαρκα παιδιά και εφήβους 12,1  2,7 ετών και μελετήθηκαν τα επίπεδα της λεπτίνης, της γκρελίνης, της αδιπονεκτίνης και της σωματομεδίνης (IGF-I) κατά τη δοκιμασία ανοχής στη γλυκόζη (OGTT). Επίσης, μελετήθηκαν τα επίπεδα της 24ωρης έκκρισης της GH και της TSH και της ημερήσιας έκκρισης της κορτιζόλης. Χρησιμοποιήθηκαν οι δείκτες HOMA-IR και ο ινσουλινογόνος δείκτης για την εκτίμηση της αντίστασης της ινσουλίνης και της λειτουργίας των β κυττάρων, αντίστοιχα. 17 ασθενείς (14,5%) είχαν IGT και σε κανένα δε διαγνώστηκε ΣΔII. Τα ποσοστά IGT και ΣΔΙΙ ήταν χαμηλότερα από αυτά μιας πολυεθνικής Αμερικανικής μελέτης. Η διαφορά εντοπίστηκε κυρίως στα προεφηβικά παιδιά (9% έναντι 25,4%), ενώ δεν παρατηρήθηκε διαφορά στους εφήβους (18% έναντι 21%). Ωστόσο, τα ποσοστά IGT ήταν υψηλότερα από αυτά που βρέθηκαν σε άλλες μελέτες από την Ευρώπη. Η γλυκόζη νηστείας, η ινσουλίνη και ο δείκτης HOMA-IR δεν προέβλεψαν την εμφάνιση IGT, όμως, η απόλυτη τιμή της ινσουλίνης στις 2 ώρες της OGTT και ο δείκτης AUCG προέβλεψαν την εμφάνιση IGT. Τα επίπεδα λεπτίνης και γκρελίνης ήταν υψηλότερα στα κορίτσια. Υπήρχε συσχετισμός μεταξύ BMI και λεπτίνης νηστείας, BMI και αδιπονεκτίνης, σωματομεδίνης (IGF-I) και λεπτίνης νηστείας, ενώ δεν υπήρχε καμιά συσχέτιση με τα επίπεδα της κορτιζόλης ή με τα 24ωρα επίπεδα της αυξητικής ορμόνης και της θυρεοειδοτρόπου ορμόνης. Συμπερασματικά, η OGTT φαίνεται να έχει τη δυνατότητα να προβλέψει την IGT, ενώ οι τιμές γλυκόζης και ινσουλίνης νηστείας και οι τιμές του δείκτη HOMA-IR, αν και υψηλότερες στους ασθενείς με IGT και ενδεικτικές για αντίσταση στην ινσουλίνη, δεν μπορούν να προβλέψουν την IGT. / The aims of the present study were: (1) to determine the prevalence of impaired glucose tolerance (IGT) and diabetes mellitus II (DMII) in obese children and adolescents of Greek origin and (2) to study the concentrations of leptin, ghrelin, adiponectin and IGF-I during an oral glucose tolerance test as well as the 24-hour concentrations of growth hormone (GH) and thyrotropin secreting hormone (TSH), and the diurnal secretion of cortisol in these children. A total of 117 obese children and adolescents aged 12.1  2.7 years underwent an oral glucose tolerance test (OGTT) and the concentrations of leptin, ghrelin, adiponectin and IGF-I were studied during the duration of the OGTT in relation to the 24-hour secretion of GH and TSH and the diurnal secretion of cortisol. For the estimation of insulin resistance and beta cell function the homeostatic model assessment (HOMA-IR) and the insulinogenic index, respectively, were used. A total of 17 patients (14.5%) had IGT and none had DMII. The overall prevalence rates of both IGT and DMII observed in the obese children and adolescents were lower than those reported in a recent multiethnic US study. Nevertheless, the difference between the data of this study and those of the US study was mostly due to the prepubertal children (9% vs. 25.4%), while no difference was observed in the pubertal population (18% vs. 21%). The prevalence rates of IGT in this study though, were greater than those reported in other European studies. Fasting glucose, insulin and HOMA-IR values were not predictive of IGT. The absolute value of insulin at 2h of the OGTT combined with the time-integrated glycemia (AUCG) strongly predicted IGT, whereas higher area under the curve for insulin (AUCI) values were found to be protective. Leptin and ghrelin concentrations were higher in the females. There was a correlation found between BMI and fasting leptin, BMI and adiponectin, IGF-I and fasting leptin although there was no correlation found with the GH, TSH or cortisol concentrations. In conclusion, the OGTT seems to be capable of predicting IGT whereas the fasting glucose and insulin concentrations are unable to predict glucose intolerance since HOMA-IR values, although higher in IGT subjects and indicative of insulin resistance, cannot accurately predict IGT. Παιδική παχυσαρκία Λεπτίνη Αυξητική ορμόνη Γκρελίνη Αδιπονεκτίνη 618.924 624 Childhood obesity Impaired glucose tolerance Diabetes type II Leptin Growth hormone Ghrelin Adiponectin Oral glucose tolerance Test
22	Pharmacometrics Modelling in Type 2 Diabetes Mellitus : Implications on Study Design and Diabetes Disease Progression Ghadzi, Siti Maisharah Sheikh January 2017 (has links) Pharmacometric modelling is widely used in many aspects related to type 2 diabetes mellitus (T2DM), for instance in the anti-diabetes drug development, and in quantifying the disease progression of T2DM. The aim of this thesis were to improve the design of early phase anti-diabetes drug development studies with the focus on the power to identify mechanism of drug action (MoA), and to characterize and quantify the progression from prediabetes to overt diabetes, both the natural progression and the progression with diet and exercise interventions, using pharmacometrics modelling. The appropriateness of a study design depends on the MoAs of the anti-hyperglycaemic drug. Depending on if the focus is power to identify drug effect or accuracy and precision of drug effect, the best design will be different. Using insulin measurements on top of glucose has increase the power to identify a correct drug effect, distinguish a correct MoA from the incorrect, and to identify a secondary MoA in most cases. The accuracy and precision of drug parameter estimates, however, was not affected by insulin. A natural diabetes disease progression model was successfully added in a previously developed model to describe parameter changes of glucose and insulin regulation among impaired glucose tolerance (IGT) subjects, with the quantification of the lifestyle intervention. In this model, the assessment of multiple short-term provocations was combined to predict the long-term disease progression, and offers apart from the assessment of the onset of T2DM also the framework for how to perform similar analysis. Another previously published model was further developed to characterize the weight change in driving the changes in glucose homeostasis in subjects with IGT. This model includes the complex relationship between dropout from study and weight and glucose changes. This thesis has provided a first written guidance in designing a study for pharmacometrics analysis when characterizing drug effects, for early phase anti-diabetes drug development. The characterisation of the progression from prediabetes to overt diabetes using pharmacometrics modelling was successfully performed. Both the natural progression and the progression with diet and exercise interventions were quantified in this thesis. Pharmacometric type 2 diabetes mellitus impaired glucose tolerance prediabetes anti-diabetes drug development insulin glucose natural diabetes disease progression lifestyle intervention short-term provocation long-term effect glucose homeostasis glucose and insulin regulation weight dropout Pharmaceutical Sciences Farmaceutisk vetenskap Endocrinology and Diabetes Endokrinologi och diabetes
23	Practitioners' Use of Clinical Practice Guidelines: An Evidence-Based Approach Santana, Sondra Michelle Phipps 01 January 2013 (has links) Pre-diabetes is a serious health problem in the United States. Distinguished by plasma glucose levels that are above the normal threshold, patients with pre-diabetes are 10 times more likely to develop type 2 diabetes. Patients with pre-diabetes suffer the same complications as patients with diabetes including diabetic retinopathy, nephropathy, and microalbuminuria. There is considerable evidence to support the idea that early identification and aggressive treatment of pre-diabetes has the potential to delay disease progression. The American Diabetes Association’s clinical practice guideline recommends management of with lifestyle modification and metformin for patients who are at risk for developing type 2 diabetes. The purpose of this project was to evaluate the implementation of the 2012 ADA clinical practice guidelines regarding the management of patients with pre-diabetes by the health care providers at a volunteer-run clinic located in a large metropolitan area in the southeastern United States. This study, even with a small sample size (n=26) revealed that the providers at the clinic had not implemented the 2012 ADA clinical practice guidelines. Clinical practice guidelines promote health care interventions that have proven benefits and improve the consistency of care provided to patients. The greatest benefits of implementing clinical practice guidelines for patients with pre-diabetes are early diagnosis and aggressive disease management. This would improve patient outcomes and in the long run, decrease the cost of medical care. University of North Florida UNF Project DNP D.N.P. Pre-diabetes clinical practice guidelines impaired fasting glucose impaired glucose tolerance metformin pharmacologic intervention prevention of type 2 diabetes Diseases Endocrine System Diseases Family Practice Nursing Medicine and Health Sciences Nursing
24	BIRTHWEIGHT AND SUSCEPTIBILITY TO CHRONIC DISEASE Issa 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. birth weight birthweight birth weight and renal volume BIRTH WEIGHT QUESTIONNAIRE chronic disease Barker Hypothesis Foetal development DOHaD gestational age Anthropometric Characteristics body composition Height weight body mass index Waist Circumference hip circumference Waist-hip Ratio obesity Central Obesity Fatness Lean Body Mass Lean Mass Fat Mass body fat mass Body Fat Percentage body fatness Body Surface Area diabetes Fasting Glucose fasting insulin level glucose tolerance Impaired Fasting Glucose Impaired Glucose Tolerance Glycosylated Hemoglobin HbA1c IFG glucose control glycaemic control Metabolic Syndrome Syndrome X blood pressure Systolic Blood-pressure Diastolic Blood-pressure Systolic Hypertension high blood pressure Hypertension Dyslipidaemia Dyslipidemia Total Cholesterol Triglyceride Low Density Lipoprotein Cholesterol Ldl Cholesterol High Density Lipoprotein Hdl Cholesterol Fibrinogen angina Angina-pectoris Stroke coronary artery disease cardiovascular disease Framingham Framingham Heart Study Framingham Score coronary heart disease Glomerular Filtration glomerular filtration rate Glomerular Hyperfiltration Glomerular Injury Glomerular Number Nephrogenesis Nephron Endowment Nephron Number NKF-K/DQQI Classification Chronic Kidney Disease (ckd) Chronic Kidney Failure Kidney Failure CKD STAGES end-stage renal disease (ESRD) end-stage renal failure Cockcroft-gault MDRD formula Serum Creatinine Urinary Creatinine albuminuria Albuminuria:creatinine Ratio Kidney Development Kidney dysfunction low birth weight low birth weight Pre-term Birth AusDiab Study case control longitudinal observational study
25	BIRTHWEIGHT AND SUSCEPTIBILITY TO CHRONIC DISEASE Issa 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. birth weight birthweight birth weight and renal volume BIRTH WEIGHT QUESTIONNAIRE chronic disease Barker Hypothesis Foetal development DOHaD gestational age Anthropometric Characteristics body composition Height weight body mass index Waist Circumference hip circumference Waist-hip Ratio obesity Central Obesity Fatness Lean Body Mass Lean Mass Fat Mass body fat mass Body Fat Percentage body fatness Body Surface Area diabetes Fasting Glucose fasting insulin level glucose tolerance Impaired Fasting Glucose Impaired Glucose Tolerance Glycosylated Hemoglobin HbA1c IFG glucose control glycaemic control Metabolic Syndrome Syndrome X blood pressure Systolic Blood-pressure Diastolic Blood-pressure Systolic Hypertension high blood pressure Hypertension Dyslipidaemia Dyslipidemia Total Cholesterol Triglyceride Low Density Lipoprotein Cholesterol Ldl Cholesterol High Density Lipoprotein Hdl Cholesterol Fibrinogen angina Angina-pectoris Stroke coronary artery disease cardiovascular disease Framingham Framingham Heart Study Framingham Score coronary heart disease Glomerular Filtration glomerular filtration rate Glomerular Hyperfiltration Glomerular Injury Glomerular Number Nephrogenesis Nephron Endowment Nephron Number NKF-K/DQQI Classification Chronic Kidney Disease (ckd) Chronic Kidney Failure Kidney Failure CKD STAGES end-stage renal disease (ESRD) end-stage renal failure Cockcroft-gault MDRD formula Serum Creatinine Urinary Creatinine albuminuria Albuminuria:creatinine Ratio Kidney Development Kidney dysfunction low birth weight low birth weight Pre-term Birth AusDiab Study case control longitudinal observational study
26	BIRTHWEIGHT AND SUSCEPTIBILITY TO CHRONIC DISEASE Issa 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. birth weight birthweight birth weight and renal volume BIRTH WEIGHT QUESTIONNAIRE chronic disease Barker Hypothesis Foetal development DOHaD gestational age Anthropometric Characteristics body composition Height weight body mass index Waist Circumference hip circumference Waist-hip Ratio obesity Central Obesity Fatness Lean Body Mass Lean Mass Fat Mass body fat mass Body Fat Percentage body fatness Body Surface Area diabetes Fasting Glucose fasting insulin level glucose tolerance Impaired Fasting Glucose Impaired Glucose Tolerance Glycosylated Hemoglobin HbA1c IFG glucose control glycaemic control Metabolic Syndrome Syndrome X blood pressure Systolic Blood-pressure Diastolic Blood-pressure Systolic Hypertension high blood pressure Hypertension Dyslipidaemia Dyslipidemia Total Cholesterol Triglyceride Low Density Lipoprotein Cholesterol Ldl Cholesterol High Density Lipoprotein Hdl Cholesterol Fibrinogen angina Angina-pectoris Stroke coronary artery disease cardiovascular disease Framingham Framingham Heart Study Framingham Score coronary heart disease Glomerular Filtration glomerular filtration rate Glomerular Hyperfiltration Glomerular Injury Glomerular Number Nephrogenesis Nephron Endowment Nephron Number NKF-K/DQQI Classification Chronic Kidney Disease (ckd) Chronic Kidney Failure Kidney Failure CKD STAGES end-stage renal disease (ESRD) end-stage renal failure Cockcroft-gault MDRD formula Serum Creatinine Urinary Creatinine albuminuria Albuminuria:creatinine Ratio Kidney Development Kidney dysfunction low birth weight low birth weight Pre-term Birth AusDiab Study case control longitudinal observational study

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