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

The rate of alloxan-induced insulin release was measured from rat islets maintained in a simple perifusion system. Insulin release during the five-minute exposure to alloxan reached its maximum rate after two to three minutes of the exposure and then rapidly declined. This insulin release was dependent upon extracellular calcium and was associated with an increased 45Ca uptake by isolated islets. Once exposed to alloxan, however, the islets did not release insulin when stimulated again with D-glucose or alloxan. These effects of alloxan on insulin release (stimulation and subsequent inhibition) and the increased 45Ca uptake were prevented by the presence of 3-0-methyl-D-glucose during the alloxan exposure. These findings indicate a close correlation between alloxan-induced insulin release and the subsequent inhibition of further insulin release. D-glucose, when present during the entire five-minute exposure to alloxan, protected competitively against alloxan inhibition of insulin release. In addition, D-glucose, when present immediately after brief (one to three minutes) alloxan exposures, reversed some of the subsequent inhibition of insulin release. These findings suggest that alloxan and D-glucose were competing for a common site on the beta-cell. The possibility of this site being a receptor responsible for the initiation of insulin release is discussed.
Diabetes 1978 Dec
PMID:Alloxan stimulation and inhibition of insulin release from isolated rat islets of Langerhans. 36 92

The role of calcium flux in mediating epinephrine modification of insulin release was investigated by using lanthanum, an inhibitor of calcium flux, in the in vitro perifusion system. Lanthanum inhibits insulin secretion stimulated by glucose and by acetylcholine to basal levels. Epinephrine and lanthanum have additive effects in inhibiting insulin secretion to glucose stimulation. The effect of epinephrine prestimulation on insulin secretion to subsequent glucose challenge varies markedly, depending on the presence or absence of bicarbonate ion: epinephrine priming is reversed in the absence of bicarbonate, and effect possibly related to reduced calcium uptake. In the presence of bicarbonate, lanthanum blocks the priming effect of epinephrine on insulin secretion. The data further support the postulated role of calcium in adrenergic effects on beta cell function.
Diabetes 1979 Jan
PMID:Effects of calcium, lanthanum, and bicarbonate ion on epinephrine modification of insulin release in vitro. 36 54

In animals the pyruvate dehydrogenase reaction is mainly responsible for the irreversible loss of glucose carbon by oxidation. Regulation of this reaction is shown to be a major determinant of glucose conservation in starvation and diabetes. Estimates of conservation in man in starvation and diabetes are reviewed. The pyruvate dehydrogenase complex is inhibited by products of its reactions; it is also regulated by a phosphorylation-dephosphorylation cycle catalysed by a kinase intrinsic to the complex and by a more loosely associated phosphatase. Inactivation is largely accomplished by phosphorylation of the tetrameric decarboxylase component (alpha2beta2) to alpha2Pbeta2. Complete phosphorylation produces the (alpha2P3)beta2 form. Both forms are completely reactivated by phosphatase action but the initial rate of reactivation of a complex containing alpha2Pbeta2 is approximately three times that of (alpha2P3)beta2. The proportion of active (dephosphorylated) complex is decreased in rat tissues by starvation and diabetes and in perfused rat heart by oxidation of fatty acids and ketone bodies. In adipose tissue in vitro, insulin increases the proportion of active complex and lipolytic hormones may decrease this proportion. It is suggested that rates of oxidation of lipid fuels may be a major determinant of the activity of pyruvate dehydrogenase in tissues in relation to the actions of insulin and lipolytic hormones and the effects of diabetes and starvation. Phosphorylation and inactivation of the complex are enhanced by high mitochondrial ratios of [acetyl-CoA]/[CoA], [ATP]/[ADP], [NADH]/[NAD+] and low concentrations of pyruvate, Mg2+ and Ca2+, and vice versa.
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PMID:Regulation of pyruvate oxidation and the conservation of glucose. 37 69

During pregnancy it is necessary for the mother with diabetes to maintain careful control of the diabetes in order to lessen both fetal and maternal morbidity and mortality. The diet must take into account not only the metabolic requirements of the mother, but also those of the developing fetus. A total weight gain of 22 to 26 pounds is recommended, with the pattern of weight gain being more important than the total amount. Pregnancy is not a time for weight reduction. Caloric requirements can be met by the addition of 300 kcal. per day to the prepregnancy meal plan, or about 36 kcal. per kilogram. This can be met by the addition of 50 gms., carbohydrate and 30 gms. protein. Diets will contain approximately 1800 to 2500 calories a day. Calcium, iron, folic acid, and sodium also require attention in meal planning. The importance of regular meals and snacks must be emphasized. In particular, bed-time snacks are important because of the tendency towards overnight hypoglycemia and ketosis.
Diabetes Care
PMID:Nutritional management in diabetes and pregnancy. 40 Jan 35

In alloxan diabetes, serum zinc, copper, iron and magnesium were significantly higher than in normal rats, while the level of serum calcium, sodium, and potassium was lower than normal. Treatment with daonil or insulin led to a normalization, as expected of the level of serum glucose and most of the other elements, except for iron and potassium. When lycanol was used for treatment, the level of all elements returned to the normal except for blood glucose, zinc and potassium.
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PMID:Serum mineral changes in alloxan diabetes before and after treatment with some hypoglycemic drugs. 40 72

Ten patients with primary hyperparathyroidism were placed on a constant 30 mEq of calcium and 120 meq of sodium diet, and alterations in their calcium balance in response to standard oral doses of chlorpropamide were studied over a 4 day control period and a 4 day treatment period. The 10 patients treated with chlorpropamide significantly increased the urinary excretion of calcium and sodium and decreased the excretion of cyclic adenosine monophosphate (AMP). The serum calcium was lowered in six of the patients treated with chlorpropamide, and three of these patients, who had diabetes mellitus and either refused or were too ill for parathyroidectomy, continued to receive chlorpropamide for periods of 9 to 36 months. These three patients experienced prolonged lowering of the serum calcium level and became less confused, lethargic, and fatigued. The interrelationships between the chlorpropamide-induced changes in excretion of calcium, sodium, and cyclic AMP still must be clarified.
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PMID:Chlorpropamide-induced changes in patients with hyperparathyroidism. 41 59

To elucidate pathogenetic factors of bone mineral loss in diabetes mellitus, bone mineral content (BMC), glucose and calcium homeostasis were evaluated in a cross-sectionsl study of 215 insulin-treated diabetics. BMC declined 10% during the first 5 years of diabetes. This coincided with cessation of insulin secretion, deterioration of metabolic control and raising urinary calcium excretion rates of calcium and phosphorus. BMC was inversely correlated to fasting blood glucose (P less than 0.02), to glycosuria (P less than 0.02) and to insulin requirement (P less than 0.002), and positively to the glucagon-stimulated serum C-peptide levels (P less than 0.005). Urinary excretion rates of calcium and phosphorus correlated positively with the degree of hyperglycaemia (P less than 0.001) and glycosuria (P less than 0.001). The skeletal calcium loss corresponded to the excess of urinary excretion during the phase of BMC reduction. There was no evidence of secondary hyperparathyroidism. The relationship between bone loss and disturbed glucose homeostasis indicates that diabetic bone loss is secondary to the metabolic abnormalities, possibly acting directly on bone.
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PMID:Bone mineral loss in insulin-treated diabetes mellitus: studies on pathogenesis. 42 86

The intravenous injection of zinc or manganese chloride immediately before and 15 minutes after alloxan or dithizone prevented the usual hyperglycemia observed 24 hours after induction of diabetes. Injection of zinc chloride in alloxan diabetes led to normalization of sodium while zinc, copper, iron and magnesium remained high and calcium and potassium remained low as in alloxan. In case of dithizone diabetes, the administration of zinc salt led to an increase in serum zinc, magnesium and potassium and to a decrease in serum calcium while the sodium level returned to normal. Manganese plus alloxan led to a normalization of serum zinc, copper, potassium and sodium. In the case of dithizone plus manganese only magnesium was raised while the other elements were unchanged when compared to animals injected with dithizone only. Chromium and cobalt lowered the blood glucose to a certain extent however it did not affect most of the elements. The same changes occurred in all elements as with alloxan or dithizone alone. Pretreatment with ATP led to a normalization of serum zinc, copper, magnesium, sodium and potassium, while in case of iron it remained high and calcium remained low as that found in alloxan diabetic rats.
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PMID:Serum mineral changes due to exogenous ATP and certain trace elements in experimental diabetes. 44 5

Experimentally diabetic rats have low serum 1,25-dihydroxyvitamin D, intestinal malabsorption of calcium, secondary hyperparathyroidism, and bone loss. To examine the hypothesis that abnormalities similar to those in the diabetic rat might explain human diabetic osteopenia, we studied calcium metabolism in 40 healthy control and 82 diabetic patients aged 18--75 yr [47 untreated: fasting plasma glucose (mean +/- SE), 267 +/- 8 mg/dl; 19 treated but hyperglycemic: glucose 305 +/- 24 mg/dl; 16 treated and in better control: glucose, 146 +/- 8 mg/dl]. Serum total calcium, ionic calcium, immunoreactive parathyroid hormone (Arnaud method, GP-1M and CH-12M antisera), 25-hydroxyvitamin D (Haddad method), and 1,25-dihydroxyvitamin D (Lambert method) concentrations were normal in all 3 groups of diabetics and were not significantly different from values in the control group. We determined absorption of calcium from the intestine by a double isotope method (100 mg Ca carrier; normal range, 40--80%) in 11 control and 13 untreated, uncontrolled diabetics (mean plasma glucose, 285 +/- 17 mg/dl). Absorption of calcium in controls was 60 +/- 3% and in diabetics was 56 +/- 3% (not significantly different). We have found no derangement of calcium metabolism in adults with insulin-requiring juvenile- and adult-onset diabetes regardless of treatment status. The experimental diabetic rat model does not appear to be useful for determining the pathogenesis of adult human diabetic osteopenia.
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PMID:Calcium homeostasis in diabetes mellitus. 46 80

A 52-year-old man with mild diabetes and acute stem cell leukaemia developed an orbitofacial mucormycosis. Cultures showed the fungus to be Rhizopus oryzae. Vigorous treatment with amphotericin B and other bactericidal and bacteriostatic antibiotics for a concurrent sepsis failed to suppress the infections, and the patient died. On post-mortem examination characteristic haematoxylin-staining, broad, aseptate fungal hyphae were found in the right eye, orbit, and lung. A striking and unusual feature of this case is the presence of brightly birefringent crystals within the severely degenerated eye. These were found by histochemical staining and x-ray diffraction studies to be calcium salts of fatty acids, apparently liberated from necrotic adipose tissue of the orbit.
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PMID:Orbitofacial mucormycosis with unusual pathological features. 50 83


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