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  • About
  • The Global ETD Search service is a free service for researchers to find electronic theses and dissertations. This service is provided by the Networked Digital Library of Theses and Dissertations.
    Our metadata is collected from universities around the world. If you manage a university/consortium/country archive and want to be added, details can be found on the NDLTD website.
381

Étude sur l’entreposage de la matière grasse chez des femmes obèses post-ménopausées présentant un taux élevé ou normal d’apolipoprotéine B

Salem, Huda 07 1900 (has links)
No description available.
382

Physico-chimie des lipopolysaccharides et réponse inflammatoire : rôle des lipoprotéines / Physico-chemistry of lipopolysaccharides and inflammatory response : role of lipoproteins

Sali, Wahib 16 December 2014 (has links)
Le LPS est un puissant agent pro-inflammatoire bactérien, dont la partie lipide A est considérée comme le principe actif. Néanmoins, la chaîne O des LPS influence leur agrégation en solution aqueuse. Notre but a été de déterminer le rôle de la chaîne O sur les effets biologiques et physiopathologiques des LPS.Nos travaux, menés selon trois axes stratégiques complémentaires, ont donné lieu aux avancées suivantes :- développement d'un dosage innovant des LPS par LC-MS/MS et d'un ratio d'inactivation des LPS sur la base d'une utilisation combinée dudit dosage et du test LAL. Ce ratio traduit la capacité d'un organisme hôte à inactiver les LPS, notamment par leur transfert aux HDL par la PLTP. Ce ratio pourrait être utile dans l'évaluation des patients à haut risque.- la longueur de la chaîne O module l'inflammation induite par les LPS. Au-delà de leur concentration d'agrégation critique, les LPS forment des agrégats dotés d’une architecture et de propriétés physico-chimiques dépendant de leur chaîne O. Ces deux paramètres déterminent l'activité biologique des LPS et leur métabolisme ;- développement d'un double marquage innovant des LPS confirmant leur voie principale d'élimination : le transport inverse du LPS. Ce travail définit donc les effets physiopathologiques induits par les LPS comme résultant de deux composantes : leur activité biologique et leur métabolisme. Toute stratégie de recherche ou thérapeutique ciblant les LPS, devrait donc prendre en compte leur structure moléculaire, leur agrégabilité et la relation entre ces deux paramètres, déterminants majeurs de l'activité biologique des LPS et de leur métabolisme. / LPS is a potent bacterial pro-inflammatory agent, consisting of hydrophilic, polysaccharide part and of a lipid A which is considered like active moiety. Nevertheless, the O chain of LPS influences their aggregation in aqueous media. Therefore, our goal has been to determine the role of O chain on the LPS biological and physiopathological effects. Our work was organized according to three main axes, and led to the following findings :- development of a new LPS assay by LC-MS/MS. The combination of this new technique with LAL test allowed us to calculate an inactivation ratio which reflects the ability of host organism to inactivate LPS, especially through their transfer to HDL by PLTP. The ratio could be useful in predicting outcome of high risk patients.- the length of O chain modulates LPS-induced inflammation. Above their critical aggregation concentration, LPS form aggregates with an architecture and physiochemical properties dependent on their O chain. Both parameters determine LPS biological activity and their metabolism.- development of an innovative dual labelling of LPS as a new tool to explore LPS elimination pathway : the reverse LPS transport. This work brings evidence that the physiopathological effects of LPS depend on two parameters : their biological activity and their metabolism. Any strategy of research or therapeutic targeting LPS should take into account their molecular structure, their aggregability and the relation between the both parameters, which are major determinants of their biological activity and their metabolism.
383

Effet des acides gras oméga-3 sur l’inflammasome NLRP3 et les facteurs de risque de diabète de type 2 chez l’humain : modèles in vivo et ex vivo

Lamantia, Valérie 12 1900 (has links)
Contexte : La dysfonction du tissu adipeux blanc (TAB) favorise les facteurs de risque de diabète de type 2 (DbT2), c’est-à-dire la résistance à l’insuline (RI), l’hyper sécrétion d’insuline glucostimulée (SIGS), le délai de clairance des gras et les concentrations élevées d’apoBlipoprotéines (apoB plasmatique) incluant les lipoprotéines de faible densité (LDL). De récentes études de notre laboratoire et d’autres suggèrent que le niveau élevé d’apoB plasmatique (hyperapoB) est une cause et non seulement une conséquence de la dysfonction du TAB. De plus, une internalisation augmentée d’apoB-lipoprotéines via les récepteurs tels que le récepteur aux LDLs (LDLR) et le cluster de différenciation 36 (CD36), favorise le risque de DbT2. Cependant, les mécanismes sous-jacents de même que les interventions nutritionnelles pour les cibler demeurent incertains. L'activation de la voie de l’inflammasome NLRP3/ interleukine (IL) -1β favorise la dysfonction du TAB et les facteurs de risque de DbT2 et est activée par les LDLs oxydées dans les cellules immunitaires. L'acide eicosapentaénoïque (AEP) et l'acide docosahexaénoïque (ADH) réduisent l'hyperapoB, l'activité de l’inflammasome NLRP3 dans les cellules immunitaires et les facteurs de risque de DbT2 chez l’humain. Ils sont synthétisés de façon endogène par l’entremise des désaturases d’acides gras δ-5 (D5D) et δ-6 (D6D). Chez l’humain, de faibles niveaux d’AEP et d’ADH circulants et d’activité de la D5D et une activité élevée de la D6D prédisent l'incidence de DbT2 et la RI par des mécanismes inconnus. Objectifs : L'hypothèse de ma thèse est que l'AEP et l’ADH améliorent les facteurs de risque de DbT2, soit la dysfonction du TAB, le délai de clairance des gras, la RI et l’hyper SIGS, ceci via une baisse de l'apoB plasmatique et de l’activité de l’inflammasome NLRP3 dans le TAB. Les objectifs sont d'examiner si: 1) les associations entre les activités de la D5D et de la D6D et les facteurs de risque de DbT2 dépendent de l'apoB plasmatique; 2) la supplémentation en AEP+ADH réduit l'apoB plasmatique, l'expression du LDLR et du CD36 dans le TAB, l'activité de l’inflammasome NLRP3 dans le TAB et les facteurs de risque de DbT2; 3) l’AEP+ADH inhibe la sécrétion d'IL-1β par le TAB humain stimulée par des signaux canoniques ou les LDLs natives. Méthodes: Des hommes et des femmes postménopausées normoglycémiques ont été testés à l’état basal et après une supplémentation en AEP (1,8 g/jour) et ADH (0,9 g/jour) de 12 semaines. Les activités de la D5D et de la D6D ont été estimées à partir des acides gras produits/précurseurs dans les phospholipides plasmatiques. Nous avons mesuré la SIGS, la RI et le disposition index lors d’un clamp Botnia. Après un repas à 66% de gras, le délai de clairance des gras a été mesuré par l’aire sous la courbe (sur 6 h) des triglycérides (TG) ou de l’apoB48 (chylomicrons) plasmatiques. Ex vivo dans une biopsie de TAB, nous avons mesuré l'expression de surface du LDLR et du CD36 par immunohistochimie, l'ARNm de NLRP3 et IL1B par RT-qPCR et la sécrétion d'IL-1β par alpha-LISA en l’absence ou en présence d’une stimulation par le lipopolysaccharide (LPS), l'adénosine triphosphate (ATP) et/ou les LDLs humaines natives et lors d’une co-incubation avec l’AEP+ADH. Résultats: À l’état basal (N=98), l'activité de la D5D corrélait négativement avec l'apoB plasmatique, la 2e phase de SIGS, la RI et le délai de clairance des chylomicrons et ces associations étaient dépendantes de l'apoB plasmatique. Inversement, l'activité de la D6D corrélait positivement avec la SIGS, la RI et le délai de clairance des chylomicrons indépendamment de l'apoB plasmatique. Chez les sujets ayant complété la supplémentation en AEP+ADH (N=30), on notait une amélioration de la 1e phase de SIGS, du disposition index et de la clairance des TGs. Des niveaux initiaux plus élevés d'apoB plasmatique, de TGs postprandiaux plasmatiques et de RI, et dans le TAB d'expression du LDLR et du CD36, de sécrétion d’IL-1β et d'ARNm de NLRP3 prédisaient une plus grande réduction de ces paramètres. En comparaison à l'acide palmitique, l’AEP+ADH inhibait la sécrétion d'IL-1β par le TAB, en l’abscence ou en présence d’une stimulation par le LPS, l'ATP et/ou les LDLs natives de ces sujets. Conclusion: Les associations inverses entre l'activité de la D5D avec les facteurs de risque de DbT2 sont dépendantes de l'apoB plasmatique. Les meilleurs répondants à la supplémentation en AEP et ADH, en termes de réduction d'apoB plasmatique, d’expression du LDLR et du CD36 dans le TAB, d'activité de l’inflammasome NLRP3 dans le TAB, de TGs postprandiaux et de RI, sont les sujets avec des niveaux initiaux élevés de ces paramètres. L’AEP et l’ADH inhibent directement la sécrétion d'IL-1β par le TAB humain induite par les LDLs natives ou d'autres signaux. Nous proposons que la supplémentation en AEP et ADH puisse cibler l'activité de l’inflammasome NLRP3 dans le TAB, induite par un niveau élevé d’apoB-lipoprotéines plasmatiques ou internalisées par les récepteurs, et ainsi aider à prévenir le DbT2. / Background: White adipose tissue (WAT) dysfunction promotes risk factors for type 2 diabetes (T2D), namely insulin resistance (IR), high glucose-stimulated insulin secretion (GIIS), delayed fat clearance and high concentrations of apoB-lipoproteins (measured as plasma apoB) including low density lipoproteins (LDL). Recent studies from our lab and others suggest that high plasma apoB (hyperapoB) is a cause and not only a consequence of WAT dysfunction. Moreover, upregulated receptor-mediated uptake of apoB-lipoproteins via LDL receptor (LDLR) and cluster of differentiation 36 (CD36), promotes the risk for T2D. However, underlying mechanisms as well as nutritional interventions to target them remain unclear. Activation of the NLRP3 inflammasome/interleukin (IL)-1β pathway promotes WAT dysfunction and risk factors for T2D and is activated by oxidized LDLs in immune cells. Eicosapentaenoic acid (EPA) and docosahexaenoic acid (DHA) reduce hyperapoB, NLRP3 inflammasome activity in immune cells and risk factors for T2D in humans. They are synthesized endogenously through δ-5 (D5D) and δ-6 (D6D) fatty desaturases. In humans, low levels of circulating EPA and DHA and D5D activity and high D6D activity predict the incidence of T2D and IR by unknown mechanisms. Objectives: The hypothesis of my thesis is that EPA and DHA improve T2D risk factors, namely WAT dysfunction, delayed fat clearance, IR and high GIIS, this via a reduction of plasma apoB and WAT NLRP3 inflammasome activity. The objectives are to examine whether: 1) the associations between the levels of D5D and D6D activities and the risk factors for T2D are dependent on plasma apoB; 2) supplementation with EPA+DHA reduces plasma apoB, WAT LDLR and CD36 expression, WAT NLRP3 inflammasome activity and T2D risk factors; 3) EPA+DHA directly inhibits IL-1β secretion from human WAT stimulated by canonical signals or native LDLs. Methods: Normoglycemic men and postmenopausal women were tested at baseline and after supplementation with EPA (1.8 g/day) and DHA (0.9 g/day) for 12 weeks. The activities of D5D and D6D were estimated from the product/precursor fatty acids in plasma phospholipids. We measured GIIS, IR and disposition index by a Botnia clamp. Following a 66% fat meal, delayed fat clearance was measured as the area under the curve (over 6 h) of plasma triglycerides (TG) or apoB48 (chylomicrons). Ex vivo in a WAT biopsy, we measured LDLR and CD36 surface expression by immunohistochemistry, NLRP3 and IL1B mRNA by RT-qPCR, and IL-1β secretion by alpha-LISA either unstimulated or stimulated by lipopolysaccharide (LPS), adenosine triphosphate (ATP), and/or native human LDLs, and during co-incubation with EPA+DHA. Results: At baseline (N=98), D5D activity correlated negatively with plasma apoB, 2nd phase GIIS, IR and delayed chylomicron clearance and these associations were dependent on plasma apoB. Conversely, D6D activity correlated positively with GIIS, IR, and delayed chylomicron clearance independently of plasma apoB. In subjects who completed the EPA+DHA supplementation (N=30), there was an amelioration in 1st phase GIIS, disposition index and TG clearance. Higher baseline levels of plasma apoB, plasma postprandial TGs, IR, WAT LDLR and CD36 surface expression, WAT IL-1β secretion and WAT NLRP3 mRNA predicted a greater reduction of these parameters. In comparison with palmitic acid, EPA+DHA inhibited IL-1β secretion from WAT, either unstimulated or stimulated by LPS, ATP and/or subjects’ native LDLs. Conclusion: The negative associations of D5D activity with risk factors for T2D are dependent on plasma apoB. Best responders to EPA and DHA supplementation to reduce plasma apoB, WAT LDLR and CD36 expression, WAT NLRP3 inflammasome activity, delayed TG clearance, and IR are subjects with elevated baseline levels of these parameters. EPA and DHA directly inhibit IL-1β secretion from human WAT induced by native LDLs or other signals. We propose that EPA and DHA supplementation may target upregulated WAT NLRP3 inflammasome activity induced by high plasma concentrations, or receptor-mediated uptake, of apoB-lipoproteins, and thus help prevent T2D.
384

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.
385

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.
386

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.

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