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

Nuclear families of non-insulin-dependent diabetic (NIDDM) patients are uncommon, as usually one or both parents have died. In order to aid identification of complete nuclear families, we have ascertained the disease process at a younger age by studying subjects with previous gestational diabetes. One hundred women who had had gestational diabetes, age (+/- SD) 38 (6) years, were screened by fasting plasma glucose (fpg). Sixty-one were found to have either fasting hyperglycaemia (5.5 < or = fpg < 7.8 mmol/l) or diabetes. Of these women 35 had both parents alive and the parents of 14 of these women agreed to the assessment of their metabolism by a continuous infusion of glucose with model assessment (CIGMA). Seven probands had impaired glucose tolerance (IGT) and seven were diabetic. They were age 35 (4) years and had body mass index (BMI) 26 (5) kg/m2. The parents were aged 62 (6) years and had BMI 29 (6) kg/m2 and their affection status was defined as presence of glucose intolerance (fpg or post-infusion achieved plasma glucose level > 2 SD of an age and obesity matched population). In the 14 families, five probands (36%) had neither parent affected, six (43%) had one parent affected and three (21%) had both parents affected. Only three probands had a parent with diabetes as defined by World Health Organisation criteria. We conclude that the study of women who have had gestational diabetes allows detection of probands with diabetes or impared glucose tolerance, who have both parents available for study.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Prevalence of diabetes mellitus and impaired glucose tolerance in parents of women with gestational diabetes. 767 91

Cushing syndrome in pregnancy is rare. This is explained by the syndrome's association with amenorrhoea, oligomenorrhoea, infertility and abortions. Cushing syndrome commonly presents with hypertension, weight gain, diabetes, striae or truncal obesity, all of which can be consistent with pregnancy in women without Cushing syndrome. We describe a case of Cushing syndrome in pregnancy secondary to an adrenal cortical tumour which was discovered after an abnormal glucose tolerance test. The woman developed classical features of Cushing syndrome including gestational diabetes and hypertension and was managed successfully to term after a unilateral adrenalectomy at 23 weeks. The case is reported not only because of its rarity but also because the diagnosis was made after a routine screening test for gestational diabetes. Early diagnosis and treatment of adrenal adenoma causing Cushing syndrome in pregnancy reduces maternal and fetal morbidity and mortality.
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PMID:Cushing syndrome in pregnancy secondary to an adrenal cortical adenoma. 767 97

The clinical characteristics of subjects with a missense glucokinase mutation, gly299-->arg, were studied in a large pedigree, BX, initially characterized by some members having Maturity Onset Diabetes of the Young (MODY). Glucose tolerance, beta cell function and insulin sensitivity were measured with Homeostasis Model Assessment (HOMA) and with a 'Continuous Infusion of Glucose with Model Assessment' (CIGMA) test. Diabetic complications were clinically assessed. Subjects with glucokinase gly299-->arg were the same age, height, and obesity as the subjects without the mutation. Diabetes was usually asymptomatic at diagnosis and was treated with diet alone in 15 of the 18 subjects. Five of the 11 adult females had been diagnosed when they developed gestational diabetes. The fasting plasma glucose concentrations at the time of study were 4.3-12.6 mmol l-1, with the higher levels being in the more obese (p < 0.05) and in the older subjects (p < 0.05). In subjects with the mutation, beta cell function was impaired, being geometric mean 63% (normal-100%) compared with 126% in the subjects without the mutation (p < 0.001) measured by HOMA and in a subset assessed by CIGMA 59% and 127% (p < 0.01), respectively. There was no difference in fasting insulin concentrations, insulin sensitivity, lipid concentrations or blood pressure between the groups. The haemoglobin A1c was raised (mean 6.5% compared with 5.5% in the subjects without the mutation), but microvascular and macrovascular complications were uncommon. The subjects with the mutation did not have microalbuminuria but had an impaired vibration perception threshold compared with subjects without the mutation.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Clinical characteristics of subjects with a missense mutation in glucokinase. 775 56

Amylin is a 37 amino-acid peptide mainly produced by the islet beta-cell. Aggregation of amylin is partly responsible for amyloid formation. Amyloid deposits occur both extracellularly and intracellularly and may contribute to beta-cell degeneration. Amylin is packed in beta-cell granules and cosecreted with insulin in response to the same stimuli but, unlike other beta-cell products, it is produced from specific a gene on chromosome 12. Basal, plasma amylin concentrations are around 5 pM, and increase fourfold after meals or glucose. Higher levels are found in cases of insulin resistance, obesity, gestational diabetes and in some patients with NIDDM. Low or absent levels are found in insulin-dependent diabetic patients. There are similarities between amylin and non beta-cell peptides such as calcitonin gene related peptides (CGRP). They may bind to the same receptor, determine similar post-receptor phenomena and qualitatively similar actions but with different degree of potency. The actions of amylin are multiple and mostly exerted in the regulation of fuel metabolism. In muscle, amylin opposes glycogen synthesis, activates glycogenolysis and glycolysis (increasing lactate production). Consequently, amylin increases lactate output by muscle and increases the plasma lactate concentration. In fasting conditions, this lactate may serve as a gluconeogenic substrate for the liver, contributing to replenish depleted glycogen stores and to increase glucose production. In non-fasting conditions, lactate can be transformed by liver in triglycerides. It is not clear at present whether amylin actions on the liver are direct or mediated by changes in circulating metabolites. A probably indirect effect of amylin in muscle is to decrease insulin- (or glucose)-induced glucose uptake, which may contribute to insulin resistance. Other actions include inhibition of glucose-stimulated insulin secretion and, in general, actions mimicking CGRP effects. Some of these actions are seen at supraphysiological concentrations. The physiopathological consequences of amylin deficiency, or excess are under active by investigated.
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PMID:Amylin/islet amyloid polypeptide: biochemistry, physiology, patho-physiology. 778 40

70 women with previous (1983-1993) history of gestational diabetes mellitus (GDM) were examined in order to assess their present carbohydrate metabolism. The through examination together with oral glucose tolerance test (OGTT) according to WHO were performed. Also the level of glycosylated hemoglobin HbA1c was measured. The following risk factors were analysed: obesity; arterial hypertension; family history of diabetes; number of past pregnancies; time that passed since the pregnancy with GDM; trimester in which GDM was diagnosed. In result 54% of all subjects were diagnosed as having diabetes mellitus, 19% had impaired glucose tolerance (IGT). The presence of diabetes or IGT significantly correlated with the number of past pregnancies, observation time and indirectly with family history of diabetes. Using both measurements of fasting blood glucose and glycosylated hemoglobin enables to diagnose nearly 80% of diabetes following GDM and as a diagnostic method is worth recommending for screening. Women who had GDM should be subjected to control examinations towards diabetes mellitus at least once a year.
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PMID:[Evaluation of carbohydrate metabolism in women with previous gestational diabetes mellitus]. 778 56

All fetuses benefit from ultrasonographic estimation of gestational age and evaluation of growth patterns. Monitoring the pregnancies of obese women is perceived as more difficult than monitoring those of nonobese women. The aim of this study was to determine if maternal obesity affects the growth and Doppler resistance indices (RI) of the fetus. Twenty-eight women with a preconception weight > 90.7 kg underwent obstetric ultrasonographic evaluations from the 20th week of gestation. Their ultrasonographic data were compared with those of controls. Ten of the obese women developed gestational diabetes and had lower umbilical artery RIs for a given gestational age (P < .0001) than did those obese women without other medical complications, those with medically controlled pregnancy-induced hypertension or those from the control population. The relation between fetal unit weight and umbilical artery RIs was established. The pattern of RI changes was similar in all groups when estimated fetal weight instead of gestational age was used as the covariant. Fetal growth and Doppler velocimetry can be monitored adequately in obese women. Gestational diabetes significantly influences the pattern of fetal growth and the impedance to flow in the umbilical artery.
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PMID:Ultrasonographic growth and Doppler hemodynamic evaluation of fetuses of obese women. 780 81

Gestational diabetes encompasses a variable spectrum of decompensated glucose tolerance, with a substantial risk for developing future NIDDM. Several easily identifiable risk factors for subsequent diabetes have been identified, notably elevated fasting glucose levels during pregnancy, early diagnosis of gestational diabetes, and obesity. By continuing to identify independent risk factors during pregnancy and in the puerperium, we can develop better intervention programs and medical therapy to prevent or delay the onset of diabetes. Glucose tolerance testing in the postpartum period followed up by annual glucose surveillance for diabetes should be performed in all women with prior GDM. They should be actively educated about their high risk of diabetes and strongly encouraged to continue their diabetes and strongly encouraged to continue their diabetic diet, achieve an ideal body weight, and implement an exercise program. Combining such a program of preventive care with contraceptive visits contributes to a complete health care program for women with prior GDM during their reproductive years.
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PMID:Maternal implications of gestational diabetes. 782 73

In order to assess the clinical consequences of gestational diabetes in the index pregnancy, a group of patients with positive oral glucose challenge test and their matched controls have been closely followed up. No differences in perinatal outcome have been pointed out, except for the higher rate (p < 0.01) among diabetic patients of preterm delivery and pregnancy-induced hypertension. The prevalence of the latter has shown no relationship to maternal obesity. In view of these data, the future risk of cardiovascular disease of this cohort of patients needs to be assessed with a follow-up study.
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PMID:Does gestational diabetes represent an obstetrical risk factor? 805 Jul 27

Diabetes occurs in more than 13 million persons in the United States, and approximately 60% of the new cases are diagnosed in women. This review examines health issues related to women with diabetes mellitus. The following issues are discussed in the review. The prevalence of diabetes is higher in Native-American, black, and Hispanic women than in white women. Women with upper-body obesity are at risk for developing non-insulin-dependent diabetes mellitus (NIDDM) and women with diabetes are at risk for developing heart disease. Diabetes, obesity, and heart disease are all modifiable by nutrition. White women with diabetes derive approximately 40% of energy from fat, which is 10% greater than the national goal. Women with a history of gestational diabetes are at risk for developing NIDDM. Women with insulin-dependent diabetes mellitus (IDDM) are at high risk of developing complications in pregnancy, and pregnancy outcomes improve with preconceptual counseling. Women with IDDM are at risk for developing eating disorders, although not to a greater extent than the nondiabetic population. Women with diabetes are at risk for developing endometrial cancer. Both IDDM and NIDDM prevention clinical trials are in progress, although none target women specifically. Dietetics practitioners are encouraged to use local and national diabetes resources.
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PMID:Diabetes mellitus--a priority health care issue for women. 807 95

The importance of the intrauterine and neonatal metabolic environment as possible teratogenic determinants of predispositions to diabetes, obesity and cardiovascular diseases is discussed. Epidemiological, clinical and experimental results suggest that gestational diabetes or even slightly impaired glucose tolerance during pregnancy are important risk factors for the development of an increased Type II- and even Type I diabetes susceptibility in the offspring. In addition, early prenatal undernutrition might also predispose to enhanced risk of Type II diabetes, whereas perinatal overnutrition seems to enhance predominantly Type I diabetes susceptibility. In this context, fetal and/or neonatal hyperinsulinism occurring during a critical period of brain development and leading to permanent malorganization of hypothalamic regulation centres for metabolism and hence to malprogramming of the hypothalamo-pancreatic system, is discussed as a possible reason for lifelong enhanced diabetes susceptibility. In view of epidemiological and experimental findings, an epigenetic maternofetal transmission of such acquired persistent modifications can run over several generations, mediated by gestational hyperglycaemia and fetal or neonatal hyperinsulinism. In conclusion, a partial prophylaxis of diabetes mellitus, obesity and cardiovascular diseases appears to be possible by prevention of gestational diabetes--even mild forms of impaired glucose tolerance during pregnancy--as well as early prenatal undernutrition and perinatal overnutrition.
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PMID:Perinatal hyperinsulinism as possible predisposing factor for diabetes mellitus, obesity and enhanced cardiovascular risk in later life. 807 2


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