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

The susceptibility of rats to alloxan undergoes a circadin rhythm. The toxicity rhythm, presumably involving injury to liver, kidney and other sites, pancreatic beta-cells in particular, is demonstrated in pooled data from 370 mature inbred Fischer or Minnesota Sprague-Dawley rats of both sexes kept in light from 06(00) to 18(00) alternating with darkness, some with free access to Purina laboratory chow with tap water at all times and some other rats subjected to one of three starvation schedules: 1) a 28-h fast before an intravenous alloxan injection; 2) a 28-h fast, except for a 4-h ad libitum feeding before injection; 3) a 28-h fast, except for a 4-h pre-injection tube-feeding of Nutrament (Mead and Johnson, Evansville, Indiana), 1.5 ml/100 g body weight. Survival time data on an additional 200 inbred Fischer rats reveal, next, that susceptibility to alloxan increases as the starvation span is lengthened from 24 to 84 h. The shortening in survival time indicative of this susceptibility increase is nonlinear; a circadian rhythmic change in susceptibility to alloxan is seen as a statistically significant wave-form indicative of the basic (persisting) rhythm, of applied interest as well to students of experimental diabetes.
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PMID:Circadian susceptibility rhythm of the rat to alloxan. 74 84

In Europe, about 1% of the women using oral contraceptives develop hypertension. Predisposing factors seem to be age, hypertension problems in past pregnancies, family history of hypertension, personal histories of kidney disorders, diabetes mellitus or adipositas, or diastolic pressure over 80 mm Hg. An overactive renin-angiotensin-aldosterone system may be an important factor in the etiology of this type of hypertension. Oterh possible factors are: reduced excretion of angiotensin 2, increased sensitivity of the arterioles to substances such as angiotensin 2 and noradrenaline, direct effect of ethinyl estradiol and mestranol on the sodium and water system, cardiovascular changes, disorders in the adrenergic system (e.g., catecholamine metabolism). Blood pressure should be checked before beginning any treatment with oral contraceptives and every 3 months after that. For the purpose of differential diagnosis angiotensin 2 in the plasma and catecholanin and its by-products should be checked (24-hour urine samples). In cases of serious hypertension hormone therapy should be discontinued at once. Primary aldosteronism and renal artery stenosis must be excluded in the differential diagnosis, for although these hypertensive disorders exhibit similar biochemical changes, they should be treated by surgical intervention. Usually hypertension is reversible after cessation of therapy with contraceptive steroids. However, some cases of irreversible hypertention, kidney failure, and malignant nephrosclerosis have been described. Hypertensive somen who wish to use oral contraceptives may, under medical supervision try a modified hormonal contraceptive (minipill without estrogen) or sequential or lower dosages.
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PMID:[Clinical aspects of hypertension under contraceptive steroids]. 79 66

Glucose tolerance and insulin responses have been examined over extended periods in severely obese, but otherwise healthy, subjects. Three significant points emerge from this study. First, it was shown that obese, supposedly ketosis resistant, subjects may deteriorate in a brief time span from a state of normal glucose disposal and adequate or increased insulin responses to insulin-deficient diabetes, culminating in ketoacidosis. Unusually high blood glucose levels complicating the ketoacidosis in two patients suggest hyperosmolarity obesity and added risk factor in severely obese diabetics. It appears that, after long-standing obesity and after years of hyperinsulinemia, a large weight gain due to prolonged overeating may impose an excessive challenge to islet cells of marginal competence. Such an event by itself or a superimposed stress or both may then cause acute insulin deficiency and/or insulin resistance leading to diabetic ketoacidosis. Hyperosmolarity may be exacerbated in the obese with cessation of food intake due to large losses of salt and water. Second, many symptoms and manifestations of hyperphagic obesity are similar to the early functional abnormalities of decompensated diabetes. The advent of the critical phase of uncontrolled diabetes, therefore, fails to alarm the obese patient and may escape timely recognition by the physician. Third, technical and mechanical difficulties due to severe obesity are apt to cause critical delays in therapy. These factors, when added to coexisting hyperosmolarity and ketoacidosis, probably account for the high mortality in these patients.
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PMID:Evolution of diabetic ketoacidosis in gross obesity. 80 48

Oedema of the umbilical cord, defined as visible oedema in a cord wish a minimal cross sectional area of 1-3 cm-2, is found in 10 per cent of deliverieo. It is seen more frequently in cetain complications of pregnancy such as abrupti placentage, maternal diabetes, macerated intrauterine death and in conditions affectint the infant including prematurity, rhesus isoimmunization, respiratory distress syndrome (RDS) and transient respiratory distress (TRD). There is a higher incidence in infants delivered by Caesarean section. There is no significant association between cord oedema and either fetal distress or neonatal asphyxia nor is there any correlation with maternal hypertension or oedema. The mechanism of production of the odema is discussed; low oncotic pressure, raised hydrostatic pressure in the placenta and umbilical cord, and an increase in total water in the feto-placental unit are considered. The presence of oedema of the cord may reflect similar changes in the lungs which antenatally predispose aninfant whose pathway for production of surfactant is immature to develop RDS and the mature infant to develop TRD. The value of cord oedema as a warning sign is stressed.
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PMID:Oedema of the umbilical cord and respiratory distress in the newborn. 80 96

1. The interaction of insulin and isometric exercise on glucose uptake by skeletal muscle was studied in the isolated perfused rat hindquarter. 2. Insulin, 10 m-i.u./ml, added to the perfusate, increased glucose uptake more than 10-fold, from 0.3-0.5 to 5.2-5.4 mumol/min per 30g of muscle in hindquarters of fed and 48h-starved rats respectively. In contrast, it did not stimulate glucose uptake in hindquarters from rats in diabetic ketoacidosis. 3. In the absence of added insulin, isometric exercise, induced by sciatic-nerve stimulation, increased glucose uptake to 4 and 3.4 mumol/min per 30g of muscle in fed and starved rats respectively. It had a similar effect in rats with moderately severe diabetes, but it did not increase glucose uptake in rats with diabetic ketoacidosis or in hindquarters of fed rats that had been "washed out" with an insulin-free perfusate. Insulin, at concentrations which did not stimulate glucose uptake in resting muscle, restored the stimulatory effect of exercise in these situations. 4. The stimulation of glucose uptake by exercise was independent of blood flow and the degree of tissue hypoxia; also it could not be reproduced by perfusing resting muscle with a medium previously used in an exercise experiment. 5. At rest glucose was not detectable in muscle cell water of fed and starved rats even when perfused with insulin. In the presence of insulin, a small accumulation of glucose, 0.25 mM, was noted in the muscle of ketoacidotic diabetic rats, suggesting inhibition of glucose phosphorylation, as well as of transport. 6. During exercise, the calculated intracellular concentration of glucose in the contracting muscle increased to 1.1-1.6mM in the fed, starved and moderately diabetic groups. Insulin significantly increased the already high rates of glucose uptake by the hindquarters of these animals but it did not alter the elevated intracellular concentration of glucose. 7. In severely diabetic rats, exercise did not cause glucose to accumulate in the cell in the absence of insulin. In the presence of insulin, it increased glucose uptake to 6.1 mumol/min per 30g of muscle and intracellular glucose to 0.72 mM. 8. The data indicate that the stimulatory effect of exercise on glucose uptake requires the presence of insulin. They suggest that in the absence of insulin, glucose uptake is not enhanced by exercise owing to inhibition of glucose transport into the cell.
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PMID:Glucose metabolism in perfused skeletal muscle. Interaction of insulin and exercise on glucose uptake. 80 2

In monkeys (Macaca mulatta) without hypothalamic lesions, food intake was found to increase with increasing age and body weight; however, food intake per kilogram body weight showed a decline over the same period of time. As the animals became older, the amount of food intake converted to body weight decreased dramatically (feeding efficiency). Water intake was shown to be closely coupled to food intake. Both daily food and water-intake data were highly reliable over a period of years. Monkeys with ventromedial hypothalamic lesions exhibited hyperphagia and increased feeding-efficiency ratios and eventual obesity. The obese animals developed symptoms of diabetes mellitus. Animals with lesions restricted primarily to the arcuate nucleus showed no hyperphagia but increased feeding efficiency. These animals exhibited decreased growth hormone release and a transitory elevation of serum insulin.
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PMID:Feeding behavior in monkeys with and without lesions of the hypothalamus. 81 9

The physiologic factors involved in vaseopressin (ADH) release and action are reviewed with emphasis on the interaction between osmotic and volume stimuli to the discharge of ADH. Abnormalities in reception of stimuli to ADH release, and in the impaired synthesis and release of ADH, are reviewed in relation to the causes of diabetes insipidus, and information on the biochemical changes which have been described in patients with nephrogenic diabetes insipidus is also discussed. We summarize the pathologic lesions and associated diseases found in 54 of our patients with diabetes insipidus. Criteria for establishing the diagnosis of diabetes insipdus are reviewed with emphasis on the dehydration test, including the importance of measuring plasma osmolality at the conclusion of water deprivation. Treatment of diabetes insipidus is briefly discussed with emphasis on the use of DDAVP and oral agents. The syndrome of inappropriate ADH secretion (SIADH) is reviewed including our experience with 39 patients. The differential diagnosis of SIADH, including the value of water loading and the measurement of ADH levels, is discussed. We comment on treatment of these patients including the use of investigational drugs. Lastly, we review the pharmacologic features and clinical relevance of some drugs which alter the release and action of ADH.
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PMID:Pathophysiologic and pharmacologic alterations in the release and action of ADH. 81 77

The effect of exogenously administered somatostatin (SRIF) on meal-stimulated secretions of the exocrine pancreas was studied in dogs with chronic pancreatic fistulas. Dogs were fed 600 gm. of raw meat, and pacreatic output of water, bicarbonate, and protein was measured. Bicarbonate and protein secretions rose markedly postfeeding in all control animals. Four hundred micrograms or 100 mug. of SRIF infused for one hour together with a meal completely prevented the postfeeding rise in pancreatic secretions. SRIF (100 mug./hr.) infused one hour after a meal suppressed pancreatic secretions to basal levels within 30 minutes. Pancreatic secretions rose promptly after discontinuation of SRIF in all dogs. These data indicate (1) SRIF completely prevents pancreatic bicarbonate and enzyme responses when given together with a meal; (2) it completely suppresses already initiated pancreatic responses when given one hour after a meal; (3) 100 mug. of SRIF is as effective as 400 mug. in suppressing the postprandial rise in pancreatic secretions. We conclude that SRIF severely interferes with pancreatic secretions during normal alimentation and that this observation should be considered if SRIF is to be used as a therapeutic agent.
Diabetes 1977 Jan
PMID:Effect of somatostatin on meal-stimulated pancreatic exocrine secretions in dogs. 83 May 67

A case of hyponatraemic coma occurring in a patient with diabetes mellitus treated with tolbutamide is described. Although chlorpropamide is known to cause water retention in some circumstances, this is a less well recognized complication of tolbutamide therapy.
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PMID:Symptomatic hyponatraemia associated with tolbutamide therapy. 87 Aug 94

The undressed body of a young man was discovered in a pit in a forest. The victim was a 27 year old depressed man, suffering from a severe diabetes. Besides personal objects, three empty insulin vials (400 I.U./vial) and empty ampules of distilled water, injection-needles and a syringe were also found in the pit. The investigation carried out at the scene, the questioning of his family and physicians, and the autopsy clarified this unusual case. In conclusion the hypothesis of "suicide" was maintained: the man administered himself a large dose of insulin; in hypoglycaemic coma he died from a bronchopneumonia in a "grave" dug by himself.
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PMID:An extraordinary case: suicide with insulin in a grave dug by the victim himself. 87 73


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