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Query: UMLS:C0011849 (diabetes)
 277,896 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The authors have elaborated a statistic survey about the pregnant women with endocrinopathies, that they have examined in the outpatient clinic from January of 1980 to December of 1988. Three hundred and twenty four women were examined in an amount of 2152 (two thousand one hundred and fifty two) observations. The incidence for 100 births was 0.54%. Maternal and fetal mobility and mortality were analysed in correlation with the maternal area of endocrinopathy (Diabetes Mellitus, Thyroid, Hypophysis and Adrenal Glands) and with the necessary therapeutic regimens. At last the A.A. made some considerations about the importance of a team approach in this area of medical care, and applied to the clinicians who work in primary care, to a better collaboration.
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PMID:[Pregnancy and endocrinopathy. Activity, pathology and results at the outpatient obstetrics-endocrinology clinics of the University of Coimbra Hospitals--January 1980 through December 1988]. 227 15

Clinical features of epinephrine release led to the finding of spontaneously elevated plasma epinephrine concentrations in five patients, in four of whom plasma norepinephrine concentrations were normal. Adrenal medullary hyperplasia was suspected in one patient, whose first cousin had multiple endocrine neoplasia type IIa, and in two others, all of whom have experienced relief from symptoms during propranolol or atenolol administration. The other two patients had unilateral adrenal cysts, with negative metaiodobenzylguanidine scans and no histological evidence of pheochromocytoma, but complete relief of symptoms by excision of the cysts. In one patient, Cushing's syndrome and associated hypertension, diabetes, and ischemic finger-tip ulceration all disappeared after surgery. It is concluded that spontaneous hyperepinephrinemic manifestations can be received by beta-blockers or, when an adrenal mass is present, by unilateral adrenalectomy even when the metalodobenzylguanidine test result is negative.
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PMID:Primary hyperepinephrinemia in patients without pheochromocytoma. 236 52

Between 1982 and 1985, cataract extraction was performed on 144 eyes of 122 diabetics, and the early and late complications of the operation were recorded. There was seldom any intraoperative hemorrhaging or any postoperative anterior chamber hemorrhaging. On the first day after the operation, increased IOP was measured more frequently in diabetic patients than in those without diabetes. Diabetic retinopathy deteriorated in 12 eyes, while hemorrhaging glaucomas occurred in 5 eyes.
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PMID:[Early and late complications in cataract extraction in diabetic patients]. 243 96

We conducted a retrospective pathology study to determine whether subjects with long-standing insulin-dependent diabetes mellitus (IDDM) have abnormalities of the adrenal medulla compared with subjects with non-insulin-dependent diabetes mellitus (NIDDM) and nondiabetic individuals. Slides were scored from 0 (no fibrosis) to 3+ (complete fibrosis). Nineteen IDDM subjects aged 30-60 yr (mean +/- SE 44.9 +/- 2.5 yr) at autopsy and with duration of diabetes 13-45 yr (26.8 +/- 1.8 yr) were studied. Twelve NIDDM subjects aged 61-84 yr (73.3 +/- 2.5 yr) with duration of diabetes 17-33 yr (22.8 +/- 1.9 yr) were studied. Twenty-two nondiabetic subjects aged 32-77 yr (53.7 +/- 2.9 yr) were studied. Four of 19 (27%) IDDM subjects had moderate to severe fibrosis compared to 1 of 12 (8.3%) NIDDM subjects and 1 of 22 (4.5%) control subjects. Thirteen of 19 (68%) IDDM subjects had a score of 1, 2, or 3 compared to 3 of 22 (13.6%) control subjects (P less than .0005). There was an association between duration of IDDM and fibrosis score (r = .46, P less than .05) and between age and fibrosis score among IDDM subjects (r = .57, P = .01). No association between age or duration of diabetes and fibrosis score was observed for NIDDM or control subjects. Adrenal medullary fibrosis may be an anatomical correlate of the diminished epinephrine secretion that occurs in response to insulin-induced hypoglycemia in some IDDM subjects.
Diabetes Care
PMID:Adrenal medullary fibrosis in IDDM of long duration. 247 15

Fifteen patients with bilateral secondary glaucoma caused by rubeosis iridis in the course of diabetes were operated; one eye was subjected to a simple trabeculectomy, the fellow-eye to filtrating trabeculectomy by Nesterow's method; antiglaucomatous operations were preceded by a panretinal photocoagulation. After at least 3 years of observation the more stable reduction of the IOP was shown after filtering trabeculectomy.
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PMID:[Trabeculectomy preceded by retinal panphotocoagulation in the treatment of secondary glaucoma with rubeosis iridis]. 248 12

Disturbances of prostaglandin I2 (PGI2, prostacyclin) production by adipose tissue contribute to the pathogenesis of diabetic ketoacidosis and may contribute to the pathogenesis of hypertension and vascular disease. We studied the cellular basis of PGI2 production in adipose tissue, measured as release of 6-keto-PGF1 alpha in response to epinephrine. Adipocytes did not produce PGI2 when nonfat cells were removed by repeated washing. The nonadipocyte cellular constituents of adipose tissue (nonfat cells) did not produce PGI2 in the absence of adipocytes. Both adipocytes and nonfat cells were required for PGI2 production in response to epinephrine. Adipocytes pretreated with 0.2 mM aspirin to inhibit PGH synthase nevertheless promoted PGI2 production when mixed with nonfat cells. Nonfat cells preincubated with aspirin did not produce PGI2 when mixed with adipocytes. The nonfat cells converted arachidonic acid to PGI2 but adipocytes did not. Epinephrine stimulated lipolysis and PGI2 production in a dose-dependent parallel manner, but the responses were distinct above 10(-6) M. Characterization of the nonfat cells by fractionation on a Percoll density gradient followed by measurement of angiotensin-converting enzyme activity and 6-keto-PGF1 alpha production indicated that the nonfat cells were predominantly vascular endothelial cells. We conclude that catecholamine-stimulated PGI2 production in adipose tissue results from the cooperation of adipocytes and vascular endothelial cells. The adipocytes provide arachidonic acid, which is converted to PGI2 by the vascular endothelial cells. Because adipose tissue is located near blood vessels throughout the body, adipocytes may be an important source of arachidonic acid for vascular endothelial cells in various circumstances in health and disease. Our findings raise the possibility that adipocytes may, under some circumstances, release arachidonic acid into the systemic circulation where it is used by vascular endothelial cells throughout the body to produce PGI2 and other eicosanoids.
Diabetes 1989 Sep
PMID:Cooperation of adipocytes and endothelial cells required for catecholamine stimulation of PGI2 production by rat adipose tissue. 250 36

We have characterized a plasma membrane phosphatidylinositol 4,5-bisphosphate (PIP2)-specific phospholipase C (PLC) and a cytosolic phosphatidylinositol (PI)-specific PLC in human liver. Epinephrine, 1 x 10(-5) M, and vasopressin, 1 x 10(-8) M, stimulated PIP2-PLC which was enhanced by guanosine 5'-O-(3-thiotriphosphate) (GTP gamma S). PI-PLC stimulation was not observed by these agents. Insulin and insulin-like growth factors (IGF-I and IGF-II) in the presence and absence of GTP gamma S did not stimulate PIP2-PLC or PI-PLC in plasma membranes and cytosol preparations nor phosphoinositide breakdown in isolated human hepatocytes. Furthermore, serendipitly we found that PIP2-PLC activity was increased in liver membranes from obese patients with type II diabetes when compared to obese and lean controls. We conclude that in human liver, insulin and IGFs are not members of the family of hormones generating inositol trisphosphate (IP3) as a second messenger. Furthermore, the increased PIP2-PLC in diabetic liver may result in: (a) increased intracellular concentrations of IP3 and thus increased Ca2+, which has been postulated to induce insulin resistance; and (b) increased diacylglycerol and thus increased protein kinase C which phosphorylates the insulin receptor at serine residues inactivating the insulin receptor kinase. While the mechanism of increased PIP2-PLC activity in diabetes is unknown, it may initiate a cascade of events that result in insulin resistance.
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PMID:Effect of insulin and insulin-like growth factors I and II on phosphatidylinositol and phosphatidylinositol 4,5-bisphosphate breakdown in liver from humans with and without type II diabetes. 254 Jan 78

A 44 year old man with longstanding diabetes mellitus gave a 6-month history of periodic attacks of flaccid quadriplegia. Following one of these episodes he was admitted for assessment. In view of persistent hyperkalaemia, hypoadrenalism was suspected and Addison's disease was confirmed biochemically. Adrenal replacement therapy restored the potassium levels to normal and resulted in no further attacks of paralysis.
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PMID:Hyperkalaemic periodic paralysis: a rare presentation of Addison's disease. 259 1

The capacity of erythrocytes to modify their glycogen stores to compensate for changes in glucose concentration in plasma was studied. Experiments in vitro and in vivo demonstrated that erythrocytes absorbed and incorporated glucose into their glycogen stores when glucose concentration in the medium was high and liberated it when the concentration was low. Epinephrine administration inhibited glucose absorption by erythrocytes, and in its presence, erythrocytes liberated glucose from their glycogen stores, being unable to compensate for this rise in glucose concentration in plasma. Similar results were obtained when endogenous secretion of epinephrine was enhanced by carotid sinus-chemoreceptor stimulation. Insulin had no effect on the capacity of erythrocytes to absorb glucose. These data suggest a role for erythrocytes in the transport of glucose to different regions in the organism's circulation and in the regulation of glucose concentration in plasma.
Diabetes 1989 Apr
PMID:Erythrocytes and glucose homeostasis in rats. 264 49

The mechanisms by which insulin and catecholamines affect low-density lipoprotein (LDL)-receptor activity were studied in freshly isolated human mononuclear leukocytes. Incubation of cells for up to 24 h in a lipid-free medium resulted in an increase in the specific binding, accumulation, and degradation of 125I-labeled LDL. Insulin stimulated the ability of the cells to bind, accumulate, and degrade the lipoprotein with high affinity, which may be caused by an increase in the LDL-receptor number without altering binding affinity. (-)-Epinephrine inhibited the specific binding, accumulation, and degradation of 125I-LDL. This effect appears to be mediated by a decrease in the number of LDL receptors and not by a change in the binding affinity. (-)-Norepinephrine, the unspecific beta-adrenergic agonist (-)-isoproterenol, and the beta 2-specific agonist terbutaline mimicked the effect of epinephrine on LDL-receptor activity. Catecholamines and beta-adrenergic agonists yielded sigmoidal log-concentration effect curves. The action of epinephrine was attenuated by the beta-antagonist (dl)-propranolol. These results demonstrate that insulin stimulates and catecholamines suppress the specific binding, accumulation, and degradation of 125I-LDL in human mononuclear leukocytes. The catecholamine action appears to be mediated by beta 2-adrenergic receptors. A suppression of LDL-receptor activity resulting from deficiency of insulin and elevated plasma catecholamine concentrations in uncontrolled insulin-dependent diabetic patients may contribute to the increased levels of LDL cholesterol observed in these patients.
Diabetes 1988 Oct
PMID:Opposite effects of insulin and catecholamines on LDL-receptor activity in human mononuclear leukocytes. 284 7


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