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

Changes in glucagon, growth hormone (GH), cortisol, renin and aldosterone accompanying the metabolic disturbances and dehydration of severe diabetic ketoacidosis were studied over a 24 h period in eight patients treated with a constant intravenous insulin infusion. Mean steady state plasma-free insulin levels achieved were 28.6--49 mu/1 in patients receiving 2 u/h but a satisfactory rate of fall of glucose was not always obtained until the infusion dose was increased to 4 u/h or more. The total insulin dose administered was positively correlated with the level of plasma glucagon and cortisol on admission. During insulin infusion, both glucagon and cortisol fell but the rate of fall was not related to dose or plasma level of free insulin achieved. In six of eight patients studied increments in plasma GH above admission levels were observed during insulin treatment. Admission values of both plasma renin activity and plasma aldosterone were raised. The renin levels were highest in newly diagnosed diabetics, and two patients with long-established diabetes showed only small increments despite profound dehydration. Plasma renin activity, but not plasma aldosterone correlated with the fluid and sodium retention over the initial 24 h treatment period, but not with potassium requirements. The urinary excretion rates of the small molecular weight proteins GH and insulin, were considerably elevated over the treatment and convalescent periods.
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PMID:Hormonal responses during treatment of acute diabetic ketoacidosis with constant insulin infusions. 10 71

This study is a description of a patient who exhibited diabetic ketosis associated with an alkalosis rather than acidosis and a review of eight previously reported cases. Precipitating factors for this syndrome are severe vomiting with loss of hydrogen, potassium, and chloride ions, and dehydration. The ingestion of alkali may also result in this mixed acid-base disturbance. Treatment consists primarily of replacement of potassium and chloride. All reported patients had received large doses of insulin for initial therapy; however, limited insulin (20 U) therapy in this patient almost completely reversed the metabolic abnormality with 12 hours.
Diabetes Care
PMID:Mixed acid-base abnormalities in diabetes. 10 96

Renin activity and aldosterone were evaluated relative to potassium levels and lead intoxication in 33 patients with a history of "moonshine" ingestion. Patients were divided into three groups: I, lead intoxicated with hyperkalemia; II, lead intoxicated without hyperkalemia; and III, not lead intoxicated without hyperkalemia. Those in group I demonstrated suppressed plasma renin activity, baseline and after furosemide, and blunted aldosterone responsiveness to furosemide. Plasma renin activity was not different in groups II and III, whereas aldosterone responsiveness was less in group II than in III. Group I patients tended to be older, had lower creatinine clearances, and six of nine had mild hyperchloremic acidosis. Diabetes and cortisol insufficiency were not present. Chronic lead intoxication due to illicit alcohol ingestion is associated with hyporeninemic hypoaldosteronism and hyperkalemia which appear to develop as the lead nephropathy progresses with duration and/or aging.
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PMID:Renin aldosterone system and potassium levels in chronic lead intoxication. 10 94

The effects of intravenous administration of potassium phosphate in the treatment of diabetic ketoacidosis were studied in nine children, ages 9 9/12 to 17 10/12 yr. During phosphate infusion (20--40 meq/L of fluid), all children maintained normal serum concentrations of phosphorus. Transient hypocalcemia occurred in six and transient hypomagnesemia in five patients. One child developed carpopedal spasms refractory to intravenous infusion of calcium gluconate but responsive to intramuscular injection of magnesium sulfate. In three patients, serum levels of intact parathyroid hormone were low at the time of hypocalcemia, an observation that suggests transient hypoparathyroidism. This study indicates that the use of potassium phosphate as the sole source of potassium replacement might potentiate ketoacidosis-induced hypocalcemia through multiple mechanisms.
Diabetes Care
PMID:Hypocalcemia, hypomagnesemia, and transient hypoparathyroidism during therapy with potassium phosphate in diabetic ketoacidosis. 11 30

Streptozotocin (STZ)-diabetic rats regularly retained sodium (Na+), and tended to retain potassium (K+) as well, in response to insulin. Diabetic patients have also been reported to exhibit antinatriuresis and antikaliuresis early in the course of insulin therapy. Insulin-related Na+ retention can occur without a marked reduction in blood glucose level and does not appear to be attributable to preexisting Na+ depletion, mineralocorticoid effect, or suppression of glucosuria. The decrease in urinary Na+ excretion (UNaV) in the rats incident to insulin administration was appreciably greater than the decrease in chloride (Cl-) or water excretion. The significance of this observation is uncertain. It may be, in part, a consequence of the nephrotoxicity of STZ. Insulin-related Na+ retention may be closely related pathogenetically to the Na+ retention of refeeding and may reflect a direct renal action of insulin or, less likely, an alteration of renal tubular metabolism in response to insulin-mediated changes in sytemic metabolism.
Diabetes 1975 Jul
PMID:Observations on sodium retention related to insulin treatment of experimental diabetes. 12 67

The ability of insulin to inhibit efflux of potassium (K) and amino acid nitrogen (AAN) from perfused livers of normal and insulin deficient rats was studied. Two groups of rats with different degrees of insulin deficiency were produced by injecting varying amounts of streptozotocin. One group, classified as being moderately diabetic (MD), had fasting plasma glucose levels between 235--425 mg%, while the other group, whose plasma glucose levels greater than 425 mg%, were considered to have severe diabetes (SD). Two other groups of rats were food restricted in order to attain body weights comparable to the two groups of diabetic rats, and livers from these animals were used for control perfusions. The results indicated that the ability of insulin to suppress efflux of K and AAN from perfused livers of rats with MD was comparable to that seen in control perfusions. On the other hand, insulin could not suppress the efflux of either K or AAN from perfused livers of rats with SD. These results indicate that normal hepatic responsiveness to insulin can be lost secondary to the production of insulin deficiency.
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PMID:Insulin responsiveness of isolated perfused livers from rats with streptozotocin induced diabetes. 14 26

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.
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PMID:[Seasonal fluctuations in the electrolyte content in diabetes mellitus]. 15 64

Although epinephrine stimulates insulin release by activation of beta-adrenergic receptors, its dominant effect (mediated by stimulation of alpha-adrenergic receptors) is an inhibition of insulin secretion that is powerful enough to suppress the secretory activity of insulin's most potent stimulants. The insulin-secretory response to potassium chloride (KCl) infusion, however, is not suppressed; in fact, in ureter-ligated dogs simultaneously infused with 360 microgram. epinephrine per hour and 2 mEq. KCl per kilogram per hour, insulin release is actually increased about threefold (over controls). Propranolol blockade of beta-adrenergic receptors essentially abolishes the insulin response to KCl infusion, with and without epinephrine. It is unlikely that KCl, like epinephrine, provokes insulin release by direct stimulation of the beta-adrenergic receptors of the beta cells of the pancreatic islets. However, potassium in some way enhances the beta adrenergic (secretory) activity of epinephrine and blunts its usually dominant alpha-adrenergic (inhibitory) effect.
Diabetes 1978 May
PMID:Epinephrine enhancement of potassium-stimulated immunoreactive insulin secretion. Role of beta-adrenergic receptors. 20 80

The acid-base and electrolyte balance of 30 women studied at delivery and in their infants during the first 48 h. 18 women were diabetics, 10 of these were delivered vaginally (DMvag) and 8 by elective caesarean section (DMcs). 12 healthy women were vaginally delivered (HMvag). The infants of diabetic mothers (IDM) received active infusion therapy. At birth the DMvag and their infants (IDMvag) had a more pronounced metabolic acidosis than the DMcs and their babies (IDMcs). The largest metabolic acidosis occurred, however, in the group of HMvag and their infants (IHMvag). After birth no significant differences were obtained in the acid-base and electrolyte balance between IDMvag and IDMcs. The plasma potassium level remained lower in IDM than in IHM. The study stress the importance of adequate management of diabetes in pregnancy in combination with active intravenous therapy during delivery and to the infant in the immediate neonatal period. The slightly larger metabolic acidosis seen in combination with vaginal delivery suggests that this mode of delivery should not be attempted uncritically in diabetic women.
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PMID:Acid-base and electrolyte balance in infants of diabetic mothers. Vaginal delivery versus caesarean section. 23 97

Potassium homeostasis was evaluated in 13 patients with diabetes mellitus. In eight, plasma renin activity was low; plasma aldosterone concentration was decreased in all; seven had a history of spontaneous hyperkalemia. After administration of glucose orally, there were paradoxical increases in serum potassium levels in seven patients. After potassium loading, maximal values and increments of serum potassium were higher and fractional potassium excretion was lower in the diabetic than in the control subjects, although the differences were not statistically significant. Abnormalities of potassium homeostasis in diabetes are probably related to insulin and mineralocorticoid deficiency. Diabetic patients with hypoaldosteronism have the potential for severe hyperkalemia should renal or extrarenal mechanisms for potassium homeostasis be challenged by severe acidosis be challenged by severe acidosis, diminished renal function, marked hyperglycemia, or administration of potassium salts or potassium-sparing diuretics.
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PMID:Potassium homeostasis in chronic diabetes mellitus. 32 62


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