PubMed Health⌕ Search

Biomedical subjects

B Ludvik

Publications and source records attributed to B Ludvik.

51 records · Page 3Linked to original sources
PubMed1991

Basal and stimulated plasma levels of pancreatic amylin indicate its co-secretion with insulin in humans.

Amylin is a 37-amino acid pancreatic polypeptide, probably involved in the pathophysiology of Type 2 (non-insulin-dependent) diabetes mellitus. We have determined amylin in human plasma by extraction-based radioimmunoassay (Sep-Pak C18). Of 23 healthy control subjects plasma amylin was determined as 11.9 +/- 3.5 ng/l. Of 27 patients with Type 2 diabetes receiving insulin the amylin levels were lower, and in 16 patients with Type 2 diabetes on oral medication they were higher than in the control subjects; 8.2 +/- 4.4 ng/l (p less than 0.01) vs 18.8 +/- 9.9 ng/l (p less than 0.05). In 14 Type 1 (insulin-dependent) diabetic patients we found extremely low mean amounts of amylin: 2.9 +/- 1.9 ng/l (p less than 0.002). Thus, basal amylin appears to be associated with the capacity to release insulin. An oral glucose load stimulated the release of amylin, this was more pronounced in patients with Type 2 diabetes than in healthy subjects. An excellent correlation of mean amylin with mean insulin concentrations was obtained (r = 0.949). In patients with Type 2 diabetes amylin was reduced congruent to decreases in C-peptide during a hyperinsulinaemic, euglycaemic glucose clamp experiment (r = 0.971 for linear correlation between C-peptide levels and amylin). We conclude, that amylin and insulin are co-secreted in humans, and that the amylin release is under feedback-control by insulin.

Adult↗
PubMed1991

Effects of dichloroacetate and bicarbonate on haemodynamic parameters in healthy volunteers.

1. It has been shown that sodium bicarbonate has no effect or could even be detrimental in various forms of metabolic acidosis. Dichloroacetate, a stimulator of the pyruvate dehydrogenase complex, might offer an alternative treatment. The present study therefore examines the metabolic and haemodynamic effects of dichloroacetate and sodium bicarbonate in healthy volunteers. 2. On 2 different days, sodium dichloroacetate (50 mg/kg body weight) or sodium bicarbonate (1.5 mmol/kg body weight) was given intravenously as a single bolus in 10 healthy volunteers. Haemodynamic parameters were measured using a microprocessor-controlled system. Measurements were performed before and 30 and 60 min after infusion. 3. After administration of dichloroacetate, cardiac index increased from 2.3 +/- 0.03 to 2.7 +/- 0.1 1 min-1 m-2 (P less than 0.05), peripheral vascular resistance decreased from 266 +/- 9.7 to 240 +/- 1.7 kPa s l-1 (2662 +/- 97 to 2398 +/- 169 dyn s cm-5, P less than 0.05), oxygen availability increased from 442 +/- 16 to 535 +/- 30 ml min-1 m-2 (P less than 0.05) and serum lactate concentration fell from 1.4 +/- 0.14 to 0.6 +/- 0.1 mmol/l (P less than 0.05). With infusion of sodium bicarbonate there were no significant effects on any of these variables. 4. Our results show that dichloroacetate administered intravenously reduces the serum lactate concentration. The main effects of dichloroacetate itself are on the haemodynamic variables. Dichloroacetate increases cardiac index and oxygen availability and decreases peripheral vascular resistance, whereas sodium bicarbonate has no effect on haemodynamic or metabolic parameters. These data give some further insights in the actions of dichloroacetate and support the use of dichloroacetate as alternative therapy in various forms of metabolic acidosis.

Adult↗
PubMed1991

Decrease of stimulated amylin release precedes impairment of insulin secretion in type II diabetes.

Amylin, a 37-amino acid polypeptide, has been identified as the major protein component of pancreatic amyloid deposits in patients with non-insulin-dependent (type II) diabetes mellitus. Amylin is stored and released together with insulin and has been proposed to play a major role in the pathogenesis of type II diabetes. To compare amylin release and its proportion to insulin secretion under different metabolic conditions, oral and intravenous glucose tolerance tests (OGTT and IVGTT, respectively) were performed in healthy, lean control subjects, obese patients with normal and impaired glucose tolerance (NGT and IGT, respectively), and obese type II diabetic patients. Compared with control subjects, basal and stimulated amylin secretion during OGTT was significantly higher in obese patients with NGT and IGT but not in type II diabetic patients. The integrated amylin response was significantly higher in obese patients with NGT than lean control subjects and type II diabetic patients matched for degree of obesity. The amylin-insulin ratio decreased slightly in obese subjects with NGT and IGT and significantly in type II diabetic patients. Amylin secretion was significantly stimulated during IVGTT in control subjects and obese patients with NGT and IGT but not in type II diabetic patients. These findings suggest that amylin is physiologically released by pancreatic beta-cells in a constant ratio to insulin in nondiabetic subjects. Glucose-stimulated amylin secretion is increased in obese subjects with NGT and IGT. In type II diabetes mellitus, amylin secretion relative to that of insulin is decreased, and amylin is not stimulated by IVGTT.

Adult↗
PubMed1991

The effects of ramipril on glucose tolerance, insulin secretion, and insulin sensitivity in patients with hypertension.

To evaluate a possible influence of the angiotensin-converting enzyme inhibitor ramipril on glucose tolerance and insulin sensitivity, an oral glucose tolerance test (oGTT) and an euglycemic clamp were performed in 10 nonobese, nondiabetic patients with mild hypertension before and after treatment with ramipril for 14 days. Following ramipril treatment, systolic and diastolic blood pressures were significantly lower (152.5 +/- 10.6/97.5 +/- 4.3 vs. 136.5 +/- 18.9/79.5 +/- 16.4 mm Hg). Therapy with ramipril showed no influence on glucose tolerance (serum glucose of 106.8 +/- 32.8 vs. 109.1 +/- 33.9 mg/dl at 120 min during the oGTT), insulin secretion (53.0 +/- 45.7 vs. 41.1 +/- 10.6 microU/ml at 120 min), and insulin sensitivity (glucose infusion rate of 180.8 +/- 60.7 vs. 199.8 +/- 77.5 mg/m2/min after 3 h of clamp). In conclusion, short-term treatment of hypertension with ramipril has no influence on glucose metabolism in nondiabetic patients.

Aged↗
PubMed1991

[Role of amylin in the pathogenesis of type II diabetes mellitus].

Amylin, a peptide, which was isolated from the islet amyloid of type II diabetics, might play a potential role in the pathogenesis of type II diabetes mellitus. In in vitro and in vivo studies it has been shown that amylin has an effect on insulin secretion as well as on insulin sensitivity. From measurements of plasma amylin levels it is known that amylin is cosecreted with insulin and patients with hyperinsulinemia have also elevated amylin levels. In patients with impaired glucose tolerance and type II diabetes amylin levels are decreased compared to insulin. A secretory defect of amylin and its local accumulation in the islets of type II diabetics might be a cause for the insulin secretory defect in type II diabetes. Additionally, amylin can induce peripheral insulin resistance, which might also be a cause for type II diabetes mellitus. Amylin is a new pancreatic peptide, which might play an important role in the pathogenesis of diabetes mellitus.

Amyloid↗
PubMed1989

[Gestagen receptor-positive, solid-cystic acinar-cell tumor of the pancreas].

In a 16-year-old girl with left upper abdominal pain of two months' duration fine-needle biopsy (guided by computed tomography) revealed a solid-cystic acinar-cell tumour of the pancreas. The tail of the pancreas was resected and the spleen removed. On inspection, the tumour--about 9 cm in diameter--was encapsulated and consisted of soft, brownish, partly haemorrhagic tissue. Histologically and immunohistochemically the diagnosis of an acinar-cell tumour was confirmed. Analysis of steroid hormone receptors revealed a high progestogen content. Since the operation the patient has remained symptom-free without any sign of tumour recurrence.

Adolescent↗
PubMed1988

[Lack of effect of ACE inhibition on severe proteinuria in diabetic nephropathy--a 6-month-long study].

The effect of angiotensin converting enzyme inhibition with captopril therapy (3 x 12.5 mg/d) on heavy proteinuria and kidney function was investigated in 10 insulin-treated diabetic patients over a period of 6 months. Urinary protein excretion increased from 3706 mg/day (SD 1491) to 5405 (SD 2699) after 6 months of treatment (p = 0.05); serum creatinine rose from 248 mumol/l (SD 163) to 283 (SD 186) (p less than 0.01), whereas there was no significant difference in blood pressure before (150/80 mm Hg--SD 23/6) and after therapy (150/90 mm Hg--SD 23/10). HbA1c as a marker of metabolic long-term control decreased from 8.3% (SD 1.0) to 7.3% (SD 1.0) (p less than 0.05). No beneficial effects of low dose angiotensin converting enzyme inhibition on heavy proteinuria could be demonstrated in this group of patients with advanced diabetic nephropathy. In particular, progressive deterioration of kidney function was not influenced by the captopril treatment. In diabetic patients with incipient diabetic nephropathy presenting with microalbuminuria, further studies concerning a possible therapeutic effect are necessary.

Adult↗
PubMed1988

[Malignant aldosteronoma in the differential diagnosis of Conn syndrome].

Primary aldosteronism-characterized by hypertension, hypokalemia and metabolic alkalosis--is caused by benign adenomata or bilateral adrenal hyperplasia in most cases. Aldosterone producing carcinomata of the adrenal cortex are very rare tumors. As the histological classification is difficult, the diagnosis is often drawn from tumor size, very high levels of plasma aldosterone, severe hypokalemia and malignant behaviour. The prognosis is very poor: Overall median and 5 year survival rate from diagnosis of adrenocortical carcinoma are 14 months and 24%.

Adenoma↗
PubMed1987

[Peripheral and right atrial plasma levels of atrial natriuretic peptide and their relation to mean atrial pressure].

Atrial myocytes produce natriuretic and vasodilating peptides. Animal experiments have shown that atrial natriuretic peptide (ANP) is released after stretching the atria and drained via the coronary vein effluent. In this study ANP-plasma levels were measured in 14 patients. Blood samples were simultaneously collected from the right atrial cavum and from an antecubital vein. In the right atrial samples, ANP-plasma concentrations were significantly higher than in samples drawn from a peripheral vein (140.3 +/- 114.8 pg/ml vs 96.9 +/- 69.2 pg/ml; p less than 0.05), but a significant linear correlation was found between both values (r = 0.88; p less than 0.001). In patients with elevated atrial pressures significantly higher ANP-levels could be detected than in patients with normal atrial pressures (204 +/- 115 pg/ml vs 55.3 +/- 18.5 pg/ml; p less than 0.05). Mean right atrial pressure correlated to ANP-levels in right atrial blood (r = 0.79; p less than 0.001) as well as to ANP-levels in peripheral blood (r = 0.68; p less than 0.01). These results indicate that higher ANP plasma levels can be measured in samples drawn from a site close to ANP production. On the other hand, atrial pressure might influence the amount of circulating ANP.

Adolescent↗
PubMed1986

Thyroid hormones and pericardial effusion may influence plasma levels of atrial natriuretic peptide (ANP) in humans.

Fluid and electrolyte homeostasis is impaired in patients suffering from hypothyroidism and myxedema because myxedema induces retention of salt and water. We have measured plasma levels of human atrial natriuretic peptide (hANP) in 8 female patients who had been totally thyroidectomized because of thyroid carcinoma. Estimations of the hormone were done 4 weeks after diagnostic withdrawal (searching for iodine retaining metastases) and after 2 weeks and 4 weeks of reinitiation of thyroid suppressive therapy by L-thyroxine. hANP levels, although within the normal range (10-80 ng/l) throughout the study, were positively linked to the amount of pericardial effusion (determined by echocardiography), which was highest initially and decreased or vanished with duration of L-thyroxine therapy. Additionally, a positive correlation between thyroid hormone levels and hANP was obtained when the counteracting effect of pericardial effusion was allowed for by partial correlation analysis. Our findings might facilitate explanation of mild polyuria in hyperthyroidism and impaired water excretion in hypothyroidism.

Adult↗