Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0011860 (type 2 diabetes)
 57,723 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Glucose transporters (GLUT) catalyse the transport of glucose in many human tissues, including the placenta. On the other hand glucose concentrations can affect both glucose transport activity and level of GLUT mRNA and protein. Up to now very few studies, concerning GLUT in the placenta appeared and studies in vivo in human diabetic pregnancy are lacking. Therefore we investigated placental GLUT 1 and GLUT 3 mRNA in 10 diabetic (5 IDDM, 2 NIDDM, 3 GDM) and 9 non-diabetic women. GLUT 1 mRNA was found significantly correlated with maternal age (> 30 vs < 30 years: p < 0.025), with placental weight (> 575 vs < 575 g: p < 0.05), while GLUT 3 mRNA decreased significantly in late gestation of diabetic women (38-40 vs < 38 weeks: p < 0.025). In addition GLUT 3 was significantly lower in the diabetic than in non-diabetic women in late gestation. These preliminary results deserve to better elucidate feto-maternal carbohydrate metabolism at the placental level in normal as well as diabetic pregnancy.
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PMID:Glucose transporters (GLUT 1, GLUT 3) mRNA in human placenta of diabetic and non-diabetic pregnancies. 954 63

Presence of antithyroid autoantibodies (ThyAb) during pregnancy is strictly related to the risk of developing post partum thyroiditis (PPT) and this risk is increased in IDDM pregnant women. Gestational diabetes mellitus (GDM) is defined as carbohydrate intolerance of variable severity that begins, or is first diagnosed, during pregnancy. GDM is considered a risk factor for both type 1 and type 2 diabetes and various non-organ specific autoantibodies have been found to be associated with GDM, although there is little information on the association of GDM with thyroid autoimmunity. In this study oral glucose tolerance and prevalence of ThyAb were evaluated in a group of 41 pregnant women at increased risk of developing GDM and in a healthy control group. Our results showed that 22% of GDM risk group had impaired glucose gestational tolerance (IGGT) or GDM at the time of oral glucose tolerance test (OGTT). Moreover, ThyAb prevalence found in the women at increased risk of GDM (14.6%) was similar to that observed in healthy pregnant controls (12.5%). Nevertheless ThyAb frequency was higher in those GDM risk women with family history of diabetes (30.7%).
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PMID:Thyroid autoimmunity in pregnant women at risk for GDM. 954 80

The TRoglitazone In the Prevention Of Diabetes (TRIPOD) trial is a single-center, randomized, placebo-controlled, double-masked study. The primary aim of the TRIPOD trial is to test the hypothesis that chronic administration of troglitazone to nondiabetic women with prior gestational diabetes mellitus (GDM) will improve whole-body insulin sensitivity and reduce the incidence of non-insulin-dependent diabetes (NIDDM). Because troglitazone is already known to lower blood glucose concentrations in persons who have developed NIDDM, an additional aim of the project will be to determine whether early intervention with troglitazone will achieve better final glycemic control than can be achieved by later intervention. In addition, since troglitazone treatment is expected to improve insulin sensitivity and may prevent or delay a decline in glucose tolerance, we also plan to determine whether long-term troglitazone treatment alters the development or progression of atherosclerosis. In this article we describe the experiment's design, the study's endpoints and methods for determining those endpoints, methods for assessing quality of life, and proposed methods for statistical analyses. The unique two-phase study design of the TRIPOD trial will permit testing not only of the biological question about reversal of insulin resistance and prevention of diabetes, but also of the clinical question about whether early intervention is superior to late intervention. Results from this trial will have an important impact on the monitoring and treatment of patients at high risk for NIDDM.
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PMID:TRIPOD (TRoglitazone In the Prevention Of Diabetes): a randomized, placebo-controlled trial of troglitazone in women with prior gestational diabetes mellitus. 955 Dec 85

Type 2 diabetes is extremely common and increasing in the United States. The pathophysiology of type 2 diabetes is a combination of increased insulin resistance and inadequate secretion. The main risk factors for diabetes are family history, obesity, sedentary lifestyle, ethnic background, age, and a history of gestational diabetes. Diet and exercise, the cornerstones of diabetes management, will improve insulin sensitivity and indirectly augment insulin secretion. Until recently, the only pharmacological approaches to diabetes were sulfonylureas and insulin, which either augment insulin secretion or replace insulin, thus acting only on the insulin side of the equation. Recently, a series of new drugs have become available that are capable of decreasing hepatic glucose output (metformin), slowing postprandial glucose absorption (acarbose), and improving peripheral insulin sensitivity (troglitazone). With these drugs, either alone or in combination, and behavioral therapies, it is now feasible to achieve good to outstanding glycemic control in most individuals with type 2 diabetes.
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PMID:Focus on insulin resistance in type 2 diabetes: therapeutic implications. 955 58

The classification of diabetes mellitus and the tests used for its diagnosis were brought into order by the National Diabetes Data Group of the USA and the second World Health Organization Expert Committee on Diabetes Mellitus in 1979 and 1980. Apart from minor modifications by WHO in 1985, little has been changed since that time. There is however considerable new knowledge regarding the aetiology of different forms of diabetes as well as more information on the predictive value of different blood glucose values for the complications of diabetes. A WHO Consultation has therefore taken place in parallel with a report by an American Diabetes Association Expert Committee to re-examine diagnostic criteria and classification. The present document includes the conclusions of the former and is intended for wide distribution and discussion before final proposals are submitted to WHO for approval. The main changes proposed are as follows. The diagnostic fasting plasma (blood) glucose value has been lowered to > or =7.0 mmol l(-1) (6.1 mmol l(-1)). Impaired Glucose Tolerance (IGT) is changed to allow for the new fasting level. A new category of Impaired Fasting Glycaemia (IFG) is proposed to encompass values which are above normal but below the diagnostic cut-off for diabetes (plasma > or =6.1 to <7.0 mmol l(-1); whole blood > or =5.6 to <6.1 mmol l(-1)). Gestational Diabetes Mellitus (GDM) now includes gestational impaired glucose tolerance as well as the previous GDM. The classification defines both process and stage of the disease. The processes include Type 1, autoimmune and non-autoimmune, with beta-cell destruction; Type 2 with varying degrees of insulin resistance and insulin hyposecretion; Gestational Diabetes Mellitus; and Other Types where the cause is known (e.g. MODY, endocrinopathies). It is anticipated that this group will expand as causes of Type 2 become known. Stages range from normoglycaemia to insulin required for survival. It is hoped that the new classification will allow better classification of individuals and lead to fewer therapeutic misjudgements.
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PMID:Definition, diagnosis and classification of diabetes mellitus and its complications. Part 1: diagnosis and classification of diabetes mellitus provisional report of a WHO consultation. 1034 46

We examined antepartum clinical characteristics along with measures of glucose tolerance, insulin sensitivity, pancreatic beta-cell function, and body composition in Latino women with gestational diabetes mellitus (GDM) for their ability to predict type 2 diabetes or impaired glucose tolerance (IGT) within 6 months after delivery. A total of 122 islet cell antibody-negative women underwent oral and intravenous glucose tolerance tests (OGTT; IVGTT), hyperinsulinemic-euglycemic clamps, and measurement of body fat between 29 and 36 weeks' gestation and returned between 1 and 6 months postpartum for a 75-g OGTT. Logistic regression analysis was used to examine the relationship between antepartum variables and glucose tolerance status postpartum. At postpartum testing, 40% of the cohort had normal glucose tolerance, 50% had IGT, and 10% had diabetes by American Diabetes Association criteria. Independent antepartum predictors of postpartum diabetes were the 30-min incremental insulin:glucose ratio during a 75-g OGTT (P = 0.0002) and the total area under the diagnostic 100-g glucose tolerance curve (P = 0.003). Independent predictors of postpartum IGT were a low first-phase IVGTT insulin response (P = 0.0001), a diagnosis of GDM before 22 weeks' gestation (P = 0.003), and weight gain between prepregnancy and the postpartum examination (P = 0.03). All subjects had low insulin sensitivity during late pregnancy, but neither glucose clamp nor minimal model measures of insulin sensitivity in the 3rd trimester were associated with the risk of IGT or diabetes within 6 months' postpartum. These results highlight the importance of pancreatic beta-cell dysfunction, detectable under conditions of marked insulin resistance in late pregnancy, to predict abnormalities of glucose tolerance soon after delivery in pregnancies complicated by GDM. Moreover, the association of postpartum IGT with weight gain and an early gestational age at diagnosis of GDM suggests a role for chronic insulin resistance in mediating hyperglycemia outside the 3rd trimester in women with such a beta-cell defect.
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PMID:Gestational diabetes: antepartum characteristics that predict postpartum glucose intolerance and type 2 diabetes in Latino women. 970 32

The available data suggest that the frequency of diabetes in pregnancy is highly variable, generally reflecting the underlying pattern of NIDDM in the particular population. Different ethnic groups in the same environmental setting experience widely variable risk. Impaired glucose tolerance is usually more prevalent than diabetes in women of childbearing age. Maternal age, overweight, parity, and family history of diabetes all predispose to gestational diabetes mellitus (GDM). Incidence of GDM is low in the absence of risk factors, suggesting that selective screening programs may be cost-effective. The worldwide epidemic of glucose intolerance predicted by the latest World Health Organization studies will undoubtedly increase the burden of GDM, especially in the developing countries.
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PMID:Epidemiology of glucose intolerance and gestational diabetes in women of childbearing age. 970 21

Hypertension in pregnancy and gestational diabetes have in common a lack of universally accepted classification and nomenclature that hinders comparison of data between research groups and contributes to the lack of consensus in the literature on these conditions. The inter-relationship of hypertension and gestational diabetes can be considered from three viewpoints according to whether hypertension is present before, during, or after the pregnancy. The first question is whether hypertension predating pregnancy predisposes to gestational diabetes. Epidemiological evidence and physiological argument based on the common etiologic factor of insulin resistance would suggest that gestational diabetes should be more common in the presence of preexisting hypertension. The limited clinical data available support this hypothesis. There are three issues concerning the coexistence of hypertension and gestational diabetes: whether gestational diabetes predisposes to pregnancy-induced hypertension, whether pregnancy-induced hypertension predisposes to gestational diabetes and what effect the combination has on morbidity and mortality. A number of studies have investigated whether pregnancy-induced hypertension is more common in women with gestational diabetes, but no consensus has been reached. There is little direct clinical evidence on the reverse issue, but data are presented to suggest that pregnancy-induced hypertension may only predispose to gestational diabetes when its etiology is gestational hypertension and not preeclampsia. The issue of how the coexistence of pregnancy-induced hypertension and gestational diabetes affects maternal or neonatal morbidity and mortality is largely unanswered. The last question is whether gestational diabetes has any prognostic significance with regard to the future development of hypertension in the mother. It is well known that gestational diabetes predisposes to subsequent NIDDM and that NIDDM is associated with a high incidence of essential hypertension. Once again insulin resistance may be a unifying factor. However, there is no direct clinical evidence that gestational diabetes predisposes to future hypertension.
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PMID:Hypertension in women with gestational diabetes. 970 24

Women with a history of gestational diabetes mellitus (GDM) are at increased risk of future diabetes, predominantly type 2 diabetes, as are their children. The extent of this risk depends both on the diagnostic criteria used to identify GDM and on maternal risk factors, some of which are potentially modifiable whereas others are not. The unmodifiable risk factors are ethnicity, pre-pregnancy weight, age, parity, family history of diabetes, and degree of hyperglycemia in pregnancy and immediately postpartum. The modifiable risk factors are persistent obesity, future weight gain, and subsequent pregnancies. Additional modifiable risk factors in these women are likely to be levels of physical activity, dietary fat, and avoidance of other lifestyle factors that adversely influence insulin resistance, such as smoking and certain drugs. Diabetic prevention strategies need to address the potentially modifiable risk factors using the unmodifiable risk factors to identify women most at risk.
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PMID:Risk and prevention of type 2 diabetes in women with gestational diabetes. 970 26

We sought to test the hypothesis that long-term postnatal development may be modified by metabolic experiences in utero. We enrolled offspring of women with pregestational diabetes (this included type 1 and type 2 diabetes) and gestational diabetes in a prospective study from 1977 to 1983. Fetal beta-cell function was assessed by measurement of amniotic fluid insulin (AFI) concentration at 32-38 weeks' gestation. Postnatally, offspring were seen yearly for neuropsychological testing, measurement of anthropometrics, and modified glucose tolerance testing. Neuropsychological control subjects were followed longitudinally. Additional control subjects had anthropometrics measured once, and a random subset of these had a single oral glucose challenge at 10-16 years. The rates of major neuropsychological disturbances in our cohort did not differ significantly from national estimates. However, aberrant maternal metabolism was associated with poorer intellectual performance and psychomotor development. The macrosomia observed at birth in offspring of diabetic mothers (ODM) resolves by 1 year of age. Obesity recurs in childhood; and by 14-17 years, the mean BMI is 24.6 +/- 5.8 kg/m2 in ODM versus 20.9 +/- 3.4 kg/m2 in control subjects. Obesity in adolescence is associated with sex, mother's weight, and AFI concentration. Impaired glucose tolerance (IGT) is found in 36% of ODM and is also associated with elevated amniotic fluid insulin in utero. In confirmation of our original hypothesis, aberrant maternal metabolism is associated with poorer intellectual and psychomotor development, obesity, and IGT in offspring. Excessive insulin secretion in utero, as assessed by AFI concentration, is a predictor of both obesity and IGT in adolescence. This study is a long-term prospective evaluation of the effects of maternal diabetes on pregnant women and their offspring. In this article, we report the results of the correlations between indexes of maternal and fetal metabolism during pregnancy and the offspring's subsequent physical, metabolic, and psychological development from birth through adolescence.
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PMID:Long-term effects of the intrauterine environment. The Northwestern University Diabetes in Pregnancy Center. 970 42


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