Thesis (M. Phil.)--University of Hong Kong, 2008. / Also available online.

Thesis (Ph.D.)--University of Melbourne, School of Rural Health, 2009. / Typescript. Includes bibliographical references.

Thesis (Ph. D.)--Rutgers University, 2008. / "Graduate Program in Nutritional Sciences." Includes bibliographical references.

Thesis (M.Med.Sc.)--University of Hong Kong, 2002. / Includes bibliographical references (leaves 74-83) Also available in print.

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This literature review has been analyzed and synthesized to clarify the problems associated with gestational diabetes mellitus. Gestational diabetes is a metabolic disorder with medical complications that increase perinatal outcomes of morbidity and mortality. Due to the long-range implications of gestational diabetes on the mother and the child conceived, screening, management and interventions should be utilized. This review consists of literature from the last four years, 1996 to 1999, in regards to different aspects of gestational diabetes. The analysis reflects that universal screening consensus has not been attained and whether an alternative management can be more effective. The interventions of patient education, diet therapy, exercise, monitoring of the condition, and the emotional and personal support counseling are what nurses do best. It is the foundation of health care and health prevention to the patient.

Thesis (Ph. D.)--University of Hong Kong, 2010. / Includes bibliographical references (leaves 168-194). Also available in print.

Although the risk of malformations in the offspring of diabetic mothers remains the leading cause of perinatal mortality, the pathogenesis has not been elucidated. The hypothesis of this study was that protein glycation and oxygen free radicals play a role in hyperglycemia-induced malformations. CD-1 mouse embryos (0-2 somites) were cultured under hyperglycemic conditions for 48 hours with the exogenous addition of anti-glycating agents and oxygen free radical scavengers. The exogenous addition of aspirin (ASA) and D-lysine reduced significantly the malformations and embryonic glycated protein levels. Salicylate, arachidonic acid (AA), and to a lesser extent, indomethacin also exerted protective effects, but with no effect on glycated protein levels. We hypothesize that ASA, salicylate and indomethacin are protective by exerting free radical scavenging action; and ASA and D-lysine are acting as potent anti-glycating agents. Moreover, we suggest that AA may have inhibited hyperglycemia-induced malformations through the protective action of prostaglandins against free radical damage. Serum media lipid peroxidation (LPO) was reduced in the ASA and indomethacin groups possibly due to either a direct free radical scavenging action and/or the inhibitory effects of these agents on cyclooxygenase activity thereby decreasing the oxygen free radicals produced by this enzyme system. On the other hand, AA was associated with an increased level of LPO in the serum media. As the evidence has shown, the cause of hyperglycemia-induced malformations appears to be multifactorial and no one agent can completely eliminate the problem, although protective action can be exerted at different levels of the glycation-free radical cascade of tissue damage.

Our objectives were to measure concentrations of glucose, insulin, insulin-like-growth-factor-binding-protein-1 (IGF BP1) and beta-hydroxybutyrate (BOHB) in amniotic fluid (AF), and establish if these concentrations were associated with emergence of maternal gestational diabetes mellitus (GDM). AF samples (n=408) were collected following routine amniocentesis (12-22 weeks gestation). Glucose and insulin concentrations were elevated in our GDM mother-infant pairs, where GDM was associated with a 176g increase in birth weight. Logistic regression showed that AF glucose but not insulin was associated with developing GDM. Non-linear Bayesian probability plots showed that when 2nd trimester glucose was plotted against insulin increases in both were predictive of the subsequent emergence of GDM. In conclusion, our findings show that: (1) AF glucose but not insulin predicts subsequent emergence of GDM and (2) these observed elevations provide evidence that the fetus of GDM mothers is being exposed early in-utero to metabolic perturbations (i.e. elevated glucose) that may have important long-term metabolic consequences for their future development.