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Query: UMLS:C0011860 (type 2 diabetes)
 57,723 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The nomenclature of human diabetes mellitus (DM) has been revised, and this classification has been accepted throughout the medical world and literature. The major categories of diabetes are: insulin-dependent DM, type I or IDDM; noninsulin-dependent DM, type II or NIDDM; secondary DM or type S; impaired glucose tolerance, IGT; gestational diabetes; and previous abnormality of glucose tolerance, PrevAGT. A review of the literature has shown that over half of the documented diabetic dogs, with a single medical diagnosis, appear to be type I, IDDM, with a substantial proportion being type S, and the remainder being type II, NIDDM. Obesity is frequently associated with IGT and NIDDM. Diabetic cats most commonly have pancreatic islet destruction associated with pancreatic amyloidosis; they are insulin deficient, IDDM. The commonest causes of secondary diabetes in dogs are pancreatic damage, hyperadrenocorticism and hypersomatotropism secondary to persistent progesterone influence. Progestogen therapy is the most frequently reported cause of secondary diabetes in cats. Diabetes in horses is type S, usually secondary to a functional pituitary tumor but occasionally following chronic pancreatitis. The blood glucose ranges for normal, IGT and diabetic animals, and the normal serum insulin values of various species is tabulated.
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PMID:Definition of diabetes mellitus. 351 69

The frequency of abnormal glucose tolerance in the first 12 months after gestational diabetes was found to be 33.3%, which is much higher than previously accepted. Women with gestational diabetes (Group 1 = 54 requiring insulin, Group 2 = 32 treated with diet alone) attending a metropolitan teaching hospital over a 3 1/2 year period were followed-up after delivery to determine their subsequent glucose tolerance. Of 86 seen 3 months after delivery, 2 had developed insulin-dependent diabetes mellitus (IDDM) and 2 noninsulin dependent diabetes mellitus (NIDDM), diagnosed by glucose tolerance testing. Another 38 returned for follow-up glucose tolerance testing at 12 months; of these 3 had impaired glucose tolerance (IGT), 7 had NIDDM, and one who had had NIDDM at 3 months now showed IGT after 9 months dietary treatment. Thus, 12 months after delivery, the cumulative prevalence of abnormal glucose tolerance was 14/42 (33.3%), 10 of the 42 being frankly diabetic (26%). Of the remaining 44 patients, 21 have not yet reached 12 months or were pregnant again, and 23 did not attend for glucose tolerance testing. Although the trend was for gestational diabetes mellitus (GDM) to recur earlier and more severely in subsequent pregnancies, in 3 instances the diabetes did not recur. Major congenital malformations occurred in 4 of the 86 babies (4.7%); minor malformations were found in a further 13 (15%) with no difference in frequency between Group 1 and Group 2.
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PMID:Gestational diabetes--infant malformations and subsequent maternal glucose tolerance. 352 46

One hundred ninety-nine gravida with gestational diabetes mellitus (GDM) defined as "carbohydrate intolerance of varying severity with onset or first recognition during pregnancy" have been stratified into subgroups on the basis of fasting plasma glucose and evaluated for further phenotypic and genotypic heterogeneity. A significantly greater proportion of the women in all our groups were older and heavier than in a "control" population of 148 consecutive gravida with documented normal oral glucose tolerance. After correction for age and weight by covariate analysis, absolute insulinopenia in response to oral glucose could be demonstrated in all GDM groups, although exceptions were present in each. The incidence of diabetes in the mothers of our patients with GDM was 8-fold greater than in controls; the incidence in fathers did not deviate from control patterns. HLA-DR3 and DR4 antigens were more frequently present in GDM and the increase was statistically significant in blacks. At the time of diagnosis, cytoplasmic islet cell antibodies (ICA) were significantly more common in GDM associated with elevated fasting plasma glucose than in controls; the frequency of ICA was 18.4% (7/38) in women with fasting plasma glucose greater than or equal to 130 mg/dl. Our findings indicate that GDM entails genotypic as well as phenotypic diversity and may include patients with slowly-evolving Type I diabetes mellitus, as well as patients with Type II diabetes mellitus, and women with asymptomatic diabetes which antedated the pregnancy (i.e. pregestational diabetes mellitus). Appreciation of this heterogeneity should be incorporated into any evaluation of intervention strategies for women with GDM or into prognoses concerning their postpartum metabolic status.
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PMID:Gestational diabetes mellitus: a syndrome with phenotypic and genotypic heterogeneity. 352 23

In order to better understand the role of A- and B-cell function in diabetic pregnancy, we studied four groups of pregnant women at week 34-36 of gestation. Seventeen were healthy controls (C), 24 had gestational diabetes (GD), 16 had type 2 diabetes (NIDD) and 37 had type 1 diabetes (IDD). At times -20, 0, 20, 30, 45, 60, 90 and 120 min from the beginning of a 30 min infusion of 30 g of arginine intravenously, plasma glucose, glucagon (IRG) and C-peptide (CPR) were measured. Plasma glucose was higher in diabetic than in control subjects. IRG values were also higher in the GD and the NIDD women. CPR values were similar to, or slightly higher than control values in the GD and the NIDD and were much lower in the IDD women. All three variables increased during the arginine infusion in all groups, with the exception that CPR remained unchanged in the IDD. The CPR/IRG molar ratio was similar in control, GD and NIDD women; in the IDD, it was much smaller than in the other groups and was not affected by arginine. In all the diabetic patients, IRG was negatively correlated with the maternal weight gain and in the IDD IRG was positively correlated with the increase in the insulin need and with the CPR levels. In conclusion diabetes appeared to enhance the A-cell function also in pregnancy, possibly impairing the 'facilitated anabolism' and stressing the 'accelerated starvation' which are typical of normal pregnancy. Glucagon was confirmed as one possible determinant of the insulin resistance seen in diabetic pregnancy.
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PMID:Endocrine pancreatic function in insulin-dependent diabetic pregnant women. 353 67

NIDDM is characterized by decreased insulin secretory responses to glucose and to nonglucose stimuli, hyperglucagonemia, and decreased tissue sensitivity to insulin. However, it has been unclear which of these abnormalities, if any, precedes the others. Since women with histories of gestational diabetes mellitus (GDM) are at high risk for eventual development of NIDDM, we measured B- and A-cell function and tissue sensitivity to insulin in eight normoglycemic, postpartum women with recent histories of GDM and in eight control subjects pair-matched for age and percent of ideal body weight. Fasting plasma glucose levels in subjects with former GDM tended to be slightly higher than in matched controls (98 +/- 3 versus 92 +/- 2 mg/dl, P = 0.07). Basal plasma insulin in subjects with former GDM was significantly higher than in controls (22 +/- 4 versus 14 +/- 2 microU/ml, P = 0.05). During an intravenous glucose tolerance test (IVGTT), relative first- and second-phase insulin responses to glucose were decreased in subjects with former GDM (2316 +/- 560 versus 7798 +/- 1036% of basal X min, P = 0.004; and 8340 +/- 946 versus 14,509 +/- 2556, P = 0.04). An index of sensitivity to insulin, SI, calculated from the IVGTT, was also lower in former GDM (1.23 +/- 0.69 X 10(-4) versus 3.58 +/- 0.78 X 10(-4) min-1/microU/ml, P = 0.001). Acute insulin responses to 5 g i.v. arginine were measured at plasma glucose levels of approximately 95, 215, and 600 mg/dl. The response at 600 mg/dl is termed the AIRmax and is used as an index of glucose-regulated insulin secretory capacity.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Insulin resistance and impaired insulin secretion in subjects with histories of gestational diabetes mellitus. 389 96

Because the supplementation of pyridoxine (vitamin B6) improves the glucose tolerance in gestational diabetes and adult onset diabetes, pyridoxine deficiency has been considered to be one of the factors that cause diabetes mellitus. We produced pyridoxine deficient rats by giving pyridoxine-free food with deoxypyridoxine which competitively the activity of pyridoxal phosphate. In these pyridoxine deficient rats plasma insulin during the glucose tolerance test was significantly low as compared with controls. In vitro experiments of pancreas perfusion showed that secretion of insulin and glucagon was impaired in the pyridoxine deficiency. Since the restriction of diet-calorie caused a decrease in arginine-induced secretion of insulin and glucagon from the isolated pancreas, the impairment of the endocrine pancreas may depend on malnutrition. Pyridoxine deficiency is surely one of the factors that impair the endocrine pancreas by multifactorial derangement of metabolism besides the tryptophan-nicotinic acid pathway.
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PMID:The endocrine pancreas in pyridoxine deficient rats. 703 87

Once thought to be solely a disease of insulin deficiency, diabetes mellitus now is recognized as a disorder with multiple pathogenetic mechanisms. Newer terminology identifies those uncommon patients with true insulin deficiency as having insulin-dependent diabetes (IDDM), while the majority of patients with diabetes have some residual insulin secretion but may have a disorder of insulin receptor number or affinity. These patients have non-insulin dependent diabetes (NIDDM). Other patients may have gestational diabetes, impaired glucose tolerance, a potential for glucose intolerance, or a previous history of diabetes. A few patients will have diabetes secondary to a known cause, such as pancreatitis or Cushing's syndrome. Understanding this nosological approach to diabetes should enhance the clinician's decisions regarding therapy.
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PMID:Classification and pathogenesis of the diabetes syndrome: a historical perspective. 705 Feb 15

Pregnancy with maternal diabetes is exceptionally contra indicated. Maternal IDDM and NIDDM required strict glycemic control and must be supervised during all the pregnancy. It is important to early evaluate the risk of gestational diabetes and necessary to have diabetologic, obstetrical and neonatologic managements. In these conditions, pregnancy in diabetes has a good prognostic. These women (IDDM, NIDDM, GDM) must be enrolled in a follow-up program.
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PMID:[Diabetes and pregnancy]. 749 64

In a prospective study, neonatal morbidity of newborn children of diabetic mothers and its association with the maternal metabolism was determined. Particular attention was directed on the somatic outcome of the children and their frequent metabolic imbalances. In addition, we determined the influence of maternal biological and somatometrical variables on the somatic outcome of newborns. Dependent upon the mothers' and children' variables, risk groups of newborns (fetopathy groups) were defined to optimize clinical care and surveillance of newborns. A total of 810 children were included born to mothers with primary insulin dependent diabetes mellitus (IDDM), non insulin dependent diabetes (NIDDM), or gestational diabetes (GDM). Among the study population, 41.7% of children had macrosomia, 27.2% had a weight-length index > 1.2, 17.9% developed hypoglycemia and 19.5% hyperbilirubinemia within the initial 72 hours after birth. The somatic outcome of the children was significantly associated with pregnancy duration, maternal age, weight, height, and HbA1. Increasing maternal HbA1 prior to delivery (categorized in < 8.5%, 8.6-10%, > 10%) was associated with increased relative risk of incidence of neonatal morbidity. Finally, risk groups (fetopathy groups I-III) were defined according to maternal HbA1 value and somatic outcome of the newborns. The importance of these fetopathy groups for criteria of neonatal morbidity is demonstrated. Based upon categorization of newborn children into fetopathy groups, children should be allocated to specific concepts of appropriate surveillance and clinical care. The fetopathy classification may also serve as an independent tool for retrospective quality control of diabetic pregnancy.
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PMID:[Risk groups of newborn infants of diabetic mothers in relation to their somatic outcome and maternal diabetic metabolic status in pregnancy]. 749 17

Non-insulin-dependent diabetes mellitus (NIDDM) is normally treated by oral hypoglycaemic agents, but their use is excluded during pregnancy because of their potential teratogenic and hypoglycaemic effects on the fetus. This caveat was recently questioned as glyburide was shown to cross an isolated cotyledon in vitro in insignificant amounts. In the present study, placental transport of glyburide in vivo was examined as an indispensable step towards clinical trials. Tritiated glyburide, C14 albumin or C14-labelled diazepam were injected into 13, 9 and 11 pregnant rats, respectively and the radioactivity was measured thereafter in maternal blood and in whole fetal extracts. The ratios between radioactivity in fetal tissue to that in maternal blood for glyburide (0.535 +/- 0.068) were similar to those of diazepam (0.641 +/- 0.057) which readily crosses the placenta. However, they differed significantly from those for albumin (0.048 +/- 0.0004) which does not cross. Moreover, glyburide in fetal tissue consistently reflected its concentration in maternal blood when measured at consecutive intervals after intravenous injection in the mother. In contrast, albumin in fetal tissue was low at all time points regardless of its levels in maternal blood when measured at different times after injection. These data suggest that glyburide crosses the placenta of pregnant rats and should therefore be considered with caution as a hypoglycaemic agent in the treatment of gestational diabetes.
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PMID:Glyburide crosses the placenta in vivo in pregnant rats. 755 74


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