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Biomedical subjects

J Knudtzon

Publications and source records attributed to J Knudtzon.

At least 55 records · Page 3Linked to original sources
PubMed1986

Effects of hypersecretion of growth hormone and prolactin on plasma levels of glucagon and insulin in GH3-cell-tumor-bearing rats, and the influence of bromocriptine treatment.

Plasma levels of prolactin, growth hormone, glucagon insulin and glucose were measured in non-treated control rats, bromocriptine-treated control rats and GH3-cell-tumor-bearing rats with and without bromocriptine treatment. Bromocriptine treatment increased plasma levels of glucagon, insulin and glucose in control rats. Tumor-bearing rats had increased body weight and increased plasma levels of prolactin, growth hormone, glucagon, insulin and glucose. Bromocriptine treatment reduced body weight and decreased the plasma levels of prolactin, glucagon and insulin, as compared to non-treated tumor-bearing rats. The drug had no effect on plasma levels of growth hormone and glucose. These results indicate that, in GH3-cell-tumor-bearing rats, prolactin, glucagon and insulin are more sensitive to the action of bromocriptine than growth hormone.

Animals↗
PubMed1986

Hypoinsulinemic and hyperglycemic effects of beta-endorphin in rabbits.

The present study was designed to investigate the in vivo effects of beta-endorphin on plasma levels of glucagon, insulin and glucose in rabbits, and to elucidate some of the mechanisms involved. beta-Endorphin (50 micrograms) injected intravenously into fasted rabbits, decreased plasma levels of insulin (-4.5 +/- 1.3 microU/ml, P less than 0.05) and increased plasma levels of glucose (+2.7 +/- 0.4 mmol/l, P less than 0.05). Similar hypoinsulinemic and hyperglycemic effects were observed for 25 and 2.5 micrograms beta-endorphin in fasted and 50 and 0.5 micrograms beta-endorphin in fed rabbits. beta-Endorphin produced slight and transient increases in plasma levels of glucagon at the highest dose in fed rabbits, only (+80 +/- 9 pg/ml, P less than 0.05). The beta-endorphin-induced hypoinsulinemia was not inhibited by phentolamine, yohimbine, propranolol or atropine, which is in consistency with a direct inhibitory effect of beta-endorphin on the beta-cell in rabbits. The beta-endorphin-induced hyperglycemia was reduced by naloxone (+0.8 +/- 0.1 mmol/l) but not by N-methyl-naloxone (ORG 10908) a peripheral opiate receptor blocking drug (+2.2 +/- 0.2 mmol/l), suggesting a central nervous action on opiate receptors. This central action of beta-endorphin was probably not mediated by catecholamine release or other stimulation of adrenergic or muscarinic receptors, since the beta-endorphin-induced hyperglycemia was not inhibited by phentolamine, yohimbine, propranolol or atropine. These results suggest that the beta-endorphin-induced hyperglycemia was caused, at least in part, by a peripheral inhibition of insulin release and a central stimulation on glucoregulation.

Animals↗
PubMed1986

Effects of pro-opiomelanocortin-derived peptides on plasma levels of glucagon, insulin and glucose.

Pro-opiomelanocortin (POMC) is a prohormone for several peptides including corticotropin, melanocyte stimulating hormones and beta-endorphin. POMC-derived peptides have been demonstrated in many tissues, including the hypothalamus and the endocrine pancreas, which play important roles in the control of plasma levels of glucagon, insulin and glucose. This article reviews the present knowledge concerning in vitro and in vivo effects of POMC-derived peptides on glucagon, insulin and glucose levels involving several possible mechanisms: direct effects on the endocrine pancreas (including endocrine, paracrine and peptidergic regulation) and glucose production, and indirect effects involving the hypothalamus, the autonomic nervous system and the adrenal gland.

Adrenocorticotropic Hormone↗
PubMed1986

Growth hormone therapy of short stature.

Considerable progress has been made in the diagnosis and treatment of growth hormone-related short stature. Knowledge about growth hormone releasing factor (GRF) and somatomedin C has provided the possibility of distinguishing between hypothalamic and pituitary growth hormone deficiency and growth hormone resistance. It has been shown that treatment with GRF may stimulate growth in certain cases of growth hormone deficiency. Recombinant DNA techniques may, in the near future, provide sufficient amounts of GRF, growth hormone and possibly somatomedin C for clinical use. At present, many countries have prohibited the use of human pituitary growth hormone due to a possible risk of transmission of Creutzfeldt-Jakob disease. It has become increasingly clear that several short children without classical growth hormone deficiency, may increase their growth velocity during growth hormone treatment. There are many medical, psychological, ethical and economical implications involved in the extended treatment of children with short stature. It is necessary to maintain a restricted approach towards the treatment of children with short stature, and such treatment should be prescribed and controlled by a limited number of well-trained paediatric endocrinologists. This article reviews some of the present knowledge in this rapid developing field of paediatric endocrinology.

Child↗
PubMed1986

Twins discordant for vater association. Obstructed labor of the second twin due to ascites and persistent cloaca without communication to the exterior.

The unusual delivery of a dead second twin with rare malformations is presented. The first twin, born live following a normal labor, had no malformations. The birth of the second twin was obstructed by massive ascites, and its abdomen had to be perforated before delivery. The sex could not be determined due to lack of the internal genitalia and the fetal appearance of the external genitals. The left kidney and ureter were hypoplastic. The right ureter and distal part of the colon were dilated and opened into a large primitive cystic cloaca without communication to the exterior. The ascites was probably caused by the urinary obstruction. These malformations probably represent one of the earliest arrested developments of the embryonic hindgut. The presence of a tracheo-esophageal fistula and a single umbilical artery, together with the anal atresia and the renal anomalies, could indicate that the anomalies formed part of the VATER association.

Abnormalities, Multiple↗
PubMed1985

Involvement of the autonomic nervous system in the in vivo TRH-induced increases in the plasma levels of glucagon, insulin and glucose in rabbits.

Thyrotropin-releasing hormone, TRH, increases the plasma levels of glucagon, insulin, glucose and free fatty acids in rabbits. However, TRH has no direct effects on the release of hormones neither from the endocrine pancreas in humans nor from the isolated perfused rat pancreas. The aim of the present study was to investigate if the effects of TRH in rabbits were mediated by the autonomic nervous system. The TRH "Roche"-induced hyperglucagonemia was inhibited by phentolamine (an alpha-receptor blocking drug), yohimbine (an alpha-2 -receptor blocking drug) and atropine. The TRH "Roche"-induced hyperinsulinemia was inhibited by propranolol (a beta-receptor blocking drug). The TRH "Roche"-induced hyperglycemia was inhibited by all four drugs. The TRH "Roche"-induced increases in the plasma levels of free fatty acids were not inhibited by the sympathetic and parasympathetic blocking drugs. The effects of TRH "Roche" on the plasma levels of glucagon, insulin and glucose cannot be explained by increases in the plasma levels of catecholamines. TRH, given intravenously into rabbits, may possibly act on regions in the central nervous system which control carbohydrate metabolism and the release of glucagon and insulin from the endocrine pancreas by sympathetic and parasympathetic mechanisms.

Animals↗
PubMed1985

Different acute in vivo effects of bacterial derived and pituitary growth hormone preparations on plasma levels of glucagon, insulin and free fatty acids in rabbits.

Intravenous injection of high doses of bacterial derived growth hormone (1 and 2 mg Somatonorm) did not affect the plasma levels of glucagon, insulin and free fatty acids in fasted and fed rabbits. On the other hand, 1 and 2 mg human extracted growth hormone (Crescormon) had stimulatory effects on plasma levels of glucagon, insulin and free fatty acids. These results indicate that the observed stimulatory effects in the rabbits were not due to the growth hormone molecule itself. It was shown by gel filtration and SDS electrophoresis that Crescormon contained constituents that were not present in Somatonorm. The differences in the observed metabolic effects of bacterial derived and pituitary growth hormone preparations in the rabbits could possibly be attributed to a human pituitary lipid-mobilizing factor LMF.

Animals↗
PubMed1985

Chronic recurrent abdominal pain in childhood due to mesenterium ileocolicum commune. Two cases with normal rotation of the intestine.

Mesenterium ileocolicum commune with normal rotation of the midgut is described in an 11-year-old girl and a 12-year-old boy. Both had had recurrent abdominal pain for several years before the diagnosis was made. Barium enema showed the entire colon to be located in the middle and left part of the abdomen. Operation showed displacement of the right colon due to the mesenterium ileocolicum commune. The boy also had congenital bands across the duodenum, which could explain previous episodes of vomiting and delayed emptying of the stomach after a barium meal. The girl had only rudimentary transduodenal bands. Fixation of the right colon, lysis of duodenal bands and appendectomy were performed in both cases. Postoperatively both children have been asymptomatic. These two cases, with a common ileocolic mesentery and normal midgut rotation, demonstrate a rare abnormality of intestinal fixation during the third embryonic stage of development. Diagnosis of the cause underlying the chronic recurrent abdominal pain was delayed, but the patients were eventually cured by operation.

Abdomen↗
PubMed1984

Alpha-melanocyte stimulating hormone increases plasma levels of glucagon and insulin in rabbits.

Intravenous injections of 25 and 2.5 micrograms alpha-melanocyte stimulating hormone (alpha-MSH) increased plasma levels of glucagon, insulin and free fatty acids in fasted and fed rabbits. 45 micrograms beta-melanocyte stimulating hormone (beta-MSH) had similar effects, whereas 22 micrograms gamma-2-melanocyte stimulating hormone (gamma-MSH) was inactive. The alpha-MSH-induced increases in the plasma levels of glucagon, insulin and free fatty acids were not inhibited by alpha- or beta-adrenergic blocking drugs. The alpha-MSH-induced increases in the plasma levels of insulin were, however, augmented by phentolamine (an alpha-adrenergic receptor blocking drug). The plasma levels of glucose were increased by 25 micrograms alpha-MSH in fed rabbits, only, and were decreased by alpha-MSH during alpha-receptor blockade. The acute in vivo effects of alpha-MSH and beta-MSH on the plasma levels of glucagon, insulin and free fatty acids were rather similar to those previously reported for corticotropin (ACTH). It is possible that the 4-10 ACTH sequence, present in alpha-MSH, beta-MSH and ACTH, but not in gamma-MSH, is a message sequence for the observed effects. However, ORG 2766, a 4-9 ACTH analogue, was inactive. The mechanism by which alpha-MSH increased the plasma levels of glucagon and insulin in rabbits remains to be determined. It is possible, that the effects were mediated by both a central nervous action and a direct action on the endocrine pancreas.

Adrenergic alpha-Antagonists↗
PubMed1984

Adrenergic effects on plasma levels of glucagon, insulin, glucose and free fatty acids in rabbits.

Adrenergic effects on plasma levels of glucagon, insulin, glucose and free fatty acids were studied in fasted rabbits by infusing epinephrine, norepinephrine, isoproterenol, phentolamine (an adrenergic alpha-receptor blocking drug) and propranolol (an adrenergic beta-receptor blocking drug). The adrenergic effects on the plasma levels of insulin, glucose and free fatty acids were similar to those found in other species. The plasma levels of insulin were increased by beta-receptor stimulation (isoproterenol, phentolamine + epinephrine) and decreased by alpha-receptor stimulation (epinephrine, norepinephrine, propranolol + epinephrine). The plasma levels of glucose were increased by both alpha- and beta-receptor stimulation, and the epinephrine-induced hyperglycaemia was only blocked by combined infusions with phentolamine and propranolol. The plasma levels of free fatty acids were increased by saline and further increased by beta-receptor stimulation (isoproterenol), while epinephrine and norepinephrine gave variable results. Alpha-receptor stimulation (propranolol + epinephrine) slightly decreased the plasma levels of free fatty acids. The plasma levels of glucagon, however, were mainly increased by alpha-receptor stimulation (epinephrine, norepinephrine, propranolol + epinephrine) and increased only to a minor extent by beta-receptor stimulation (isoproterenol, phentolamine + epinephrine) in rabbits. This is in contrast to results reported for humans, where beta-receptor stimulation seems to be most important in stimulating glucagon release.

Animals↗
PubMed1984

Acute in vivo stimulatory effects of human pituitary lipid-mobilizing factor on plasma levels of glucagon and insulin in rabbits.

The lipid-mobilizing factor LMF is prepared from deep-frozen human pituitary glands by alkaline extraction, followed by acetone precipitation at pH 4.8, Sephadex gel filtration and DEAE-cellulose chromatography. In addition to its adipokinetic effect in rabbits, LMF also increased the plasma levels of glucagon and insulin in rabbits in doses of 15 to 100 micrograms. The LMF-induced increases in the plasma levels of glucagon were most pronounced in fasted rabbits, whereas the increases in the plasma levels of insulin were most pronounced in fed rabbits. Glucose infusions decreased the LMF-induced hyperglucagonaemia and increased the LMF-induced hyperinsulinaemia. Somatostatin did not inhibit the LMF-induced hyperglucagonaemia with statistical significance, but inhibited the LMF-induced hyperinsulinaemia. The plasma levels of glucose were slightly decreased by 20 and 40 micrograms LMF in fasted rabbits and were unchanged in fed rabbits. In fasted rabbits, LMF had a toxic effect and 100 micrograms LMF killed one rabbits. Human growth hormone (hGH), prepared from the pituitary glands after removal of LMF, also increased the plasma levels of glucagon and insulin in rabbits. It is possible that the observed effects of LMF and hGH were due to the presence of some biologically active substances from the pituitary gland. These postulated substances could be involved in the pituitary control of the endocrine pancreas, and work is in progress to isolate them from the LMF preparation.

Animals↗
PubMed1984

Adrenergic effects on plasma levels of glucagon, insulin, glucose and free fatty acids in rabbits--influences of selective blocking drugs.

Species differences concerning the effects of alpha- and beta-receptor stimulation on glucagon release and carbohydrate metabolism have been reported. The aim of the present study was to investigate how the subtypes of alpha- and beta-receptors regulate the plasma levels of glucagon, insulin, glucose and free fatty acids in fasted rabbits. Epinephrine-induced 1) hyperglucagonaemia, 2) hypoinsulinaemia and 3) hyperglycaemia were significantly inhibited by alpha-2 receptor blockade (yohimbine), and not influenced by alpha-1 receptor blockade (prazosin). Isoproterenol-induced 1) hyperglucagonaemia was not affected by beta-1 or beta-2 receptor blockade, 2) hyperinsulinaemia was inhibited by a lower dose of beta-2 (ICI 118.551) than beta-1 receptor blockade (metoprolol), 3) hyperglycaemia was inhibited by beta-2 receptor blockade and 4) increases in the plasma levels of free fatty acids were blocked by beta-1 receptor blockade. It is concluded that in fasted rabbits: 1) plasma levels of glucagon are mainly increased by alpha-2 receptor stimulation, 2) plasma levels of insulin are decreased by alpha-2 receptor stimulation, and increased more by beta-2 than by beta-1 receptor stimulation, 3) plasma levels of glucose are increased by alpha-2 and beta-2 receptor stimulation and 4) the plasma levels of free fatty acids are increased by beta-1 receptor stimulation.

Adrenergic alpha-Antagonists↗
PubMed1984

Acute in-vivo effects of adrenocorticotrophin on plasma levels of glucagon, insulin, glucose and free fatty acids in rabbits: involvement of the alpha-adrenergic nervous system.

Intravenous injection of 8.5 nmol (1-24)ACTH increased the plasma levels of glucagon, insulin, glucose and free fatty acids in rabbits. The (1-24)ACTH-induced hyperglucagonaemia and hyperinsulinaemia started 3 and 20 min after the injection respectively. Similar increases in the plasma levels of glucagon, insulin and free fatty acids were found with 5.3 nmol (1-39)ACTH, whereas (1-4)ACTH, (4-10)ACTH, (1-10)ACTH, (11-24)ACTH, (7-38)ACTH and (18-39)ACTH (corticotrophin-like intermediate lobe peptide) injected at doses of approximately 8 nmol were inactive. Infusions with the alpha-adrenergic blocking drug, phentolamine, reduced the (1-24) ACTH-induced hyperglucagonaemia and hyperglycaemia, and augmented the (1-24)ACTH-induced hyperinsulinaemia, which now became significant after 5 min. Infusions with the beta-adrenergic blocking drug, propranolol, did not diminish the (1-24)ACTH-induced effects, but killed the rabbits after 2-4 h. It is concluded that the acute in-vivo effects of ACTH in rabbits are modulated by the involvement of alpha-adrenergic receptors, which increased the plasma levels of glucagon and glucose, and delayed and diminished the ACTH-induced increases in the plasma levels of insulin. The (1-24)ACTH-induced increases in the plasma levels of free fatty acids were not influenced by the adrenergic blocking drugs.

Adrenocorticotropic Hormone↗