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Query: UMLS:C0028754 (obesity)
 124,988 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The obstetric performance and pregnancy outcome in 208 massively obese patients who were delivered over an eight-year period were compared with those of nonobese control subjects. The incidence of obesity in their infants was also compared. No significant increase in the incidence of urinary tract infection, diabetes, breech presentation, cesarean section, forceps delivery, or maternal and infant morbidity was noted in the obese women. Significantly increased incidences of hypertensive disorders of pregnancy (p less than 0.01), gestational diabetes (p less than 0.01), inadequate weight gain (p less than 0.001), and wound or episiotomy infection (p less than 0.05) were observed in the study group. The mean birth weight of the infants of obese women was 209 grams greater than that of the control subjects. A significantly increased number of the obese patients were delivered of excessive-sized infants. Despite this, the incidence of obesity in infants of obese women was not significantly increased at birth or six months of age. By 12 months of age, however, these infants were significantly more obese than the control infants.
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PMID:Pregnancy in the massively obese: course, outcome, and obesity prognosis of the infant. 67 88

A questionnaire regarding the screening procedure for gestational diabetes was sent to all maternity hospitals in Denmark in 1990. Only 15 out of 51 departments used the screening procedure as proposed by Guttorm & Pedersen. Glucosuria was a clinical risk factor in 49 of 51 departments. There was no agreement about the histories and clinical risk factors. The factors used were family history of diabetes, obesity, a previous infant weighing 9 lbs or more, a previous infant born with low gestational age, habitual abortion, previous perinatal deaths, previous preterm delivery, hydramnios, excessive fetal growth or glucosuria in the present pregnancy. No department used universal screening.
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PMID:[Screening for gestational diabetes in Denmark]. 141 25

Regular exercise may diminish the risk for atherosclerotic vascular disease in patients with non-insulin-dependent (type II) diabetes and in the general population. The basis for this effect of exercise may be its ability to diminish or prevent hyperinsulinemia, insulin resistance, and/or increases in intra-abdominal adipose mass. These abnormalities are associated with premature atherosclerotic vascular disease, essential hypertension, type II diabetes, and certain dyslipoproteinemias, and most likely precede them. They also have been implicated in the pathogenesis of these disorders. We propose that the high prevalence of hyperinsulinemia and insulin resistance in individuals leading a western life-style accounts for the reported benefit of physical activity in preventing coronary heart disease in the general population. We also propose that exercise (and diet) are most likely to be effective when initiated in young individuals, before the onset of irreversible vascular alterations, and when life-style changes may be more acceptable. Early identification of such individuals may be possible on the basis of family history, the presence of components of the hyperinsulinemia-insulin resistance syndrome, and/or central obesity. One such group that may already have been identified is women with gestational diabetes.
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PMID:Diabetes, exercise, and atherosclerosis. 146 16

The influence of ethnic origin, body mass index, and parity on the frequency of gestational diabetes was assessed in 11,205 consecutive women attending a multiracial antenatal clinic in London, where all women were screened for gestational diabetes. Logistic regression was used to model the relationship between gestational diabetes and ethnic origin, age, body mass index (BMI), and parity. Results were presented as adjusted odds ratios, where the reference categories are White women, age < 25 years, BMI < 27, and parity < 3. Ethnic origin was the dominant influence on the prevalence of gestational diabetes. Women from ethnic groups other than White had a higher frequency of gestational diabetes than White women (2.9% vs 0.4%, p < 0.001). Compared to White women the relative risk of gestational diabetes in the other ethnic groups was: Black 3.1 (95% confidence limits 1.8-5.5), South East Asian 7.6 (4.1-14.1), Indian 11.3 (6.8-18.8), and miscellaneous 5.9 (3.5-9.9). Increasing age was an independent risk factor. The relative risk was higher in women > or = 35 years in all ethnic groups other than in South East Asian women. Obesity (BMI > or = 27) was a further independent risk factor in all ethnic groups except in the Indian and South East Asian women. Parity > or = 3 increased the relative risk of gestational diabetes in the White, Black, and South East Asian women only.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:High prevalence of gestational diabetes in women from ethnic minority groups. 147 22

The authors revealed during dispensarization of pregnant women suffering from essential hypertension that the disease is relatively frequently associated with some metabolic disorders, i. e. obesity, gestational diabetes or impaired glucose tolerance. They draw attention to a similarity with Reaven's syndrome in non-pregnant women. The authors recommend to screen for diabetes all obese pregnant women and those with hypertension to detect an impaired glucose metabolism and prevent foetopathies in neonates of thus affected mothers. The authors consider obesity one of the subsidiary criteria in the differential diagnosis of essential hypertension and preeclampsia.
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PMID:[Gestational diabetes mellitus and disorders of glucose tolerance in pregnant women with essential hypertension]. 149 70

In obesity, impaired glucose tolerance (IGT), non-insulin-dependent diabetes mellitus (NIDDM), and gestational diabetes mellitus (GDM), defects in glucose transport system activity, contribute to insulin resistance in target tissues. In adipocytes from obese and NIDDM patients, we found that pretranslational suppression of the insulin-responsive GLUT4 glucose transporter isoform is a major cause of cellular insulin resistance; however, whether this process is operative in skeletal muscle is not clear. To address this issue, we performed percutaneous biopsies of the vastus lateralis in lean and obese control subjects and in obese patients with IGT and NIDDM and open biopsies of the rectus abdominis at cesarian section in lean and obese gravidas and gravidas with GDM. GLUT4 was measured in total postnuclear membrane fractions from both muscles by immunoblot analyses. The maximally insulin-stimulated rate of in vivo glucose disposal, assessed with euglycemic glucose clamps, decreased 26% in obesity and 74% in NIDDM, reflecting diminished glucose uptake by muscle. However, in vastus lateralis, relative amounts of GLUT4 per milligram membrane protein were similar (NS) among lean (1.0 +/- 0.2) and obese (1.5 +/- 0.3) subjects and patients with IGT (1.4 +/- 0.2) and NIDDM (1.2 +/- 0.2). GLUT4 content was also unchanged when levels were normalized per wet weight, per total protein, and per DNA as an index of cell number. Levels of GLUT4 mRNA were similarly not affected by obesity, IGT, or NIDDM whether normalized per RNA or for the amount of an unrelated constitutive mRNA species. Because muscle fibers (types I and II) exhibit different capacities for insulin-mediated glucose uptake, we tested whether a change in fiber composition could cause insulin resistance without altering overall levels of GLUT4. However, we found that quantities of fiber-specific isoenzymes (phopholamban and types I and II Ca(2+)-ATPase) were similar in all subject groups. In rectus abdominis, GLUT4 content was similar in the lean, obese, and GDM gravidas whether normalized per milligram membrane protein (relative levels were 1.0 +/- 0.2, 1.3 +/- 0.1, and 1.0 +/- 0.2, respectively) or per wet weight, total protein, and DNA. We conclude that in human disease states characterized by insulin resistance, i.e., obesity, IGT, NIDDM, and GDM, GLUT4 gene expression is normal in vastus lateralis or rectus abdominis. To the extent that these muscles are representative of total muscle mass, insulin resistance in skeletal muscle may involve impaired GLUT4 function or translocation and not transporter depletion as observed in adipose tissue.
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PMID:Gene expression of GLUT4 in skeletal muscle from insulin-resistant patients with obesity, IGT, GDM, and NIDDM. 153 55

Variations in nutritional intake during pregnancy have measurable effects on the circulating levels of maternal nutrients, maternal weight gain, and birth weight of the offspring. A growing body of evidence indicates that alterations in maternal metabolism can also have long-term consequences in the offspring in relation to adult adiposity, glucose tolerance, and perhaps intellectual development. Therefore, recommendations for diet during pregnancy must be made with great care, and with as much scientific understanding as possible. Nutritional advice traditionally given to all pregnant women, including those with gestational diabetes mellitus (GDM) or noninsulin-dependent diabetes, does not allow for individual differences in caloric needs as a function of the degree of maternal obesity and thus, may encourage excessive weight gain. Evidence reviewed below suggests that adjusting caloric intake to meet new guidelines for weight gain during pregnancy may be advantageous in reducing maternal blood sugar and insulin levels, without producing abnormalities in other metabolic variables. Modest caloric reduction which limits excessive weight gain in the mother may also be associated with a small reduction of fetal weight. However, more stringent dietary manipulations in obese gravida should be discouraged as a routine measure until more knowledge is available from large-scale clinical trials about their effects on the entire panoply of maternal nutrients and their impact on the offspring.
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PMID:Caloric restriction in gestational diabetes mellitus: when and how much? 161 76

Gestational diabetes mellitus (GDM) is a strong predictor of glucose intolerance later in life. Former GDM (n = 145) and control (n = 41) subjects were studied 3-4 yr after the index pregnancy. They were subjected to a 75-g oral glucose tolerance test (OGTT) with measurements of insulin, C-peptide, and proinsulin in the basal state and every 30 min for 180 min. In the former GDM group, 5 subjects (3.4%) had developed non-insulin-dependent diabetes mellitus (NIDDM), and 32 (22%) had developed impaired glucose tolerance (IGT; by World Health Organization criteria). In the control group, 2 (4%) had IGT. In the GDM group, IGT or NIDDM was significantly associated with obesity (body mass index [BMI] greater than or equal to 25 kg/m2) and earlier diagnosis of GDM during pregnancy (P less than 0.001). Nonobese (BMI less than 25 kg/m2) GDM subjects with normal glucose tolerance at follow-up had significantly higher mean glucose (P less than 0.01), insulin (P less than 0.05), and proinsulin (P less than 0.001) values during the OGTT than control subjects, whereas there was no significant difference in C-peptide values. A comparison between control subjects with normal OGTT and BMI less than 25 kg/m2 (n = 39) and GDM subjects (n = 39) selected to have a comparable area under the glucose curve, BMI, and age demonstrated no group differences in glucose, C-peptide, or insulin levels, whereas the proinsulin levels were significantly higher (P less than 0.001) during the glucose load. The molar ratio between proinsulin and insulin was also significantly higher among the former GDM subjects.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Follow-up of women with previous GDM. Insulin, C-peptide, and proinsulin responses to oral glucose load. 174 43

Several maternal plasma fuel abnormalities have been described in gestational diabetes mellitus (GDM), and all may contribute to the development of fetal macrosomia, generally because of the surfeit of calories they provide. Elevated maternal plasma glucose and amino acid concentrations represent key disturbances, because they are also well-known fetal pancreatic beta-cell secretagogues. Fetal hyperinsulinemia contributes to macrosomia in a special way by selectively accelerating fuel utilization and storage in insulin-sensitive fetal tissues. Maternal obesity intensifies the insulin resistance already present in late pregnancy and probably exaggerates the metabolic abnormalities attending GDM that impact on fetal growth and development. However, the means by which maternal obesity per se promotes the development of heavy babies in nondiabetic pregnancies remains poorly defined. Significant correlations exist between newborn birth weight and the levels of maternal plasma glucose, amino acids, free fatty acids, and triglycerides in diabetic pregnancies. However, the relative influence of each disturbance on fetal birth weight remains controversial and requires more detailed investigation.
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PMID:Impact of maternal fuels and nutritional state on fetal growth. 174 67

Sonographic measurement of fetal humeral soft tissue thickness (STT) was performed in 93 women with gestational diabetes mellitus during the third trimester. STT measurements revealed accelerated growth in large for gestational age infants at 31 wk gestation. This new measurement proved to be the most accurate predictor of excessive fetal size compared with other standard ultrasound parameters (sensitivity 82%, specificity 95%, positive predictive value 90%). Asymmetrical growth was more evident in infants with large STT measurements in utero. Humeral STT measurement may distinguish large fetuses with truncal obesity from those that are symmetrically large, thereby allowing prediction of risk for birth trauma before delivery.
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PMID:Sonographic measurement of fetal humeral soft tissue thickness in pregnancy complicated by GDM. 174 68


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