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Biomedical subjects

K Kosaka

Publications and source records attributed to K Kosaka.

At least 451 records · Page 25Linked to original sources
PubMed1978

Insulin binding and glucose metabolism in adipocytes of streptozotocin-diabetic rats.

To investigate the mechanism of the cellular insulin insensitivity of diabetic rats, insulin binding, glucose transport, and glucose oxidation were studied in adipocytes from streptozotocin-diabetic rats. Increased insulin binding was found in cells from diabetic rats, and this was due to an increased number of insulin receptors rather than a change in receptor affinity. Basal and insulin-stimulated glucose oxidation was decreased in adipocytes from diabetic rats when the data are expressed in absolute terms or as percent increased above basal. Although the absolute rate of basal and insulin-stimulated glucose transport was decreased in adipocytes from diabetic rats, the percent increase above basal of insulin-stimulated glucose transport was not decreased. In conclusion, although the cellular insulin insensitivity exists in adipocytes from diabetic rats, the number of insulin receptors was increased, coupling between insulin receptors and the glucose transport system is intact in adipocytes from diabetic rats, and a defect in intracellular glucose metabolism rather than glucose transport plays a major role in the insulin insensitivity of adipocytes from diabetic rats.

Adipose Tissue↗
PubMed1978

Effects of antiinsulin receptor autoantibody on the metabolism of rat adipocytes.

We have studied the effects of the serum from a patient with an unusual form of diabetic syndrome with extreme insulin resistance on the metabolism of rat adipocytes in vitro. This serum and IgG fractions from it inhibited the [125I]insulin binding to isolated adipocytes and stimulated the 2-deoxyglucose uptake, glucose oxidation, and the incorporation of amino acids into protein. In addition, these fractions inhibited the lipolysis induced by beta 1-24 ACTH in isolated adipocytes. The insulin-like effects of this serum and the effects of insulin were not additive at their maximal concentrations. The inhibition of [125I]insulin binding was due to a decrease in receptor affinity rather than to a change in receptor number by Scatchard plot analysis. Both the inhibition of insulin binding and the insulin-like effects on rat adipocytes were neutralized by antihuman IgG. In addition, these insulin-like effects were abolished by trypsin treatment of adipocytes. These facts suggest that this serum has a circulating antibody directed at or near the insulin receptor itself and that this antibody mimics the insulin effect on rat adipocytes by binding to the insulin receptor in vitro.

Adipose Tissue↗
PubMed1978

Induction of growth hormone and prolactin secretion by luteinizing hormone-releasing hormone and its blockade by bromoergocriptine in acromegalic patients.

In an attempt to evaluate the effect of LRH on GH and PRL secretion, LRH in a dose of 100 micrograms was injected iv to 22 patients with active acromegaly. A definite increase in both serum GH and PRL levels was observed in one patient, while four other subjects responded to LRH to secret either GH or PRL. The effectiveness of LRH on GH and PRL release was not correlated with the age or sex of patients, the basal levels of serum GH or PRL, the GH response to TRH administration, or the increase in serum gonadotropin concentrations after LRH injection. In three patients, this LRH-induced GH and PRL release was completely blocked by pretreatment with 2-bromo-alpha-ergocriptine (CB154). The results suggest that elevations of GH and PRL after LRH occur rather sporadically in acromegalic patients and that the action of LRH on GH release is occasioned by a different mechanism from that of TRH.

Acromegaly↗
PubMed1978

Degradation and secretion of insulin in hepatic cirrhosis.

To clarify the mechanism of hyperinsulinism of hepatic cirrhosis, plasma insulin and C-peptide levels before and after oral glucose loads were measured in 34 patients with cirrhosis, 15 patients with chronic hepatitis, and 25 normal subjects. While plasma immunoreactive insulin (IRI) levels during oral glucose tolerance testing (OGTT) were significantly increased in cirrhotics, plasma immunoreactive C-peptide (CPR) levels were elevated slightly. The C-peptide to insulin ratio throughout OGTT was significantly smaller in cirrhotics than in normal subjects (P less than 0.01). A decreased hepatic insulin degradation rate has been suggested to one of the main causes of hyperinsulinism in hepatic cirrhosis. The ratio of the difference between basal and 30-min CPR values and basal and 30-min OGTT blood glucose values [delta CPR: delta BS(30)'] as well as the delta IRI: delta BS(30') ratio was significantly decreased in cirrhotics (P less than 0.01). These results indicate that insulin secretion in response to a glycemic stimulus is reduced in cirrhotics. Both the ratios of the sums of six IRS and CPR values of OGTT (sigma CPR: sigma IRI) and delta CPR: delta BS(30') and sigma CPR: sigma BS(30') were found in inverse relationship with indocyanine green retention rate in cirrhotics.

Adult↗
PubMed1978

Comparison of the early time courses of the release of insulin that follow injections of tetragastrin, tolbutamide, xylitol, and glucose into the pancreatic artery of dogs.

The early time courses of insulin release were studied by injecting insulinotropic substances directly into a dog's pancreatic artery. Blood samples from the pancreatic vein were collected every five seconds continuously over 90 seconds and were assayed for their insulin concentrations. Injections were repeated two to five times, with intervals of 30 minutes. Insulin release was stimulated within one minute after injection of each of tetragastrin, tolbutamide, xylitol, and glucose, but the time courses of the release of insulin were different with different stimulants: Tetragastrin and tolbutamide increased insulin release faster than did glucose; xylitol produced a slower insulin release than did glucose. The slower insulin-releasing effects of glucose and xylitol than the other agents would be compatible with the theory that their metabolism is required to cause release of insulin, but it is also possible that the glucoreceptor mechanism may require a longer lag time than the other receptor mechanisms for the perception and transfer of the signal to release insulin.

Animals↗
PubMed1978

Effects of anti-insulin receptor autoantibodies on the metabolism of human adipocytes.

We studied the effect of sera from two patients who had an unusual form of diabetic syndrome with extreme insulin resistance on the metabolism of human adipocytes in vitro. The IgG fractions from sera A and B, which were obtained from two patients (1 and 2) with insulin-resistant diabetes, inhibited [125I] insulin binding to human adipocytes and, at the same time, stimulated glucose oxidation and inhibited the lipolysis induced by levarterenol in human adipocytes. On the other hand, the IgG fraction from the C serum, which was obtained from patient 2 after her diabetic syndrome had completely disappeared as a result of immunosuppressive therapy, did not inhibit [125I] insulin binding to human adipocytes, stimulate glucose oxidation, or inhibit lipolysis in human adipocytes. These facts suggest that these IgG fractions bind to or near the insulin receptor of human adipocytes, that they exhibit their insulin-like effect by binding to the insulin receptor in vitro, and, furthermore, that they are responsible for the extremely insulin-resistant diabetes. However, the apparent discrepancy between the effects of these IgG fractions on man in vitro and in vivo is puzzling and needs to be explained.

Adipose Tissue↗
PubMed1978

Effect of ACTH on the relaxation of guinea pig trachea with various bronchodilators.

The effect of ACTH on the actions of various bronchodilators was examined using the isolated guinea pig tracheal smooth muscle. Relaxing effects of isolated guinea pig tracheal smooth muscle with 1-isoproterenol hydrochloride, salbutamol hemisulfate, hexoprenaline hydrochloride and epinephrine except prostaglandin E2 and aminophylline were markedly potentiated by combining ACTH. These results may suggest that ACTH has a direct effect on guinea pig tracheal smooth muscle by potentiating the actions of various beta-receptor stimulators.

Adrenocorticotropic Hormone↗
PubMed1978

Establishment and characterization of a human cancer cell line that produces human colony-stimulating factor.

A human colony-stimulating factor (CSF) producing cell line, T3M-1, has been established from explant cultures of a human squamous cell carcinoma of the oral cavity that secretes human CSF. It has been continously propagated during the past 15 months. The cells grew in a monolayered sheet with about 17 hr of population-doubling time and showed a colony-forming capacity with about 5% plating efficiency. The cells exhibited an epithelioid morphology resembling the structure of the original tumor, and they showed "tumor takes" when inoculated into nude mice. Karyotypic analysis revealed the cell line to be a human aneuploid one with a hypotriploid mode, including the Y-chromosome(s) and at least 10 common markers. T3M-1 cells possess the characteristic function of human CSF production in vitro, and a marked neutrophilia was observed in nude mice bearing the tumors produced by inoculation with the T3M-1 represents a new human cell line that secretes human CSF.

Animals↗