Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UMLS:C0011849 (diabetes)
 277,896 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Results of examination of 257 patients suffering from diabetes mellitus demonstrated a reduction of sodium, potassium and magnesium content in their plasma. Erythrocytes also displayed a reduction of potassium and magnesium, and some increase of sodium content. Reduction of electrolyte level in the plasma and erythrocytes was more pronounced in winter; the erythrocyte sodium content was less in summer than in winter. The 24-hour sodium potassium and magnesium excretion is increased, during winter in particular. The efficacy of treatment of diabetic patients with panangin and potassium chloride for the purpose of elimination of magnesium and potassium deficiency was demonstrated. A conclusion was drawn on the expediency of using these drugs in the complex treatment of diabetic patients, particularly in winter.
 ...
PMID:[Seasonal fluctuations in the electrolyte content in diabetes mellitus]. 15 64

Renal clearance studies were performed on rats both during the administration of streptozotocin and sequentially during the following 8 days as hyperglycemia progressed. Although GFR was depressed 30 min after the drug administration, GFR steadily rose during the following days to become 52% greater than control levels. Renal size did not change during this short period, and it is suggested that glomerular hemodynamic changes are responsible. A maximal tubular reabsorptive capacity for glucose (TmG) could not be satisfactorily demonstrated in normal rats, although glucose reabsorption was significantly depressed at high-filtered loads. At comparable filtered loads, glucose reabsorption in diabetic rats was almost complete in contrast to normal rats, and the increases in GFR and renal tubular sodium reabsorption are presumed to be the major factors. The administration of insulin to normal and diabetic rats was followed by a significant diuresis as well as an increase of 1% to 4% in the fraction of filtered sodium excreted although GFR was unaltered. This shows that even a 35% to 60% reduction in the filtered load of glucose can significantly depress renal sodium reabsorption. It is concluded that this is a good animal model in which to study the effects of diabetes on renal function as well as the in vivo interrelationships of sodium and glucose reabsorption.
 ...
PMID:Acute effects of streptozotocin diabetes on rat renal function. 15 16

Five patients with growth failure but few other abnormal clinical signs are presented. Two were shown to have primary hypopituitarism, three had primary hypothyroidism. All received levothyroxine sodium and grew 7.0 to 12.5 cm during the first year and 6.2 to 8.7 cm during the second year of treatment. Three of the adolescent patients developed signs of signs of puberty within six to nine months of initiation of levothyroxine therapy. One hypopituitary patient had femoral epiphysial dysgenesis, hypopglycemia, and undescended testes. One hypothyroid patient had been treated for diabetes mellitus for 8.5 years and may be the youngest patient reported with such a disease combination. We conclude that in a few patients with growth failure without specific clinical signs, diagnosis and differentiation between primary hypothyroidism and primary hypopituitarism can only be made by specific endocrinologic testing.
 ...
PMID:Primary hypothyroidism. Differentiation from primary hypopituitarism. 17 81

To determine the cause of selective aldosterone deficiency in two patients with diabetes mellitus, studies of renin and of aldosterone-precursor metabolites were performed under conditions of sodium depletion and ACTH stimulation. Plasma renin concentration was elevated in both patients, and stimulated plasma renin activity was low in one and normal in the other. Fractionation of plasma extracts demonstrated the presence of "big renin," a relatively inactive precursor of renin. Metabolites of aldosterone precursors were increased, suggesting deficient 18-hydroxylase in one patient and dehydrogenase in the other. The results suggest that hypoaldosteronism in diabetic patients may result from combined defects in both renin and aldosterone biosynthesis.
 ...
PMID:Big renin and biosynthetic defect of aldosterone in diabetes mellitus. 18 84

Experiments with rats were set up to study the interaction of hormones with Na+, K+-ATP-ase and Ca2+-ATP-ase of the sarcoplasmatic reticulum fragments and with pyruvate-dehydrogenase of the myocardial mitochondria in healthy rats and the ones with alloxan diabetes. Insulin was found to activate, while epinephrine and c-AMP to inhibit Na+, K+-ATP-ase. The Ca2+-ATP-ase is activated with epinephrine and c-AMP. In alloxan diabetes Na+, K+-ATP-ase is inhibited and Ca2+-ATP-ase and pyruvate-dehydrogenase--activated.
 ...
PMID:[Effect of insulin, adrenaline and cyclic adenosine monophosphate on the activity of transport adenosine triphosphatases and pyruvate dehydrogenase of the rat myocardium under normal conditions and in insular insufficiency]. 19 87

Several characteristics of the binding of insulin and glucagon to human circulating mononuclear leukocytes have been studied. Functional analysis (latex bead ingestion) revealed that cell mixtures, as prepared according to Boyum and used generally in studies of insulin resistance in humans, consist of 20-29% phagocytic monocytes, with the remainder being lymphocytes. Partial separation of monocytes from lymphocytes on columns of Sephadex G-10, followed by correlation of insulin binding with cell type, confirms that the monocyte is the binding species. Insulin influenced neither glucose uptake nor the further conversion of glucose to lipids and CO2 by the leukocytes. The transport of alpha-aminoisobutyrate, a nonmetabolizable amino acid, into these cells was also unaffected by insulin. Monocyte/lymphocyte mixtures specifically bound glucagon and prostaglandin E1. At physiological concentrations of these hormones, steady states were reached in 15 min and 45 min, respectively. In contrast to the 8-10-fold increases in cellular cyclic AMP produced by prostaglandins, the effect of glucagon was very small but apparently real. Under appropriate preincubation conditions, sodium azide and iodoacetamide inhibited phagocytosis and insulin binding in parallel. The binding of glucagon was unaffected by these agents. Although both antimycin A and actinomycin D inhibited phagocytosis of the monocytes, only the former inhibited insulin binding; there was only a slight effect on glucagon binding. We would conclude that the binding of insulin to human circulating monocytes, although reflective of insulin resistance in diabetes mellitus and obesity, may not be to traditional receptors. In contrast, the binding of glucagon to lymphocyte/monocyte mixtures may be to function-linked receptors.
 ...
PMID:Hormone receptors: VI. On the nature of the binding of glucagon and insulin to human circulating mononuclear leukocytes. 20 May 11

In the rat, the administration of beta1-24-corticotrophin during 7 days following an uninephrectomy enhances significantly the compensatory hypertrophy of the remaining kidney. There is no increase in renal compensatory hypertrophy when ACTH is injected to previously adrenalectomized rats. This action of ACTH could be related to the diabetes mellitus induced by this hormone or to an increase in sodium reabsorption by the tubular epithelial cells.
 ...
PMID:[Enhancement of compensatory renal hypertrophy by beta-1-24 corticotropin in the rat]. 20 74

The widespread use of corticosteroids in clinical practice emphasises the need for a thorough understanding of their metabolic effects. In general, the actions of corticosteroids on carbohydrate, protein, and lipid metabolism result in increased hepatic capacity for gluconeogenesis and enhanced catabolic actions upon muscle, skin, lymphoid, adipose and connective tissues. Because of the morbidity associated with steroid therapy, the clinician must carefully consider in each case the gains that can reasonably be expected from corticosteroid therapy versus the inevitable undesirable side effects of prolonged therapy. Thus, it is important to remember that the enhanced anti-inflammatory activity of the various synthetic analogues of cortisol is not dissociated from the expected catabolic actions of glucocorticoid hormones. Replacement therapy with physiological doses of cortisol in primary or secondary adrenal insufficiency is intended to simulate the normal daily secretion of cortisol. Short term, high dose suppressive glucocorticoid therapy is indicated in the treatment of medical emergencies such as necrotising vasculitis, status asthmaticus and anaphylactic shock. With improvement of the underlying disorder, the steroid dosage can be rapidly tapered and then discontinued over a 2 to 3 day period. Long term, high dose suppressive therapy is often commonly used to treat certain diseases (see sections 4.7.2 and 4.7.3). In this setting, suppression of the hypothalamic-pituitary-adrenal axis may persist for as long as 9 to 12 months following steroid withdrawal if steroid doses are administered in the supraphysiological range for longer than 2 weeks. In general, higher doses, longer duration of usage, and frequent daily administration are all correlated with the severity of pituitary ACTH suppression. When steroid therapy is to be withdrawn, gradual tapering of the dosage is necessary; the steroid dosage should also be given as a single morning dose if possible. Rapid or total withdrawal of the steroid therapy may be associated with exacerbation of the underlying disease or with a steroid withdrawal syndrome. An additional important point to remember in any withdrawal programme is that the steroid dosage should be appropriately increased for an exacerbation of the underlying disease or for intercurrent major stress. Alternate day therapy is recommended as a steroid maintenance programme for patients requiring high dose glucocorticoid therapy over a prolonged period of time. Thus, it is usually employed to maintain a therapeutic benefit which had previously been extablished by daily steroid treatment. Complications resulting from corticosteroid therapy include: (1) proximal muscle weakness; (2) osteopenia; (3) unmasking of latent diabetes mellitus; (4) sodium retention and/or elevation of mean arterial blood pressure; (5) adverse psychiatric reactions; (6) development of glaucoma; and (7) reactivation of latent infections (such as tuberculosis).
 ...
PMID:Corticosteroids: clinical pharmacology and therapeutic use. 20 58

In order to elucidate a possible relationship between (Na+ + K+)-activated ATPase and intestinal absorption of actively transported monosaccharides enzyme activity was measured in mucosal cells from alloxan diabetic rats. The general effect of increasing capacity of active, Na+-dependent transport processes in diabetes mellitus is associated with a significantly enhanced (Na+ +K+)-activated ATPase activity in mucosal homogenate from diabetic animals. To study the localization of these effects within the cell we isolated purified brush borders and their substructures. To enable a comparison to be made between preparation procedures of diabetic and control animals the fractions were controlled by electronmicroscopy and by measuring the sucrase activity. In the purified brush border fraction of alloxan treated rats there was no significant increase in (Na+ + K+)-activated ATPase activity. Based on these results we conclude that the (Na+ + K+)-activated ATPase in the basolateral membranes was increased in alloxan diabetes, and it seems very likely that this enzyme is involved in the regulation of Na+-dependent transport processes.
 ...
PMID:[Effect of alloxan diabetes on (Na+ + K+)-activated ATPase in brush border membrane of the mucosal cell of rat small intestine]. 21 7

Brattleboro rats homozygous for hypothalamic hereditary diabetes insipidus (DI rats) were used to investigate the following questions: a) Do exogenous and endogenous angiotensin II (AII) have an antidiuretic effect in diabetes insipidus? b) Does AII mediate the antidiuresis induced by furosemide? The following results were obtained: 1. AII (5 mg/kg s.c. in oil) and furosemide (50 mg/kg i.p.) decreased urine flow and increased urinary sodium excretion. Furosemide led to a two-fold increase of AII plasma concentrations and a decrease of plasma sodium levels. 2. SQ 14 225 (2 x 2.5 mg/kg p.o.), an angiotensin I-converting enzyme inhibitor, led to an increase of urine flow and to a slightly elevated urinary sodium excretion. 3. When the formation of AII was blocked by SQ 14 225 (2 x 2.5 mg/kg p.o.), AII plasma concentrations were 2.5-fold decreased, but furosemide still reduced urine flow. We conclude that plasma AII might have an antidiuretic action in DI rats. However, AII does not mediate the antidiuresis induced by furosemide.
 ...
PMID:Inhibition of the renin-angiotensin-system in Brattleboro rats with hereditary hypothalamic diabetes insipidus. 21 21


<< Previous 1 2 3 4 5 6 7 8 9 10 Next >>