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

The purpose of the investigations was the determination of the maximum gastric secretion during hyperglycaemia in healthy subjects as well as in patients with short-term and long-term diabetes. After the stimulation with pentagastrine, given in the dose of 6 microgram per kg of body weight in 0.9% sodium chloride solution continuous intravenous infusion, there were determined MAO, parietal and nonparietal secretions, the concentrations of sodium, potassium, chloride, calcium and magnesium, and the total secretin of these electrolytes in gastric juice. In healthy subjects hyperglycaemia was induced by intravenous infusion of 30% glucose solution. Under the influence of hyperglycaemia the decrease of MAO (p less than 0.001) in healthy subjects as well as in diabetics was found. In healthy subjects the decrease of the total potassium, chloride and magnesium secretion in gastric juice (p less than 0.001) was observed. In patients with long-term diabetes the decrease of the secretion of sodium, potassium, chloride, magnesium and calcium was observed. There were no differences in gastric secretion in both groups of diabetics. The inhibitory effect of hyperglycaemia on the parasympathetic system and the decreased release of endogenous gastrine may be the causes of these changes. Insulin may also inhibit gastric secretion.
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PMID:[Maximal gastric secretion in hyperglycemia in normal subjects and in diabetics]. 59 33

Interrelations among plasma renin activity (PRA), aldosterone and cortisole levels, 0lood volume, exchangeable sodium, urinary catecholamines, and blood pressure were studied in 35 normal subjects and 60 age-matched non-azotemic patients with diabetes mellitus (60% with hypertension, 15% with orthostatic hypotension). Basal PRA, plasma aldosterone, cortisol, blood volume, plasma potassium, and urinary electrolytes were comparable in diabetic and normal subjects. Diabetic patients, however, had a 10% increase in body sodium (P less than 0.01), and 8% of them showed normal postural PRA responses and subnormal aldosterone responses; 22% had subnormal PRA and normal aldosterone responses, and 17% had subnormal responses of PRA and aldosterone. Non-PRA-related aldosterone responses could not be explained by ACTH or electrolytes. Orthostatic decreases in blood pressure correlated (P less than 0.01) with both catecholamine excretion and basal PRA. This suggests that in diabetes mellitus, body sodium is increased. Basal PRA and plasma aldosterone are usually normal, but their postural responses are frequently impaired. Absent aldosterone responses, despite normal PRA responsiveness, may reflect an adrenal abnormality or an ineffective form of renin. Marked postural aldosterone stimulation, unrelated to PRA, ACTH, or electrolytes, points to a potent unknown factor in aldosterone control. Low levels of free peripheral catecholamines and PRA may be complementary factors contributing to postural hypotension.
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PMID:Sodium, renin, aldosterone, catecholamines, and blood pressure in diabetes mellitus. 60 91

To examine the role of basal insulin and glucagon secretion in potassium and sodium homeostasis, somatostatin, a potent inhibitor of insulin and glucagon secretion, was infused for 5 h into healthy human subjects, maturity-onset diabetes, juvenile-onset diabetics, and normal dogs. Infusion of somatostatin resulted in an increase in serum potassium (0.5-0.6 meq/liter) in normal subjects and maturity-onset diabetics, but not in juvenile-onset diabetics despite equivalent reductions in plasma glucagon in all three groups. A similar rise in serum potassium was observed in normal conscious dogs given somatostatin and was reversed by insulin replacement. Urinary excretion of potassium was unaffected by somatostatin. In dogs given intravenous potassium chloride in doses (0.375 meq/kg per h) which do not alter basal insulin levels, the rise in serum potassium (0.6 meq/liter in controls) increased 100% when somatostatin was administered together with the KCl infusion. Addition of replacement doses of insulin to the somatostatin infusion resulted in increments in serum potassium which were comparable to infusion of KCl alone. Urinary potassium excretion rose after KCl administration and was unchanged by the addition of somatostatin. Serum sodium concentration was unaffected by somatostatin administration in both the human and dog studies. However, urinary sodium excretion displayed a biphasic response falling by 20-60% within the first 2 h of somatostatin administration and then rising to values 50-80% above basal levels at 3-4 h. Inulin and p-aminohippurate clearances were unaffected by somatostatin. It is concluded that (a) potassium homeostasis is influenced by basal insulin levels in the absence of which serum potassium concentration rises and potassium tolerance declines; (b) this effect of insulin is mediated via extrarenal mechanisms of potassium disposal; (c) somatostatin has a biphasic effect on urinary sodium secretion, the mechanism of which remains to be established.
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PMID:Influence of basal insulin and glucagon secretion on potassium and sodium metabolism. Studies with somatostatin in normal dogs and in normal and diabetic human beings. 62 Dec 84

Dichloroacetate is known to reduce plasma glucose and triglycerides in diabetic and starved animals and to lower plasma lactate under various experimental conditions. To investigate its metabolic effects in man, we administered oral doses (3 to 4 g) of dichloroacetate as the sodium salt to patients with diabetes mellitus or hyperlipoproteinemia or both for six to seven days. Dichloroacetate significantly reduced fasting hyperglycemia an average of 24 per cent (P less than 0.01) from base line and produced marked, concomitant falls in plasma lactate (73 per cent; P less than 0.05 to less than 0.01) and alanine (82 per cent; P less than 0.01 to less than 0.001). In addition, it significantly decreased plasma cholesterol (22 per cent; P less than 0.01 to less than 0.001) and triglyceride (61 per cent; P less than 0.01) levels while increasing (71 per cent; P less than 0.01) plasma ketone-body concentrations. Plasma insulin, free fatty acid and glycerol levels were not affected. Serum uric acid rose, whereas excretion and renal clearance fell. Some patients experienced mild sedation, but no other laboratory or clinical evidence of adverse effects was noted during or immediately after the treatment phase.
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PMID:Metabolic effects of dichloroacetate in patients with diabetes mellitus and hyperlipoproteinemia. 62 8

Syntheses of human, dog, rat, and duck C-peptides and their analogues and preliminary results on the total synthesis of human proinsulin are described. In the syntheses of the C-peptides, chain elongation was performed exclusively by the azide-fragment condensation method in solution. The synthetic human, dog, rat, and duck C-peptides and their analogues were proved to be homogeneous by several analytic means. With these synthetic peptides, radioimmunoassay systems for dog, rat, and duck C-peptides were developed. For the total synthesis of human proinsulin, 10 protected peptide hydrazides were prepared, and the linearly protected hexaoctacontapeptide having the proposed sequence of human proinsulin was constructed by the azide-fragment condensation method in solution starting from the C-terminal undecapeptide (HP 75-86). After deblocking of the alpha-amino protection, the partially protected hexaoctacontapeptide was treated with sodium in liquid ammonia. The ensuing sulfhydryl form was converted to the S-sulfonate form, which was reduced and then air-oxidized. The oxidized material was purified by gel filtration on Sephadex G-50 (fine) followed by ion-exchange chromatography on DEAE-cellulose. The cross-reactivity in the insulin radioimmunoassay of the ensuing product was 62.5 per cent of porcine proinsulin on a weight basis at B/Bo = 60 per cent. Acid hydrolysis and amino acid analysis of this product gave the theoretically expected ratios. In addition, this peptide, as well as the S-sulfonate form of the hexaoctacontapeptide, showed displacement curves superimposable on that of synthetic human C-peptide on an equimolar basis in the human C-peptide radioimmunoassay (antiserum 527). These results confirm the synthesis of human proinsulin.
Diabetes 1978
PMID:Syntheses of C-peptides and human proinsulin. 63 37

Weight reduction is almost always successful in cases of essential hypertension if and when the weight loss is accompanied by a drastic sodium reduction. (2) Weight normalization is of remarkable help in complete reversal of abnormal glucose tolerance, decrease in insulin requirement in manifest diabetes mellitus, and - in many patients with mild diabetes - discontinuation of oral hypoglycemic agents. (3) Weight loss will occasionally relieve gout patients of their symptoms. The majority of hyperuricemic patients will benefit with a lowering of serum uric acid levels. (4) An unresolved issue is the influence of weight reduction on the cholesterol metabolism - short- and long-term results are by no means predictable. Whereas the triglycerides in obese patients almost always return to lower serum concentrations, and with them the hyperlipoproteinemias of type IIB, III and IV, the type IIA is only rarely seen in association with obesity. Therefore, information on this lipid abnormality is very limited regarding the effect of weight loss.
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PMID:The workinghman's diet. II. Effect of weight reduction in obese patients with hypertension, diabetes, hyperuricemia and hyperlipidemia. 63 8

The changes in plasma renin activity (PRA) and plasma aldosterone concentration (PA) in response to dietary sodium restriction and upright posture were evaluated in 7 patients with juvenile-type, insulin-dependent, uncomplicated diabetes mellitus and in 5 healthy volunteers. All patients had normal blood pressure, 24-hour urine protein excretion and endogenous creatinine clearance. Renal sodium conservation and concentrating ability were grossly normal and 5 patients so tested, had normal renal acidification. PRA and PA were normal in every subject suggesting that abnormalities of the renin-aldosterone axis are late complications of diabetes mellitus usually associated with hypertension and nephropathy or neuropathy.
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PMID:Renin-aldosterone responsiveness in uncomplicated juvenile-type diabetes mellitus. 64 May 77

Plasma aldosterone (PA) and plasma renin activity (PRA) were determined in 44 diabetics, of whom nine were normotensive but not nephropathic (group 1), 10 were hypertensive but not nephropathic (group 2), and 25 were hypertensive and nephropathic (group 3); they were kept in balance on a diet composed of 10 to 20 mEq. of sodium (Na) and 100 mEq. of potassium (K). Supine PA in group 1 was 38 +/- 7 ng. per deciliter, whereas in normals it was 24 +/- 2 ng. per deciliter (P less than 0.05); beyond that, neither supine nor upright PA or PRA differed significantly from normal in groups 1 and 2. By contrast, in group 3, supine PA was 13 +/- 1 ng. per deciliter and PRA 2.0 +/- 0.2 ng./ml. and upright PA was 39 +/- 7 ng. per deciliter and PRA 3.8 +/- 0.5 ng./ml., all significantly lower than those in the other groups (P less than 0.01). Nine patients, one in group 1 and eight in group 3, had low supine and upright PA and PRA; four had hyperkalemia. An additional nine patients in group 3 had low upright PA, with normal or low PRA; two had hyperkalemia. Of the 18 patients with low upright PA, K correlated with glucose (R = 0.46, P less than 0.05). These results suggest (1) the renin-aldosterone system generally responds normally in diabetics without nephropathy but responds subnormally when nephropathy is present, (2) hyporeninemic hypoaldosteronism is frequent in diabetics with nephropathy but may occur in the absence of clinical nephropathy, and (3) hyperkalemia in some diabetic patients may be secondary to hypoaldosteronemia and hyperglycemia.
Diabetes 1978 Jul
PMID:Aldosterone responsiveness in patients with diabetes mellitus. 65 19

Adult-onset diabetics have markedly diminished or absent acute insulin responses to glucose that can be partially restored by sodium salicylate infusion. To determine whether this restoration of the acute insulin response is glucose dose dependent and whether complete restoration can be achieved, adult-onset diabetics with a mean fasting plasma glucose value of 216 +/- 20 mg. per deciliter (x +/- S.E.) were stimulated with various doses of intravenous glucose. Restoration occurred in a glucose dose-dependent manner. Complete restoration could not be achieved with the maximal tolerable glucose dose (80 gm.). Second phase insulin secretion also improved in a glucose dose-dependent manner. These findings are compatible with the hypothesis that defective insulin secretion in adult-onset, hyperglycemic diabetics is not due to absolute deficiency of insulin but may be a result of defective recognition of glucose signals by pancreatic B-cells--a defect that can be partially reversed by sodium salicylate.
Diabetes 1978 Jul
PMID:Restoration of the acute insulin response by sodium salicylate. A glucose dose-related phenomenon. 65 22

In maturity onset diabetes the blood levels of total blood keto acids in terms of pyruvic, serum citric, calcium are significantly higher than in normal adults, while there is a decrease in reduced-blood glutathione, serum zinc, potassium and sodium levels. There were no significant differences between diabetes and normal adults in the serum levels of copper, ceruloplasmin oxidase activity, iron and magnesium.
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PMID:Blood-reduced glutathione, pyruvic acid, citric acid, ceruloplasmin oxidase activity and certain mineral changes in diabetes mellitus before and after treatment. 68 21


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