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Biomedical subjects

K Kosaka

Publications and source records attributed to K Kosaka.

At least 469 records · Page 26Linked to original sources
PubMed1977

Multiple system degeneration and involving thalamus, reticular formation, pallido-nigral, pallido-luysian and dentato-rubral systems. A case report.

An autopsy case of multiple system degeneration is characterized by the following; (1) progressive dementia and abnormal sleep patterns, followed by Parkinsonian symptoms with terminal akinetic mutism; (2) severe symmetrical degeneration in the thalamus, particularly nucl. medialis thalami, the reticular formation of the brain stem, also the pallidonigral, pallido-Luysian and dentato-rubral systems. As far as we known, there is no case in the literature, of combined system degeneration, which shows such a wide anatomical range of lesions as the present one. Clinico-pathological correlation between dementia and degeneration of the thalamus, and between abnormal sleep-consciousness mechanism and degeneration of the reticular formation are discussed. The extrapyramidal symptoms are discussed from the clinico-pathological aspect. In addition, peculiar eosinophilic bodies are described, which were most frequently found in the putamen.

Adult↗
PubMed1977

Comparative effects of native insulin and insulin-dextran complexes on the metabolism of adipose tissue.

Insulin-dextran complexes have been prepared and their biological activities compared to that of native insulin. Complexes referred to as T-70 had a molecular weight of about 450 000, T-2000 being more than 2 million. Insulin-dextran T-70 was stable and no release of free insulin from the complex was observed upon its incubation with adipose tissue. Insulin-dextran T-70 mimicked the effects of native insulin upon adipose tissue metabolism. It also lowered blood sugar. These effects necessitated, on an insulin molar basis, concentrations of the complex that were 10-times greater than those needed for native insulin. Maximal concentrations of insulin complex T-70 or native insulin elicited similar quantitative effects. This suggested that when the concentration of insulin-dextran T-70 was high enough, the complex occupied a sufficient number of receptor sites to produce maximal stimulation of the tissue. In contrast, insulin-dextran T-2000 was barely effective, indicating that, probably due to its size, it was unable to reach receptor sites. The size, stability and metabolic effects of insulin-dextran T-70 observed in this study give additional support to the concept that insulin action is probably mediated via a series of events initiated at the level of the plasma membrane of adipocytes.

Adipose Tissue↗
PubMed1977

Effect of vasoactive intestinal polypeptide infused intrapancreatically on glucagon and insulin secretion.

Synthetic vasoactive intestinal polypeptide (VIP) was infused at a dose of 50 ng/kg/min for 10 min into the cranial pancreaticoduodenal artery in anesthetized dogs. Both mean blood flow and plasma glucagon concentration in the cranial pancreaticoduodenal vein were significantly enhanced during the infusion, indicating a great augmentation in glucagon output. The pancreatic venous plasma concentration of insulin was not significantly raised, but its output increased during the infusion, again due to the increase in plasma flow. Plasma concentration of glucagon in the femoral artery was not significantly augmented, whereas that of insulin was enhanced during VIP infusion. Mean arterial plasma glucose levels rose gradually during the infusion. Intrapancreatic pretreatment with propranolol failed to exert any significant inhibiting effect upon the VIP-induced enhancement in plasma glucose, pancreatic venous blood flow, or bihormonal output. These results suggest that the vasoactive polypeptide of intestinal origin may regulate the function of the endocrine pancreas and that this effect may not be mediated mainly via the beta-adrenergic receptor system.

Animals↗
PubMed1977

Radioimmunoassay of main urinary metabolite of prostaglandin F2alpha in normal subjects.

Radioimmunoassay of 5alpha, 7alpha-dihydroxy-11-keto-tetranor-prosta-1,16-dioic acid, main urinary metabolite of prostaglandin F2alpha (PGF2alpha-MUM), was performed in normal subjects. Twenty-four hours secretion of PGF2alpha-MUM were 29.04 +/- 9.73 microgram in males and 18.22 +/- 5.88 microgram in females on an average. And an oral administration of aspirin resulted in the remarkable decrease of PGF2alpha-MUM in both sexes.

Aspirin↗
PubMed1977

Effect of alpha adrenoreceptor stimulants infused intrapancreatically on glucagon and insulin secretion.

To see the effect of alpha adrenergic receptor stimulation upon in vivo basal secretion of glucagon and insulin, phenylephrine and methoxamine were infused at a dose of 236 pmol/kg/min and 2.36 nmol/kg/min, respectively, for 10 min into the cranial pancreaticoduodenal artery in anesthetized dogs. During the infusion of either drug pancreatic venous blood flow was markedly diminished, resulting in a significant decrease of basal output of both glucagon and insulin. Intrapancreatic administration of the stimulants exerted neglible effects on the plasma levels of both hormones in the systemic circulation. Pretreatment with phentolamine abolished the alpha stimulant-induced inhibition of bihormonal output. Under alpha blockade which per se results effectively in a stimulation of insulin release, basal output of glucagon was not significantly augmented. These results suggest that the alpha receptors on the A cell of the islets may be involved in the similar inhibitor mechanism, but less potently than those on the B cell under basal physiological adrenergic control in the canine.

Animals↗
PubMed1977

Insulin secretion in hypoglycemia after adrenal vein ligature or splachnicotomy.

During bonito insulin-induced hypoglycemia in dogs, pancreatic venous dog insulin concentration (IRI), radioimmunoassayed differentially from bonito insulin, was progressively diminished in response to local glucose infusion (0.6 mg/kg - min) for 4 min into the superior pancreaticoduodenal artery. Basal arterial plasma glucose was significantly lower after bilateral splanchnicotomy (BSNC) than after bilateral adrenal vein ligature (BAVL). During local glucose infusion in both normoglycemia and hypoglycemia, the increment of pancreatic venous IRI was significantly greater after BAVL or BSNC than in the controls, and the increment of pancreatic venous glucose was also significantly greater after BAVL than in the controls or after BSNC. It is suggested that under the stress of major surgery the splanchnic nerves partially suppress insulin secretion in normoglycemia as well as in hypoglycemia, and epinephrine released from the adrenal medulla may interfere with glucose-mediated insulin secretion in profound hypoglycemia.

Adrenal Glands↗
PubMed1977

Effects of fasting and refeeding of insulin receptors and glucose metabolism in rat adipocytes.

To investigate the mechanism of insulin insensitivity during fasting and hyperresponsiveness to insulin after refeeding, insulin binding, 2-deoxyglucose uptake and glucose oxidation were measured in adipocytes from three groups of rats: control, 48 h fasted, and 48 h refed after 48 h fasting. In 48 h fasted rats, fat cell diameters were decreased to five-sixths of that of the controls and plasma insulin levels were decrease to less than half of the controls; however, after 48 h refeeding, these parameters were restored to normal. In adipocytes from fasted rats, insulin binding was increased but insulin-stimulated 2-deoxyglucose uptake glucose oxidation were significantly decreased as compared to that of the controls. In adipocytes of refed rats, insulin bindings was slightly increased as compared to the controls, accompanied by a slightly decreased 2-deoxyglucose uptake and completely restored glucose oxidation. Conclusions from these studies are that both disorders in coupling of insulin-receptor complexes to glucose transport systems and intracellular glucose metabolism play major roles in the insulin insensitivity of adipocytes from fasted rats, whereas, in adipocytes from refed rats, intracellular glucose metabolism, rather than glucose transport, is mainly involved in restoring insulin sensitivity.

Adipose Tissue↗
PubMed1977

Effect of bromoergocriptine on TRH-induced growth hormone and prolactin release in acromegalic patients.

In an attempt to evaluate the dynamics of growth hormone (GH) and prolactin secretion in acromegalic patients, the response of serum GH as well as prolactin to 2-bromo-alpha-ergocriptine (CB154) alone or to CB154 combined with thyrotropin-releasing hormone (TRH) was studied in 8 subjects with this disease. Oral administration of CB154 unequivocally decreased serum prolactin levels in all of the 8 patients, while GH-inhibitory action of the drug was observed only in 6 subjects who responded to TRH with secretion of GH. The response of serum GH to TRH was not qualitatively and quantitatively altered by the treatment of patients with CB154 in a daily dose of 5 mg for two weeks. This treatment, on the other hand, remarkably suppressed basal levels of prolactin and completely blocked TRH-induced prolactin release in all of the subjects. The results suggest that there exists a dissociation between GH and prolactin responses to CB154 in acromegalic patients, and that CB154 and TRH may not share a common site of action on GH release in this pathologic state.

Acromegaly↗
PubMed1977

Heterogeneity of prolactin and TSH response to TRH in hypotonadotropic hypogonadism.

To evaluate prolactin and TSH secretion in isolated gonadotropin deficiency, thyrotropin-releasing hormone (TRH), in a dose of 500 microgram, was administered iv to fifteen male subjects with this disorder. In 4 out of 8 untreated patients, TRH-mediated prolactin release was significantly blunted and this attenuated response was not improved in one patient after treatment with testosterone for 1 year. In 7 patients who were treated with testosterone for 2 to 8 years, four failed to show a normal prolactin response after TRH injection. TRH-induced TSH secretion, on the other hand, was attenuated in two out of 8 untreated and in two of 8 treated patients with hypogonadotropic hypogonadism. The decreased TSH reserve was not necessarily associated with the poor prolactin response to TRH. It was concluded that heterogeneity exists in TRH-mediated prolactin and TSH release in "isolated" gonadotropin deficiency syndrome.

Adolescent↗
PubMed1977

A radioreceptor assay for insulin: direct measurement of dog pancreatic vein serum insulin.

A simple radioreceptor assay for insulin rat liver membranes as receptor sites, with sufficient specificity precision, and sensitivity to detect 10 ng or 276 muU/ml of serum insulin, has been developed. In the presence of standard porcine insulin at the concentration of 1.0 ng/tube, approximately 8% of 125I-porcine insulin was bound to the plasma membranes and ninety-five per cent of this binding was inhibited by 1.0 microgram of standard insulin per tube. Four animal insulins inhibited the binding of 125I-insulin while ACTH, glucagon, human growth hormone, and oxytocin were inert. Insulin values in dog pancreatic vein sera obtained during and after glucose loading and measured by the present radioreceptor assay agreed well with immunoreactive insulin. The ratio of IRI to the measurement by radioreceptor assay was 1.09 +/- 0.18 for the same sera.

Adrenocorticotropic Hormone↗
PubMed1977

Association of human leukocyte antigen (HLA)-B5 and -BW22-J with hepatic cirrhosis of apparently unknown etiology.

The majority of patients with hepatic cirrhosis in Japan do not have a history of acute hepatitis or alcoholism. Twenty-nine patients with hepatic cirrhosis which were thought as random samples from cirrhotic patients without a history of acute hepatitis or alcoholism were Human Leukocyte Antigen (HLA) typed. Association of HLA-B5 and -BW22-J with hepatic cirrhosis of apparently unknown etiology was found in p less than 0.003, and p less than 0.01, respectively (128 controls). A predisposition linked to HLA-B5 or -BW22-J related gene or genes seems to play a role in the development of hepatic cirrhosis, at least in a substantial part of patients with hepatic cirrhosis of apparently unknown etiology in Japan.

Adult↗