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Query: UMLS:C0011849 (diabetes)
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The California Diabetes and Pregnancy Program (CDAPP) began in 1984 as a multicenter, collaborative project with support provided by the state Department of Health Services, Maternal and Child Health Branch. Between its inception and 1988, it expanded from three to eight perinatal regions, making the CDAPP model of care available to patients in 19 clinical affiliate sites. The care was provided by a multidisciplinary team composed of physicians, a diabetes educator, a registered dietician, a social worker, and appropriate consultants. The elements of this model of care included comprehensive patient education, active patient participation in care, maternal and perinatal medical assessment, and collection of standardized patient information adequate to allow a programmatic and medical evaluation of the CDAPP. Despite impressive growth of the program by December 1988, statewide implementation of CDAPP is incomplete.
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PMID:The California Diabetes and Pregnancy Program: implementation of a multicenter experience with diabetic pregnancies. 152 38

Diabetes in pregnancy has an influence on the development of the fetus. There are strong indications that the intrauterine diabetic milieu has long-lasting consequences. In the rat, mild diabetes during pregnancy induces decreased insulin secretion in later life, whereas severe diabetes is responsible for insulin resistance. In the human, data are available showing a long-term consequence in the offspring of type I diabetes and gestational diabetes mellitus.
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PMID:The effects of maternal diabetes on the offspring. 183 33

The records of 303 females with gestational diabetes (GD) seen from 1977 to 1988 in the Hospital La Paz in Madrid were reviewed. In some respects, two periods were separately considered, period A from 1977 to 1983 and period B from 1983 to 1988, the latter corresponding to the activity of the Diabetes and Pregnancy Unit. Significant differences in fetal mortality (0.65%) with nondiabetic pregnant women or between periods A and B were not found. Macrosomic fetuses (the most common abnormality, 18.5%) were related with maternal age, a macrosomic fetus in previous pregnancies, degree of carbohydrate intolerance at the time of diagnosis of the diabetes and need for insulin therapy. This latter feature indicates a more severe degree of metabolic involvement. Regarding risk factors, the most common were older maternal age, family history of diabetes and obesity. The pancreatic reserve in nonobese women with GD (2.1 +/- 0.8 ng/ml) was lower than in obese women with GD (3.3 +/- 0.9 ng/l) (p less than 0.001), higher than in progestational diabetic women type II (1.1 +/- 0.7 ng/ml) and type I (0.15 +/- 0.1 ng/ml) (p less than 0.001), and it was not different from that in normal pregnant women (2.15 +/- 0.6 ng/ml). Insulin therapy for the control of diabetes was required in 24.5% of pregnant women. During the period B, termination of pregnancy by means of cesarean section (25.3%) was higher than in normal pregnant women (11.2%) (p less than 0.001). After pregnancy, 13.2% of patients in period A and 39.1% in period B (p less than 0.01) complied with the evaluation of carbohydrate metabolism. Overall, 26.2% had carbohydrate intolerance and 5.9% diabetes mellitus. Although the creation of the Diabetes and Pregnancy Unit has provided a better care and follow-up of the diabetic pregnant women, has not resulted in significant differences in fetal mortality.
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PMID:[Diabetes and pregnancy. Our experience in pregnancy diabetes (1977-1988)]. 208 8

The mean additional energy requirement for pregnancy has been calculated at 285 kcal daily and it reflects the energy needs for production of the fetoplacental unit and for the maternal physiological adaptations to pregnancy. In practice there is considerable variation in energy requirement due to alterations in maternal energy expenditure. Optimal energy intakes are dictated also by the pre-pregnancy maternal weight. The outcome of pregnancy is improved in the underweight mother by an intake which produces a weight gain in pregnancy of approximately 14 kg, whereas a rise of only 7 kg may be optimal for the obese mother. Obesity with or without diabetes is associated with macrosomia and other problems and it is sensible to attempt to limit weight gain in pregnancy at a time when maternal motivation is high. Diabetes in pregnancy may arise in patients with pre-existing NIDDM or IDDM, but more commonly it is diagnosed for the first time during pregnancy and it usually disappears after delivery (gestational diabetes). Recent evidence suggests that gestational diabetes has a strong genetic component and is usually NIDDM precipitated early in life by the pregnancy. Both gestational diabetes and NIDDM are characterized by insulin deficiency and by insulin resistance. Long-term follow-up studies have demonstrated that NIDDM or impaired glucose tolerance develop in later life in 50-70% of women with previous gestational diabetes. The adverse effects of pregnancy on the mother with pre-existing diabetes may be minimized by good diabetic control as may be adverse effects on the fetus and neonate of diabetes in the mother. An increased incidence of fetal malformations persists in pregnancies with pre-existing maternal diabetes. Diabetes of any form may be associated with neonatal hypoglycaemia. The aim of therapy is to produce maternal normoglycaemia throughout pregnancy by dietary measures and insulin treatment if required. Women with pre-existing diabetes should tighten their blood glucose control from before conception. Optimization of insulin therapy and diet are required for IDDM and most NIDDM women will require insulin treatment in pregnancy. Gestational diabetics require diet and possibly insulin. Most pregnancies now proceed to term.
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PMID:Diabetes and diet in pregnancy. 224 97

The study concerns the clinical outcome and later prognosis (regarding permanent insulin treatment) of patients who develop insulin-dependent diabetes mellitus during pregnancy (which is different from gestational diabetes). Sixty-three such patients (27 +/- 1 (SEM) years old) were delivered at the Copenhagen Centre for Diabetes and Pregnancy during the years 1966-1980. Obstetric complications such as toxaemia were seen in 9.5% of these study patients and the perinatal mortality was 6.3%, both percentages being higher than in the general population (1.1%, p less than 10(-7) and 1.0%, p less than 10(-3), respectively), but similar to those observed in patients with Type 1 diabetes diagnosed before pregnancy. In contrast, the frequency of malformations was 1.6%, the same as in the general population (1.4%), but lower than that seen in patients with long-standing diabetes (8.3%, p less than 0.05). At follow-up examination 8 +/- 1 years after diagnosis all patients were diabetic; 77% were insulin treated, having no or virtually no residual B-cell function, and were clearly Type 1 diabetic patients. After delivery 80% of the patients had a remission period (median 256 days) without insulin treatment. This remission period was absent or shortest in patients with the following characteristics (p less than or equal to 0.03): low age, first parity, not overweight, and high blood glucose level at diagnosis. These prognostic parameters should be considered in obligatory, clinical follow-up plans for such patients.
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PMID:Type 1 (insulin-dependent) diabetes mellitus diagnosed during pregnancy: a clinical and prognostic study. 240 79

A longitudinal study was carried out of all patients with newly acquired insulin dependent diabetes during pregnancy (as distinct from non-insulin-dependent gestational diabetes) seen at the Copenhagen Centre for Diabetes and Pregnancy during 1966 to 1980. The series comprised 63 patients with a mean age of 27 (SEM 1) years. At diagnosis the mean fasting blood glucose concentration was 15.6 (1.3) mmol/l and mean maximal insulin dose 49 (3) IU/day. At a prospective follow up examination a mean of 8 (SEM 1) years after diagnosis 46 of 60 patients (77%) were being treated with insulin (35 (2) IU/day) and had a very low mean stimulated plasma C peptide value (0.12 (0.02) nmol/l) suggesting absent or nearly absent beta cell function. The remaining 14 patients (23%), not currently receiving insulin, appeared to be severely glucose intolerant, having a mean fasting blood glucose concentration of 13.4 (1.2) mmol/l. Thus most of these patients developing insulin dependent diabetes during pregnancy had true type I disease. Compared with the age specific incidence of type I diabetes in the background population of women the incidence was at least 70% higher in pregnant than non-pregnant women (p less than 0.001; chi 2 = 11.6; f = 1). This increased incidence occurred in the third trimester when the risk of developing type I diabetes was 3.8 times that of non-pregnant women (p less than 0.000001; chi 2 = 35.6; f = 1). Finally, the risk of developing insulin dependent diabetes during pregnancy was lower when conception occurred in the winter (p less than 0.05; chi 2 = 4.18; f = 1).
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PMID:Increased incidence of true type I diabetes acquired during pregnancy. 310 40

Diabetes in pregnancy was studied in a new animal model, the spontaneously diabetic BB Wistar rat. The BB rat appears to be superior to the drug-induced models for the investigation of the effects of maternal diabetes on fertility, fetal development, and placental function because the disease entity develops spontaneously, is accompanied by destructive insulitis similar to pancreatic lesions in the human condition, and is controlled to various degrees by daily insulin therapy.
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PMID:Diabetes in pregnancy: a preliminary study of the pancreas, placenta and malformations in the BB Wistar rat. 696 57

Diabetes mellitus in pregnancy is associated with neonatal respiratory distress syndrome due to impaired synthesis of fetal lung surfactant. Pharmacologic agents that promote fetal lung maturity are diabetogenic and have limited use in the management of diabetic pregnancy for prevention of respiratory distress syndrome. Maternal administration of a thyroid analog 3,5-dimethyl-3'-isopropyl-L-thyronine (DIMIT) results in significant enhancement of fetal lung phospholipid synthesis and accelerated lung maturity. We therefore studied the effects of DIMIT (0.5 mg/kg per d, s.c.) administration to pregnant alloxan-diabetic rabbits on days 25 and 26 of gestation. DIMIT treatment of diabetic maternal rabbits (DD) was associated with reduction of maternal blood glucose (115 +/- 13 vs. 275 +/- 72 mg/dl, P less than 0.05) and fetal glucose (64 +/- 6 vs. 274 +/- 47 mg/dl, P less than 0.001) compared with saline-injected diabetic (D) mothers. Reduction of fetal insulin levels was also associated with maternal DIMIT therapy in diabetic rabbits (56 +/- 5 (D) vs. 24 +/- 4 microunits/ml, P less than 0.001). Maternal diabetes resulted in significant reduction of fetal lung weight (370 +/- 20 vs. 520 +/- 30 mg, P less than 0.005) and lung protein content (6.5 +/- 0.7 vs. 8.7 +/- 0.7 mg/gm, P less than 0.005), which were restored to normal in offspring of DIMIT-treated diabetic rabbits. Maternal DIMIT administration caused significant reduction in fetal lung glycogen content in control (62 +/- 5.8 vs. 25 +/- 5.9 micrograms/mg protein, P less than 0.001) and diabetic (56 +/- 7 vs. 34 +/- 5 micrograms/mg protein, P less than 0.02) offspring. Whereas maternal diabetes was associated with reduction of all major phospholipid species in fetal lung-comprising surfactant, these were restored with DIMIT therapy. The results demonstrate that short-term maternal administration of DIMIT in pregnant diabetic rabbits not only promotes fetal lung phospholipid synthesis, but also appears to ameliorate maternal hyperglycemia. Thus, DIMIT is of potential benefit in the management of diabetic pregnancy.
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PMID:3,5-Dimethyl-3'-isopropyl-l-thyronine therapy in diabetic pregnancy: stimulation of rabbit fetal lung phospholipids. 703 90

A discussion of the side effects of hormonal oral contraceptive (OC) use is presented. Studies show that the estrogen component of OCs works to suppress the release of GRH (gonadotropin-releasing hormone), reducing the serum FSH level. The gestagen component desensitizes the frontal lobe of the pituitary gland to the effect of GRH and suppresses the preovulatory LH peak. OCs can cause subjective side effects such as nausea, headache, depression, which can also be observed during placebo use. Breakthrough bleeding, spotting, silent menstruation, and post-pill amenorrhea are menstrual irregularities which can be linked to OC use; 98% of those who discontinue OC use show normal biphasic menstrual cycles 3 cycles after discontinuation. A constant increase in serum triglyceride levels, small increases in cholesterol and phospholipid levels are observed among OC users. Minor cases of hyperinsulinism are observed among OC users with no history of diabetes; glucose tolerance tests should be regularly administered to OC users who have a risk of diabetes or a history of pregnancy diabetes. Serum levels of proteins are affected by OC use, probably due to the effects of OC use on liver function. Studies have shown an increased risk of thromboembolism and circulatory disorders among OC users, especially those who are over 30 years of age or who smoke. OC use has been linked to development of benign tumors of the liver and the cervix. Gestagens appear to reduce the frequency of endometrial mitosis. Other medications, e.g. analgesics, barbituates, can reduce the effectiveness of OCs. For adolescents, sequence preparations are preferred and should be administered only after a 1 year period of regular menstruation. Thorough check-ups should be performed on OC users twice yearly, and contraindications should be scrupulously observed.
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PMID:[Effects and side effects of hormonal contraceptives]. 741 48

To investigate if alterations of the amino acid metabolism may play a more important role in the etiology of diabetic microangiopathy than hitherto recognized, free amino acids in plasma were measured by means of high-performance liquid chromatography (HPLC) in healthy individuals (REF) and patients with insulin-dependent diabetes mellitus (IDDM) and non-insulin-dependent diabetes mellitus (NIDDM). Isoleucine and leucine in IDDM were within normal limits, whereas they were significantly higher in NIDDM (P < 0.01 and P < 0.001, respectively). This was not due to age differences. In order to evaluate the impact of insulin on amino acid metabolism, amino acids were also measured in pregnant women (PREG) undergoing glucose tolerance tests as a screening for pregnancy diabetes and in patients with polycystic ovary syndrome (PCO) undergoing euglycemic insulin clamp tests. Insulin considerably reduced the amino acid concentration. Isoleucine and leucine were particularly depressed. On the whole there was strong covariance between the three branched-chain amino acids, isoleucine, leucine, and valine (P < 0.0001). There was no covariance between amino acid and glucose or HbA1c concentrations. A protein meal strongly stimulated insulin production (+55 mIU/liter), whereas a galactose meal revealed only a minor increase in insulin response (+12 mIU/liter) in contrast to a tolerance test with the same amount of glucose (+67 mIU/liter). It is concluded that disturbed amino acid metabolism may be a more important causative factor in the etiology of diabetic microangiopathy than hitherto recognized and, in addition, that this may affect the therapeutic approach in both IDDM and NIDDM patients.
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PMID:Effects of insulin on free amino acids in plasma and the role of the amino acid metabolism in the etiology of diabetic microangiopathy. 834 81


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