Letteratura scientifica selezionata sul tema "Gestational glucose intolerance"

Gestational diabetes mellitus increases the risk of dysglycemia postpartum, in part, due to pancreatic β-cell dysfunction. However, no histological evidence exists comparing endocrine pancreas after healthy and glucose-intolerant pregnancies. This study sought to address this knowledge gap, in addition to exploring the contribution of an inflammatory environment to changes in endocrine pancreas after parturition. We used a previously established mouse model of gestational glucose intolerance induced by dietary low protein insult from conception until weaning. Pancreas and adipose samples were collected at 7, 30 and 90 days postpartum for histomorphometric and cytokine analyses, respectively. Glucose tolerance tests were performed prior to euthanasia and blood was collected via cardiac puncture. Pregnant female mice born to dams fed a low protein diet previously shown to develop glucose intolerance at late gestation relative to controls continued to be glucose intolerant until 1 month postpartum. However, glucose tolerance normalized by 3 months postpartum. Glucose intolerance at 7 days postpartum was associated with lower beta- and alpha-cell fractional areas and higher adipose levels of pro-inflammatory cytokine, interleukin-6. By 3 months postpartum, a compensatory increase in the number of small islets and a higher insulin to glucagon ratio likely enabled euglycemia to be attained in the previously glucose-intolerant mice. The results show that impairments in endocrine pancreas compensation in hyperglycemic pregnancy persist after parturition and contribute to prolonged glucose intolerance. These impairments may increase the susceptibility to development of future type 2 diabetes.

ObjectivesTo identify the incidence of postpartum glucose intolerance and develop a prediction model based on antenatal characteristics to predict postpartum glucose intolerance.DesignProspective cohort study.SettingGondar town public health facilities in Northwest Ethiopia.ParticipantsWomen who had gestational diabetes mellitus were advised to undergo postpartum oral glucose tolerance test at 6–12 weeks of delivery.Main outcomePostpartum glucose intolerance.Data analysisPredictors of postpartum glucose intolerance were identified using multivariable logistic regression analysis. The discriminative power of the predictor variables for postpartum glucose intolerance and the model accuracy were computed by area under the receiver operating characteristic curve and estimated by area under the curve (AUC) with 95% CI.ResultsA total of 112 (85.5%) women with gestational diabetes mellitus returned and completed the postpartum oral glucose tolerance test. The incidence of postpartum glucose intolerance was 21.4% (95% CI14.3 to 28.4), inclusive of 18.7% pre-diabetes and 2.7% diabetes. Multivariable logistic regression analysis revealed that advanced maternal age, high fasting plasma glucose level at diagnosis, overweight and/or obesity, and antenatal depression were predictors of postpartum glucose intolerance. The AUC of the final reduced model to predict postpartum glucose intolerance was 0.884 (95% CI 0.822 to 0.937). Fasting plasma glucose at diagnosis of gestational diabetes mellitus (AUC=0.736, 95% CI0.616 to 0.845) and overweight and/or obesity (AUC=0.718, 95% CI 0.614 to 0.814) were better predictors of postpartum glucose intolerance. Moreover, the AUC for the combined predictors of fasting plasma glucose at diagnosis and mid-upper arm circumference was 0.822 (95% CI 0.722 to 0.907), which was the best predictor.ConclusionsThe incidence of postpartum glucose intolerance was high among women with gestational diabetes mellitus. Antenatal predictors modestly predicted postpartum glucose intolerance. The findings suggest ongoing glucose screening is indicated for all women with gestational diabetes mellitus.

Introduction. The glucose intolerance later gestational diabetes is a very important indicator that helps establish the prognosis of diabetes in pregnant women who have had gestational diabetes (1). In this study we followed for one year to all gestational diabetes who were treated at the Hospital of Fuerteventura in endocrinology consultation,Canary Island, Spain. The aim was to study what factors might be related to glucose intolerance in the immediate postpartum.Materials and methods. All pregnant women served with the diagnosis of gestational diabetes during April 2012 to May 2013, diagnosed according to the criteria of the ADA (2), were subjected to routine procedure of specialized gynecology and endocrinology unit, first: test loading test with 50 grams of glucose, and if blood glucose was greater whom 140 mgdl,SOG was performed with 100 grams glucose three hours. All these patients were followed up with a minimum of a monthly review by both gynecology and endocrinology as was given a standard diet and as controls if necessary insulin treatment. In addition glycemia in the first quarter, glycated hemoglobin in the second and third quarter was measured, if there was family history of diabetes, as well as history of previous gestational diabetes, presence of other diseases, hypertension in pregnancy, if they had done treatment with diet or insulin. Finally, it determines if the birth was eutocic or dystocia. All the analyzes were performed in the Hospital Fuerteventura laboratory by standard autoanalyzer. SPSS v.24 program for frequency valuations and statistical analyzes. Was measured frequencies, all dependent and independent variables and logistic regression analysis, ANOVA and linear correlation with statistical significance of ≤0.05 was performed.Results. Of the 60 diabetic gestational included in the study, 49 completed the assessment of oral glucose tolerance test at 0 and 120 minutes, 81'7%, of these 57.1% were normal, 41.8% had glucose intolerance which were 26.5% impaired fasting glucose and 14’3 were intolerant, 2.5 were diabetic. In these patients: 57.6 percent had a normal vaginal delivery and 39.0% were dystocia. When we analyze all the variables according to the diagnosis of glucose intolerance, just correlated test 50 grams of glucose, ANOVA (p <0.033) with degrees of impaired glucose tolerance and there was a correlation positive linear between higher blood glucose value post 50 grams of glucose and glucose intolerance in the immediate postpartum. When we analyze dystocia, there was no correlation with any of the studied variables.Discussion. Interestingly in this study it is among correlation values loading test with 50g glucose and the presence of glucose intolerance and diabetes immediately after birth of gestational diabetes. It is known that after 50 grams of glucose greater than 200 glucose has an almost certain chance of having gestational diabetes (2) and according to some centers especially in the United States is not necessary to make a confirmatory SOG (2), however, their relationship to the immediate postpartum, it has not been seen in another study that we know until now and therefore part of their predictive value for gestational diabetes, could already give us an indication of glycemic alteration itself will happen in the immediate postpartum (3). Compared with other studies, the prevalence of glucose intolerance is similar to other high-risk populations, such as the Indian population (4), which gives the Canarian population at high risk of developing diabetes in the future. This study shows that the overload test with 50 grams of glucose is not only indicative of a very high suspicion of gestational diabetes, but can also help establish the prognosis of a future change in glucose metabolism in gestational diabetes.

Objective: Women with gestational diabetes mellitus and milder gestational impaired glucose intolerance have elevated future risks of type 2 diabetes and cardiovascular disease. However, it is unclear whether they show postpartum evidence of vascular injury/dysfunction, an early event in the natural history of cardiovascular disease. Methods: In total, 337 women underwent a glucose challenge test and oral glucose tolerance test in pregnancy, yielding four gestational glucose tolerance groups: gestational diabetes mellitus, gestational impaired glucose intolerance, abnormal glucose challenge test with normal glucose tolerance on the oral glucose tolerance test and normal glucose challenge test with normal glucose tolerance. At 3 years postpartum, they underwent repeat oral glucose tolerance test (on which 69 women had pre-diabetes/diabetes) and measurement of the following serum markers of vascular injury/dysfunction: thrombomodulin, E-selectin, P-selectin, intercellular adhesion molecule-3 and vascular cell adhesion molecule-1. Results: At 3 years postpartum, mean adjusted vascular cell adhesion molecule-1 was the only vascular marker that differed across the previous gestational glucose tolerance groups. On multiple linear regression analysis, each strata of gestational dysglycaemia was an independent predictor of lower vascular cell adhesion molecule-1 at 3 years postpartum (gestational diabetes mellitus: p = 0.005; gestational impaired glucose intolerance: p = 0.003; abnormal glucose challenge test normal glucose tolerance: p = 0.0008), as was current pre-diabetes/diabetes ( p = 0.01). Conclusion: Dysregulation of vascular cell adhesion molecule-1 may be an early event in the natural history of cardiovascular disease in women with recent glucose intolerance in pregnancy.

Abstract Pregnancy is a period marked by profound changes in a woman’s hormonal status and metabolism, including the development of a carbohydrate-intolerant state. Gestational diabetes mellitus (GDM) is defined as any degree of glucose intolerance with onset or first recognition during pregnancy. The aim of this study was to estimate and analyse the parameters of glycaemic control during pregnancy. We stratified patients into the following three groups according to OGTT results: normal glucose tolerance (NTG), gestational impaired glucose tolerance (GIGT) and GDM. We investigated 92 pregnant women, diagnosed with vital and desired pregnancy up to 12 weeks of gestation, who had signed informed consent forms. Among them, 7 pregnant women had a spontaneous abortion, while 8 pregnant women dropped out, so a total of 77 pregnant women completed the trial. Most of the women examined had no risk factors (48%), while 35% of the women had one risk factor. The current study demonstrates that normal glucose tolerance was shown in 59 (76.6%) participants, while some form of glucose intolerance (GIGT or GDM) was shown in 18 (23.4%) patients. Our findings revealed an increase in glucose intolerance with advancing pregnancy (in the second and third trimester). In conclusion, we demonstrate that the difference in the quality of glycaemic control during pregnancy is manifested in the second and third trimester, until it manifests in the first trimester. These findings underpin the clinical significance of discovering GDM.

Gestational diabetes (GDM) is defined as “carbohydrate intolerance of variable severity with onset or first recognition during pregnancy.” The definition is applicable regardless of whether insulin is used for treatment or the condition persists after pregnancy. It does not exclude the possibility that unrecognized glucose intolerance may have antedated the pregnancy”. GDM complicates 3–15% of all pregnancies and is a major cause of perinatal morbidity and mortality, as well as maternal long term morbidity. Of all types of diabetes, gestational diabetes (GDM) accounts for approximately 90–95% of all cases of diabetes in pregnancy.

During pregnancy glucose tolerance in the mother is affected. Glucose tolerance in pregnancy, as in the non-pregnant state is a continuum, represented by a distribution curve shifted to the right, with no clear divide between normal and abnormal. Many of the problems associated with overt diabetic pregnancies can be seen in infants of GDM pregnancies, such as macrosomia, neural tube defects, neonatal hypocalcemia, birth trauma and subsequent childhood and adolescent obesity. Impaired glucose intolerance (IGT) in pregnancy is also a major risk factor for the development of NIDDM (non-insulin dependent diabetes mellitus) and IGT in later life and is associated with not only an increased risk for coronary heart disease (CHD) disease but also many other morbidities and mortalities associated with overt diabetes. The problem remaining to be resolved is the precise level of glucose intolerance in pregnancy that poses a significant risk for the later health of the mother. Nor is increased gestational glucose intolerance the only reproductive event that has been linked with future NIDDM risk. Other factors have been known to predispose pregnant women to the risk of future diabetes (e.g. BMI, age and weight change). The findings of the present study suggest that the association of glucose intolerance during pregnancy, with the subsequent incidence of diabetes and certain co-morbidities in the mother, is continuous throughout the range of glucose concentrations studied. The risk of future diabetes is also affected by certain maternal characteristics (BMI at index pregnancy and at follow-up, weight change).

Les relations bien connues en cas d'hémochromatose entre surcharge en fer, insulinorésistance et stress oxydant, nous ont conduit à chercher à établir le rôle de la ferritine comme un facteur prédictif du risque de diabète gestationnel et du stress oxydant indépendamment de toute supplémentation dans une population de femmes Libanaises non anémiques. Nous avons observé qu'une ferritine élevée en début de la grossesse était un facteur prédictif d'intolérance au glucose, alors que cette relation n'était pas retrouvée avec une hémoglobine élevée, suggérant que le fer de réserve est un facteur de risque à considérer et non pas le fer fonctionnel. Le dosage de la ferritine pourrait être un marqueur biologique à prendre en considération pour évaluer le risque d'intolérance au glucose chez les femmes à risque de diabète gestationnel. La prévalence du diabète gestationnel dans la population étudiée, sur la base de nouveaux critères adoptés par l'Organisation mondiale de la santé était de ~15% alors qu'elle n'était que de 4% avec les critères de O'Sullivan actuellement utilisés dans les hôpitaux où a été recrutée notre population. Cette forte différence souligne la nécessité de l'adoption de nouveaux critères pour un meilleur dépistage et une meilleure prise en charge du fait des risques materno-fœtaux associés au diabète gestationnel. Malgré l'abaissement des valeurs de la glycémie, nous montrons que les nouveaux seuils de glycémie définissant désormais un diabète gestationnel sont toujours associés à une augmentation du stress oxydant, notamment des dommages à l'ADN. Conformément à la littérature, nous montrons qu'un statut en fer élevé, est associé à un état de stress oxydant élevé. De façon plus originale nous montrons qu'une ferritine élevée en début de grossesse aggrave l'association du stress oxydant et de l'insulinorésistance avec l'intolérance au glucose. En l`absence de modèle satisfaisant pour l`étude du diabète gestationnel expérimental, nous avons validé dans une étude préliminaire un régime riche en fructose comme modèle expérimental de diabète gestationnel. Nous montrons que ce modèle induit les mêmes modifications chez les rates et leurs ratons que celles observées lors de diabète gestationnel, de plus lorsque ce régime est enrichi en fer, des altérations oxydatives sont observées au niveau cérébral et hépatique des ratons. Ce modèle expérimental nous permettra d'étudier ultérieurement les voies de signalisation qui régissent les interactions entre fer, stress oxydant et diabète gestationnel et d'évaluer les répercussions d'une augmentation des dommages oxydatifs chez les fœtus, chez les nouveau-nés à la naissance et à distance par des études de comportement. Enfin en raison des données récentes sur l'épigénétique notre modèle expérimental pourrait nous permettre de suivre l'évolution en terme d'apparition de pathologies à l'âge adulte (insulinorésistance, diabète de type 2, déclin cognitif) des animaux nés de mère avec un diabète gestationnel. Au vu de l`ensemble de nos résultats sur les interactions entre ferritine, intolérance au glucose et stress oxydant, le bénéfice d`une supplémentation martiale durant la grossesse chez des femmes à risque de diabète gestationnel doit être évalué
The overall goal of this study was to establish the role of ferritin as a predictor for gestational diabetes mellitus and oxidative stress in non-anemic and non-iron supplemented Lebanese women. We observed that high ferritin level during the first-trimester of pregnancy was a predictor for impaired glucose tolerance, whereas high hemoglobin values yielded no significant relationship, suggesting that the iron reserve was the main indicator to be considered as a risk factor rather than the functional iron. Thus, the serum ferritin level could be used as a biological marker to assess for the risk of glucose intolerance in pregnant women. Based on the new World Health Organization criteria for gestational diabetes mellitus diagnosis, it is predicted that gestational diabetes mellitus prevalence in our population could be increased by four-fold. Since gestational diabetes mellitus has deleterious effects on the perinatal and maternal health outcomes, the implementation of these new criteria will allow for better management of blood glucose in pregnant women at risk for developing gestational diabetes mellitus. Although the new criteria adopted lower cut-off blood glucose value, hyperglycemia is still a factor that highly associated with increase oxidative stress, ultimately leading to DNA damage. Previously, we have shown that high iron status was associated with elevated oxidative stress. Furthermore, we have established that high ferritin during early-term pregnancy affected the association between oxidative stress and insulin resistance with glucose intolerance. Due to the lack of good experimental model to study gestational diabetes mellitus, we have utilized fructose-supplemented diet fed pregnant dam as an experimental animal model for our gestational diabetes studies. Data obtained in a preliminary study indicated that, this experimental animal model had identical metabolic modifications found in women with gestational diabetes mellitus. Moreover, we have showed that iron-enriched diet significantly increased the redox status of the brain and the liver of the fructose-supplemented dams. Therefore, we believed that this experimental model is good model for future studies to evaluate the signaling pathways involved in iron, oxidative stress and gestational diabetes and to assess the impact of increased oxidative damage during pregnancy on the fetus, immediately after birth and later during the developmental stages via various behavioral tests. Finally, an epigenetic study using this experimental model may allow us to understand the genetic alterations that affected the likelihood of developing insulin resistance, diabetes, or cognitive decline in pups born to the mothers with gestational diabetes. Based on the findings from our studies on the interaction between ferritin, glucose impairment, and oxidative stress, as well as the iron-supplemented diet in the dams with gestational diabetes mellitus, a caution must be exercised when supplementing a pregnant woman with iron. The use of iron-supplementation during pregnancy should be re-evaluated

Objetivo: O objetivo desse estudo foi identificar a associação entre fatores clínicos e laboratoriais com o uso de insulina em gestantes com DMG no momento do diagnóstico e analisar os possíveis fatores preditores do uso de insulina. Método: Foram estudadas, de forma retrospectiva, 294 pacientes com diabetes melito gestacional (DMG) diagnosticado por meio do teste de tolerância à glicose oral de 100 gramas (TTGO-100g) entre 24 e 33 semanas completas de gestação, cujo seguimento pré-natal foi realizado ambulatorialmente pelo setor de Endocrinopatias e Gestação da Clínica Obstétrica do Hospital das Clínicas da Faculdade de Medicina da Universidade de São Paulo, no período de 1 de julho de 2002 a 30 de junho de 2008. Os seguintes fatores clínicos e laboratoriais, que pudessem estar associados ao uso de insulina para controle glicêmico, foram analisados: idade materna, obesidade pré-gestacional - índice de massa corpórea (IMC) > 30 Kg/m2, antecedente familiar de diabetes melito (DM), tabagismo, hipertensão arterial, uso de corticosteróides sistêmicos, antecedente obstétrico de DMG e de macrossomia fetal, nuliparidade, multiparidade, antecedente obstétricos de natimortos e neomortos, idade gestacional no momento do diagnóstico, gemelidade, índice de líquido amniótico (ILA) aumentado ILA > 18 cm, polidrâmnio (ILA > 25 cm), número de valores anormais do TTGO-100g, glicemia de jejum anormal no TTGO- 100g glicemia de jejum > 95 mg/dL; média das quatro glicemias aferidas no TTGO-100g; valor da glicemia de jejum, de 1ª, 2ª e 3ª horas do TTGO-100g e hemoglobina glicada (HbA1c). A associação entre cada fator e a necessidade de insulinoterapia foi analisada individualmente (2 de Pearson / teste exato de Fisher e teste t de Student). O modelo de regressão logística para a análise multivariada foi usado para predizer a probabilidade desses fatores em relação ao uso de insulina. Resultados: Das 294 pacientes avaliadas, 39,8% (117/294) necessitaram de insulinoterapia para controle glicêmico. Observou-se correlação positiva entre o uso de insulina e obesidade pré-gestacional, antecedente familiar de DM, hipertensão arterial, antecedente obstétrico de DMG e de macrossomia fetal, número de valores anormais no TTGO-100g, glicemia de jejum > 95 mg/dL no TTGO-100g; média das quatro glicemias aferidas no TTGO-100g; valor da glicemia de jejum, de 1ª, 2ª e 3ª horas do TTGO-100g e HbA1c pela análise univariada (P<0,05). Na análise do modelo de regressão logística foram desenvolvidos dois modelos que incluíam os seguintes fatores preditores do uso de insulina: obesidade pré-gestacional, antecedente familiar de DM, número de valores anormais no TTGO-100g (só modelo 1) e valor da glicemia de jejum do TTGO-100g (só modelo 2). Os dois primeiros modelos foram novamente analisados, incluindo-se a variável HbA1c para verificação de sua contribuição na predição do uso de insulina. Curvas de probabilidade e escores foram construídos com base nas quatro combinações de fatores preditores. Conclusões: É possível estimar a probabilidade do uso de insulinoterapia para controle glicêmico em gestantes com DMG por meio de IMC pré-gestacional, antecedente familiar de DM, número de valores anormais do TTGO-100g, valor da glicemia de jejum no TTGO-100g e da HbA1c.
Objective: To determine the association between clinical and laboratory parameters and insulin requirement in pregnancies complicated by gestational diabetes mellitus (GDM), and to evaluate possible factors predicting the need for insulin therapy. Methods: A total of 294 patients with GDM diagnosed by the 100- g/3-h oral glucose tolerance test (OGTT) between 24 and 33 complete weeks of gestation were retrospectively studied. These patients were under prenatal follow-up at the Obstetric Clinic of the University of Sao Paulo School of Medicine (HCFMUSP) between July 1, 2002 and June 30, 2008. The clinical and laboratory factors which could be associated to the need for insulin therapy were analyzed: maternal age, prepregnancy obesity body mass index (BMI) > 30 Kg/m2, family history of diabetes mellitus (DM), smoking, hypertension, use of systemic corticosteroids, prior GDM, prior fetal macrosomia, nulliparity, multiparity, prior stillbirth, prior neonatal death, gestational age at diagnosis of GDM, multiple pregnancy, elevated amniotic fluid index (AFI) AFI > 18 cm, polyhydramnios (AFI > 25 cm), number of abnormal 100-g/3-h OGTT values, 100-g/3-h OGTT fasting plasma glucose > 95 mg/dL, mean of the four 100-g/3-h OGTT values, 100-g/3-h OGTT fasting/one/two/three plasma glucose values, and glycated hemoglobin (HbA1c). The association between each factor and the need for insulin therapy was then analyzed individually (Pearsons chi-square/Fishers exact or Student t test). The performance of these factors to predict the probability of insulin therapy was estimated using a logistic regression model. Results: Among the 294 patients studied, 39.8% (117/294) required insulin for glycemic control. Univariate analysis showed a positive correlation between insulin therapy and prepregnancy obesity, family history of diabetes, hypertension, prior GDM, prior fetal macrosomia, number of abnormal 100-g/3-h OGTT values, 100-g/3-h OGTT fasting plasma glucose > 95 mg/dL, mean of the four 100-g/3-h OGTT values, 100-g/3-h OGTT fasting/one/two/three plasma glucose values, and HbA1c (P < 0.05). Two logistic regression models were developed and included the following parameters: prepregnancy obesity, family history of diabetes, number of abnormal 100-g/3-h OGTT values (just model 1) and 100-g/3-h OGTT fasting plasma glucose (just model 2). The two first models were analysed another time including the variable HbA1c to verify its contribution on prediction of the need for insulin therapy. Probability curves and scores were constructed based on the four combinations of predictive factors. Conclusions: The probability of insulin therapy can be estimated in pregnant women with GDM based on prepregnancy obesity, family history of diabetes, number of abnormal 100-g/3-h OGTT values, 100-g/3-h OGTT fasting plasma glucose, and HbA1c concentration.

Ziel dieser vorliegenden, vergleichenden Literaturarbeit ist es, den heutigen Wissensstand in Bezug auf den Kohlenhydratstoffwechsel einer Frau darzustellen. Hierbei werden die physiologischen Veränderungen des Metabolismus zu verschiedenen Zeitpunkten im Leben einer Frau, begonnen mit der Kindheit und Pubertät, über Menstruation und Schwangerschaft bis hin zur Menopause, betrachtet und es werden die Ursachen und möglichen Mechanismen aufgezeigt, die zu Abweichungen der Insulinresistenz und der Insulinsekretion und damit möglicherweise zu einer Glukoseintoleranz bzw. einem Typ-2 Diabetes mellitus führen können. Der Kohlenhydratstoffwechsel wird nicht nur bezüglich der physiologischen, sondern auch in bezug auf die iatrogen verursachten Veränderungen, d.h. unter oraler hormonaler Kontrazeption, unter Hormonersatztherapie im Klimakterium, sowie hinsichtlich bestimmter Pathologien, wie dem zur Infertilität führenden polyzystischem Ovarsyndrom oder dem Gestationsdiabetes, untersucht. Ergebnis: Es scheint eine starke Verknüpfung zwischen dem weiblichen Reproduktionssystem und dem Kohlenhydratstoffwechsel zu geben, deren Interaktion von den unterschiedlichsten Faktoren beeinflusst wird. Der Frauenarzt sollte sich bei der Verschreibung hormoneller Kontrazeptiva, der Hormonersatztherapie und im Besonderen bei der Therapie des polyzystischen Ovarsyndroms sowie bei der Untersuchung seiner Patientinnen bewusst sein, dass verschiedene Lebensphasen, wie Pubertät, Schwangerschaft und Klimakterium und die damit verknüpften Veränderungen des Reproduktionssystems und der Sexualhormone auch deutliche metabolische Veränderungen nach sich ziehen können. Besonders eine erhöhte Insulinresistenz, die mit einer gesteigerten Insulinsekretion einhergeht, muss bedacht werden. Nicht nur das Syndrom X, eine Zusammenfassung von metabolischen Abnormitäten (Dyslipidämie, Insulinresistenz, Adipositas, Hypertonie), die mit einem deutlich erhöhten Risiko kardiovaskulärer Krankheiten und besonders der Atherosklerose einhergehen, sondern die daraus folgende steigende Prävalenz von Typ-2 Diabetes mellitus und das stark vermehrte Auftreten von Adipositas verlangen nach einer fachübergreifenden Zusammenarbeit zwischen Frauenärzten und Internisten.
The aim of this comparative review is to reveal the current standard of knowledge concerning carbohydrate metabolism in women. The study demonstrates the physiological changes in metabolism at various stages in a female life, from childhood and puberty, through menstruation and pregnancy and ending with the menopause, whilst also evaluating different causes and possible mechanisms that lead to aberrance in insulin resistance and insulin secretion and thereby potentially to glucose intolerance and/or type 2 Diabetes mellitus. In addition to presenting physiological alterations in glucose metabolism, this work also analyses changes generated by iatrogenic treatment such as oral contraceptives and hormone replacement therapy, as well as those caused by different pathologies like polycystic ovary syndrome or gestational diabetes. The results indicate a strong correlation between the female reproduction system and the carbohydrate metabolism. The interaction is influenced by the many very different factors. Before prescribing oral contraceptives, hormone replacement therapy in climacteric (especially during the treatment of infertility in PCOS), or examining patients, the gynaecologist needs to be aware of the fact that different phases in life along with sex steroids and connected changes in the reproductive system, might lead to severe metabolic diversifications. Special attention should be paid to an increased insulin resistance, associated with an augmentation in insulin secretion. Not only the metabolic syndrome, the simultaneous appearance of metabolic abnormalities (dyslipidaemia, insulin resistance, adiposity, hypertonia), which holds a higher risk of cardiovascular diseases, especially arteriosclerosis, but also the consequential increased prevalence of type 2 diabetes mellitus and the highly increased prevalence of adiposity, demand for a multidisciplinary collaboration between gynaecologists and internists.

Within the paradigm of developmental origins of health and disease, an intrauterine environment that stimulates fetal overnutrition has been found to contribute to the risk of subsequent obesity in the offspring. There is compelling epidemiological evidence for a positive association between maternal obesity prior to pregnancy, gestational diabetes (GD) or excessive gestational weight gain, and the development of childhood obesity (as measured by body mass index, BMI). However, the evidence is limited and inconsistent with respect to more specific measures of adiposity (body composition or fat pattern) and insulin resistance in children. Furthermore, the long-term effects of maternal borderline gestational glucose intolerance (BGGI) on the offspring have not been considered. Therefore, I sought to examine whether maternal obesity prior to pregnancy, gestational glucose intolerance across the entire spectrum, and gestational weight gain have deleterious effects on the development of obesity (both global and specific measures of adiposity) and insulin resistance in pre-pubertal children. These associations are particularly important from a public health perspective as, once identified, they may point towards potential windows for prevention of childhood obesity and related metabolic disorders. This project entailed a follow-up of an existing representative, prospective birth cohort study (Generation 1 Study, n=557) in Adelaide, South Australia, recruited during 1998-2000. At the 9-10 year follow-up, rigorous anthropometric measurements were conducted in 443 children (80% of the original cohort), of whom 163 consented to provide a fasting blood sample for the estimation of insulin resistance based on homeostasis model assessment (HOMA-IR). Information on intrauterine exposures and confounders was collected from the antenatal interviews and hospital records. Maternal age, parity, smoking, pregnancy-induced hypertension, and education at the time of pregnancy were considered as potential confounders for all the associations of interest, and child current BMI z-score as a potential mediator on the pathway between the intrauterine exposures and child insulin resistance. Data were analysed using multiple linear regression and generalized linear models. Maternal pre-pregnancy BMI was positively associated with all three obesity-related measures considered in the 9-10 year-old children (BMI z-score, percentage body fat estimated by bioelectrical impedance analysis, and waist-to-height ratio); these relationships were robust to adjustment for potential confounders (adjusted coefficients for each one kg/m2 increase in maternal pre-pregnancy BMI were 0.08 (95% confidence interval 0.06, 0.10) for child BMI z-score, 0.44 (95% CI 0.31, 0.58) for percentage body fat and 0.002 (95% CI 0.002, 0.003) for waist-to-height ratio). There was no association between maternal pre-pregnancy BMI and HOMA-IR in children (with or without adjustment); however, when child current BMI z-score was included as a mediating variable, the relationship between maternal pre-pregnancy BMI and child HOMA-IR was inverse and significant (adjusted change in child HOMA-IR for each one kg/m2 increase in maternal pre-pregnancy BMI was -0.83% (95% CI 1.63, -0.02)). Intrauterine exposure to glucose intolerance during pregnancy (either BGGI or GD) was not associated with any of the three obesity-related measures in children at 9-10 years. Children of mothers who developed GD during the index pregnancy had a higher HOMA-IR; this relationship was robust to adjustment for potential confounders (adjusted change in child HOMA-IR if exposed to maternal GD was 42.9% (95% CI 20.9, 68.9)) and partly mediated by child current BMI z-score. No association was found between exposure to maternal BGGI and child HOMA-IR (with or without confounder adjustment); however, when child current BMI z-score was added as a potential mediator, exposure to BGGI was associated with a reduction in child HOMA-IR (adjusted change in child HOMA-IR if exposed to maternal BGGI was -17.9% (95% CI -29.9, -3.96)). There were no significant associations between maternal gestational weight gain and any of the outcome measures of interest in unadjusted models. However, adjustment for pre-pregnancy BMI led to a positive association between gestational weight gain and child BMI z-score (adjusted changes in child BMI z-score for each one kg increase in maternal gestational weight gain was 0.032 (95% CI 0.007, 0.057)). Gestational weight gain was not associated with child insulin resistance, and this did not change when child current BMI z-score was included as a potential mediator on the pathway between gestational weight gain and child insulin resistance. Potential two-way interactions between the main exposures were investigated in relation to all outcomes of interest. Two significant interactions were identified: maternal pre-pregnancy BMI and glucose tolerance status, and maternal pre-pregnancy BMI and gestational weight gain, with a synergistic effect on child waist-to-height ratio. These results suggest that childhood obesity and insulin resistance have origins, at least in part, in intrauterine life, particularly in relation to maternal obesity at the time of pregnancy and GD. Further research to differentiate between genetic, environmental and intrauterine programming is recommended. That said, maternal pre-pregnancy BMI was the strongest predictor of child BMI zscore, while GD appeared to have an independent effect on child insulin resistance, and both clinical and public health actions to address these maternal factors are warranted for a range of reasons.
Thesis (Ph.D.) -- University of Adelaide, School of Population Health and Clinical Practice and School of Paediatrics and Reproductive Health, 2012

Diabetes in pregnancy is predominantly either pre-existing type 1 or type 2 diabetes mellitus, or gestational diabetes, the latter defined as diabetes or glucose intolerance first diagnosed during the pregnancy. Gestational diabetes usually arises in the late second trimester and is common, affecting from 2–6% to 15–20% of pregnant women depending on diagnostic criteria and country of origin. Gestational diabetes is most commonly diagnosed on the basis of an oral glucose tolerance test performed at 24–28 weeks’ gestation by a plasma glucose at 0 minutes of more than 5.1 (or >5.6, depending on the authority) mmol/L, or at 120 minutes of more than 8.5 (or >7.8) mmol/L. The effect of pregnancy on maternal glycaemic control ceases very quickly post-partum, hence women with pre-existing diabetes taking insulin should immediately revert to their pre-pregnancy regimen after birth, but with a lower insulin dose.

Gestational Diabetes Mellitus (GDM) happens to be a very frequent and major complication of pregnancy because of higher morbidity and mortality, both for the mother and the baby. After delivery, GDM carries the risk of higher maternal morbidity due to post pregnancy obesity, development of diabetes mellitus, obesity and also cardiovascular diseases in significant number in both the mother and child for future. As per current guidelines, GDM is diagnosed at the end of the second trimester by elevated blood glucose values when, foetal damages by metabolic and epigenetic changes had already started. As a result, treatments cannot be started before the late second or third trimester, when the process of high risk of foetal morbidity and mortality has been set in. If by any method we can predict development of GDM at earliest part of first trimester or even more overjealously, we can predict, before pregnancy, then and then only we can avoid many disasters induced by GDM. With this idea many biomarkers, both clinical and laboratory based like clinical, metabolic, inflammatory and genetic markers etc., related with early pregnancy metabolic alterations have been studied for their potential to help in the prediction of later pregnancy glucose intolerance. Though promises are seen with some biomarker-enhanced risk prediction models for GDM, but lack of external validation and translation into day-to-day clinical applications, cost effectiveness, with which they may be utilized in routine prenatal care has limited their clinical use. But future is very promising and incorporating the biomarkers which precede the onset of hyperglycaemia into a risk prediction model for GDM and may help us for earlier risk assessment, screening, and diagnosis of GDM and also prevention of its both the immediate and remote complications. This review highlights the current knowledge of the understanding of the candidacy and practical utility of these biomarkers for GDM with recommendations for further research.

The aim of this chapter is to provide nurses with the knowledge to be able to assess, manage, and care for people with type 1 and type 2 diabetes mellitus in an evidence-based and person-centred way. Diabetes mellitus is a long-term condition that can affect people of all ages; consequently, people with diabetes mellitus can be found in every healthcare environment, from hospitals to care homes. The chapter will provide a comprehensive overview of the classifications, causes, and risk factors of diabetes. The key principles of patient assessment are established, before exploring best practice to deliver care, prevent acute complications, and minimize long-term complications. Nursing assessments and priorities are highlighted throughout, and the nursing management of the symptoms and common health problems associated with diabetes can be found in Chapters 19, 22, 24, 25, 26, and 28, respectively. Diabetes mellitus is a group of metabolic conditions with hyperglycaemia occurring as the main feature. It is characterized by chronic increased blood glucose (hyperglycaemia), with disturbance of carbohydrate, protein, and fat metabolism, which results from defects in insulin secretion, insulin action, or both (World Health Organization (WHO), 1999). The hormone insulin, produced by the beta cells in the pancreas, controls blood glucose levels, keeping them within a narrow range in normal health (4–6 mmol/l before food). When blood glucose levels rise (for example, after a meal containing carbohydrates has been consumed), glucose enters the beta cells, eventually resulting in the release of insulin into the portal circulation. The classifications of diabetes mellitus (World Health Organization, 2006) are as follows….● Type 1 diabetes mellitus, previously known as insulin-dependent diabetes mellitus (IDDM) ● Type 2 diabetes mellitus, previously known as non-insulin-dependent diabetes mellitus (NIDDM) ● Gestational diabetes mellitus ● Others, such as disorders affecting the pancreas, and endocrine conditions…The features of type 1 and type 2 diabetes mellitus are outlined in Table 9.1. Gestational diabetes is carbohydrate intolerance, resulting in hyperglycaemia with onset or recognition during pregnancy (World Health Organization, 2006). However, the condition may have been present prior to pregnancy, but not been diagnosed. Diabetes mellitus may occur for other reasons, including genetic defects and diseases affecting the pancreas.