[Secretion of gastrin, pancreatic polypeptide and glucagon in persons with simple obesity].
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Biomedical subjects
Publications and source records attributed to F Kokot.
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In 76 patients with active nephrolithiasis and in 28 normal subjects the influence of an Ca-load on the calcitonin and glucagon secretion and on the serum calcium, phosphate and magnesium levels was examined. In the patients with active nephrolithiasis a significant suppression of Ca-induced calcitonin secretion and absence of glucagon secretion was found. Simultaneously the patients showed a lower decrease of serum Mg and reduced increase of serum phosphate levels. The authors suggest participation of the above mentioned biochemical and endocrine abnormalities in the pathogenesis of the active nephrolithiasis.
The concentrations of insulin (IRI), parathormone (PTH), calcitonin (CT), some electrolytes (Ca, Mg, P), vitamin D and glucose were determined in 6 patients with terminal renal insufficiency treated by CAPD.
In 72 patients with end-stage renal failure and 70 healthy subjects, the influence of blockade of opioid receptors by naloxone on secretion of prolactin, lutropin (LH), follitropin (FSH), adrenocorticotropin (ACTH), somatotropin (HGH), insulin (IRI), glucagon (IR-G), parathyroid hormone (PTH) and calcitonin (CT) was studied. Administration of naloxone stimulated luliberin-induced LH and FSH secretion quantitatively equally in patients and controls. Blockade of opioid receptors was followed by a less marked suppression of chlorpromazine-induced prolactin secretion but by a higher response of hypoglycemia-induced ACTH secretion in uremic patients than in controls. In addition, a less marked suppressive effect of naloxone was noted on hypoglycemia-induced HGH secretion in chronic renal failure as compared with controls. Blockade of opioid receptors improved significantly glucose tolerance and glucose-induced insulin secretion in uremic patients and suppressed nearly completely glucagon secretion response during the second phase of a glucose tolerance test. Finally, administration of naloxone was followed by a blunted response of Ca-induced CT secretion and suppression of PTH. Data presented in this paper suggest the existence of hyperendorphinism in end-stage renal failure.
In a group of 119 patients with advanced chronic renal failure (serum creatinine level 733 +/- 186 mumol/l) the effect of a low-protein diet supplemented with essential amino acids (EAA) or their keto analogues (KA) on uremic metabolism and rehabilitation status was investigated. The protein intake amounted to 0.4 g/kg B.W./day, the phosphorus intake 0.4-0.6 g/day and the energy supply 120-150 kJ/kg B. W./day. In 51 patients there was a substitution with EAA and in 68 patients with their KA. The mean duration of dietary treatment in this study was 19 months (6-64 months). During this time, the serum creatinine increased from 733 +/- 186 to 1,220 +/- 256 mumol/l, whereas the urea nitrogen values remained relatively constant at between 26 and 30 mmol/l. There were no signs of protein malnutrition (nitrogen balance, serum transferrin and serum protein were normal). The hemoglobin concentration remained at greater than 5 mmol/l with creatinine levels of 1,220 +/- 256 mumol/l. During the substitution with KA, there was a significantly greater decrease in serum phosphate (p less than 0.05) and parathyroid hormone (PTH) (p less than 0.01) as compared with the uremics given EAA. In addition, we found a significant increase in testosterone (p less than 0.01) in patients supplemented with KA. Despite advanced chronic renal failure there was a good degree of rehabilitation (full-time work: 21%; part-time work: 66.4%). It can be concluded that a low-protein diet supplemented with EAA or KA can improve the uremic metabolism, rehabilitation status and safely postpone the start of maintenance dialysis.
A marked improvement of renal osteodystrophy was achieved after a combined treatment with keto acids and vitamin D in patients with chronic renal failure. Results were checked by histological investigations. The biochemical background of the successful treatment was analysed. A regression of hyperparathyroidism and improvement in vitamin D status are the cause of this phenomenon.
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In 12 healthy pregnant women, 14 women with mild or moderate late pregnancy gestosis (EPH) and in 12 non-pregnant women, the influence of head out water immersion (WI) on mean blood pressure (MAP), the renin-aldosterone system, vasopressin (AVP) and atrial natriuretic hormone (ANF) was examined. WI induced a prompt fall in MAP in all examined groups. This decrease of MAP was maximal after 1 h WI, showing a tendency to rise later on in pregnant women. Simultaneously a decrease of plasma renin activity (PRA), plasma aldosterone, AVP and an increase of ANF was noted. The WI induced endocrine reaction pattern was qualitatively similar, but quantitatively different in the examined groups. In contrast to the response of non-pregnant women, healthy pregnant women and women with EPH gestosis showed a significantly smaller increase in ANF secretion induced by WI. No correlation was found between PRA, plasma AVP, aldosterone and ANF respectively. In addition changes in PRA, aldosterone, AVP and ANF did not correlate with WI-induced changes in MAP. From data obtained in this paper it seems, that WI-induced MAP changes are not related significantly to changes of the above mentioned hormonal factors.
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