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Biomedical subjects

T Toyota

Publications and source records attributed to T Toyota.

At least 361 records · Page 20Linked to original sources
PubMed1983

Disturbances of the alimentary tract motility and hypermotilinemia in the patients with diabetes mellitus.

Lower esophageal sphincter pressure (LESP), gastric emptying, small bowel transit time and plasma motilin levels were measured in diabetics and normal subjects in order to investigate the disturbances of the alimentary tract motility and the participation of motilin in these motility disorders. Hypermotilinemia was observed in all diabetics with or without autonomic neuropathy. Low response of LESP to tetragastrin found in diabetics with autonomic neuropathy could not be explained by motilin. Gastric emptying was highly correlated with fasting plasma motilin levels and a significantly accelerated gastric emptying observed in diabetics without complications or diabetics with diarrhea was considered to be due to hypermotilinemia. On the contrary, no significant correlation was observed between small bowel transit time and plasma motilin levels, suggesting no participation of endogenous motilin in the regulation of small bowel transit.

Adolescent↗
PubMed1983

Gastric inhibitory polypeptide (GIP) response to an oral glucose load in the patients with diabetes mellitus.

Plasma gastric inhibitory polypeptide (GIP) concentrations following an oral glucose load were measured in 27 diabetics and 10 normal subjects. Plasma GIP concentrations increased significantly from the mean basal value following an oral glucose load in both groups. Diabetics showed significantly higher levels of plasma GIP in association with delayed and diminished peak increases in plasma insulin levels. When diabetics were divided into two groups according to their basal levels of blood glucose, moderate and severe diabetics exhibited more exaggerated increments of plasma GIP than mild diabetics. This exaggerated GIP response to an oral glucose load in proportion to the glucose intolerance indicates a relative failure of the beta cell response to GIP in diabetics and that the mechanism involved in hypersecretion of GIP would be diminution of the inhibition of GIP release caused by insulin in diabetics.

Adult↗
PubMed1983

Morphometrical quantitation of pancreatic endocrine cells in patients with carcinoma of the pancreas.

A morphometrical study of the tumor-free pancreatic regions has been performed in 18 patients with carcinoma of the pancreas, who were divided into three groups, i.e., diabetics, patients exhibiting impaired glucose tolerance (IGT) and normoglycemics. Tissues were stained for A, B, D and PP cells by immunocytochemistry and, for comparative purposes, the results were expressed as the number of cells/mm2. The diabetic and the IGT groups presented reduced A and B cell populations, with B cell counting lower in diabetics than in the IGT group. In addition, an inverse correlation was found between the number of B cells and the fasting plasma glucose (FPG) values, which suggests that the destruction of B cells may be the primordial cause of the glucose abnormality found in those patients. Possibly, a destructive process and fibrosis, similar to those occurring in chronic pancreatitis, are implicated in the reduction of such endocrine cells.

Adenocarcinoma↗
PubMed1983

Diabetic scleredema.

Many skin lesions are specific for diabetes mellitus. Necrobiosis lipoidica, lipoatrophy and idiopathic bullae (bullosis diabeticorum) are usually associated with diabetes. However, diabetic scleredema has not been noticed by internists, although dermatologists have paid attention to such a cutaneous manifestation. We reported a clinical case of a female diabetic patient aged 15 who had been afflicted with diabetic scleredema. She had been treated with insulin since 5 years of age. She noticed stiffness of the skin in April 1980. Skin biopsy showed thickness of the dermis and accumulation of acid mucopolysaccharide. After control of blood glucose with continuous subcutaneous insulin infusion (CSII) and administration of tocopherol acetate and hyaluronidase, the skin lesion improved. Etiology of diabetic scleredema is unknown. Such skin lesion which is observed frequently in insulin dependent obese patients is different from a category of scleredema of Buschke.

Adolescent↗
PubMed1983

Immunologic aspects of the nonobese diabetic (NOD) mouse. Abnormalities of cellular immunity.

Experiments were performed on 12-wk-old nonobese diabetic (NOD) mice to investigate the immunologic background of the condition, using ICR mice as controls. The results indicate the following: (1) absolute decreases in number of T lymphocytes, (2) depression of natural killer activity, (3) normal responsiveness in delayed type hypersensitivity and functional depression of killer T cells against allogeneic tumors, (4) diminished resistance to herpes virus infection, and (5) enhanced production of polyclonal antibodies to T cell-dependent antigens. These features are similar to those noted in other autoimmune diseases of man and in their experimental models in laboratory animals. Elucidation of the pathogenetic mechanism of autoimmune diabetes mellitus in NOD mice, therefore, may contribute to the diagnosis, treatment, and prevention of a wide variety of autoimmune diseases.

Animals↗
PubMed1982

[The effect of calcium on the release of gastric inhibitory polypeptide (GIP) - with reference to the release of GIP in patients with hyperparathyroidism (author's transl)].

Plasma gastric inhibitory polypeptide (GIP), insulin, glucagon concentrations and blood glucose levels in response to the ingestion of 100 g glucose were measured in 5 patients with hyperparathyroidism in order to elucidate the effect of hypercalcemia on the release of these hormones. In addition, the effect of acute hypercalcemia on the release of these hormones in response to glucose ingestion was investigated in normal subjects. Fasting plasma GIP concentration in patients with hyperparathyroidism was significantly greater than the value in seventeen normal subjects. Significantly higher responses of plasma GIP and insulin were observed after the glucose ingestion in the patients with hyperparathyroidism as compared with the values in the normal subjects, and integrated GIP and insulin responses to the glucose ingestion for 120 min in the patients with hyperparathyroidism were significantly greater than the values in the normal subjects. On the other hand, plasma glucagon concentration after the glucose ingestion in the patients with hyperparathyroidism remained unchanged, although plasma glucagon concentrations after the glucose ingestion decreased significantly from the basal value in the normal subjects. Blood glucose levels after the glucose ingestion in two groups increased significantly from the basal value in the same manner. In nine normal subjects calcium infusion (4 mg/kg bolus injection followed by continuous infusion of 4 mg/kg/hr for 3 hr) caused a significantly high concentration of plasma calcium (11.5 approximately 13.0 mg/dl) from the basal value. Significantly higher responses of plasma GIP and insulin to the glucose ingestion were observed during calcium infusion as compared with the values during saline infusion. On the other hand, plasma glucagon concentration after the glucose ingestion was not significantly changed during calcium infusion in contrast with a significant decrease of plasma glucagon after the glucose ingestion during saline infusion. Consequently, calcium was considered to play a major part in the release of GIP and insulin. The characteristic response of plasma glucagon during calcium infusion was considered, at least in part, to protect the hypoglycemia caused by hyperinsulinemia.

Adult↗
PubMed1982

Release of gastric inhibitory polypeptide (GIP) during calcium infusion and in hyperparathyroidism.

Gastric inhibitory polypeptide (GIP) is a candidate hormone for an incretin which stimulates or potentiates insulin secretion. We elucidated that, in five patients with hyperparathyroidism, GIP and insulin responded remarkably to glucose ingestion, and that hypercalcaemia appeared to have a stimulatory effect on glucose-induced GIP release as well as on insulin release. In nine healthy subjects a 2% calcium solution was continuously infused intravenously and a hypercalcaemic state was maintained. This caused GIP to respond significantly more to glucose ingestion. In spite of GIP being considered an incretin in the normoglycaemic state, GIP does not markedly stimulate insulin secretion. However, in the hypercalcaemic state in healthy subjects, glucose-induced GIP and insulin secretion is significantly greater than in the normocalcaemic state. The potentiated response of insulin to glucose may be caused, in part, by GIP.

Adult↗
PubMed1982

Infusion-free hemodiafiltration: simultaneous hemofiltration and dialysis with no need for infusion fluid.

A new simultaneous hemofiltration and dialysis system was developed which has no need of infusion fluid. The system employs two hemodiafilters in a direct series. An ultrafiltration rate and dialysate flow rate control system was employed to control the dialysate flow at the inlet and outlet, and the difference in volume was arranged to be the amount of water removed from the body. When the blood circuit was narrowed between the two hemodiafilters, the ultrafiltration was performed at the first hemodiafilter; at the second one, the dialysate moved to the blood side as a dilution fluid. To remove pyrogens and bacteria, tap water was subjected to activated charcoal, ion exchange and reverse osmosis treatment, followed by preparation of the dialysate. In clinical evaluation, this system showed marked improvement in clearance of middle and large molecules.

Adult↗
PubMed1982

Platelet sensitivity to adenosine diphosphate and to prostacyclin in diabetic patients.

We studied the platelet sensitivity to adenosine diphosphate (ADP) and to prostacyclin (PGI2) in order to clarify the mechanism of the onset or development of diabetic retinopathy. The platelet sensitivity to ADP in diabetics with simple and proliferative retinopathy was significantly increased as compared with that in diabetics without retinopathy and in controls. The platelet sensitivity to PGI2 in diabetics with simple and proliferative retinopathy was decreased significantly as compared with the normal value. There was a significant negative correlation between the platelet sensitivity to ADP and that to PGI2 in all diabetics. Since the effect of PGI2 on platelets is to inhibit its aggregation, the decreased sensitivity to PGI2 implies a tendency to accelerate platelet aggregation. The increased platelet aggregation due to the alteration of the platelet sensitivity is considered as an important factor in diabetic microangiopathy.

Adenosine Diphosphate↗
PubMed1982

Impaired insulin secretion in the spontaneous diabetes rats.

Dynamics of insulin and glucagon secretion were investigated by using a new model of spontaneous diabetes rats produced by the repetition of selective breeding in our laboratories. The perfusion experiments of the pancreas showed that the early phase of insulin secretion to continuous stimulation with glucose was specifically impaired, although the response of the early phase to arginine was preserved. The glucose-induced insulin secretion in the nineth generation (F8) which had a more remarkably impaired glucose tolerance was more reduced than in the sixth generation (F5). No significant difference of glucagon secretion in response to arginine or norepinephrine was noted between the diabetes rats and control ones. The present data indicate that the defective insulin secretion is a primary derangement in a diabetic state of the spontaneous diabetes rat. This defect in the early phase of glucose-induced insulin secretion suggests the specific impairment of the recognition of glucose by the pancreatic beta-cells. The spontaneous diabetes rats are very useful as a model of disease for investigating pathophysiology of non-insulin dependent diabetes mellitus.

Animals↗
PubMed1982

Remission of insulin resistant diabetes in two patients with anti-insulin receptor antibodies.

Since Kahn et al. reported in 1976 insulin resistant diabetes due to anti-insulin receptor antibodies, an unusual form of diabetes mellitus (type B) has been found in many countries. We had two diabetic patients with anti-insulin receptor antibodies, associated with either acanthosis nigricans or systemic lupus erythematosus. Remission occurred 15 months after the onset of insulin resistant diabetes. One patient unfortunately died of acute pneumonia and the other has been followed up. The anti-insulin receptor antibodies were measured according to the method of Omori and Hirata by using the pellet of human placental membrane. The anti-insulin receptor antibodies in both cases diminished as remission occurred. Reverse hemolytic plaque assay (PFG) detected immunoglobulin-producing cells. In Case 2, the plaque forming cells were twenty times as many as the normal value. Immunosuppressive therapy with cyclophosphamide reduced the immunoglobulin secreting cells as remission occurred. The patients with insulin resistance (type B) should be treated with enough insulin inspite of the presence of insulin resistance. Besides, cyclophosphamide, 6-mercaptopurine and prednisolone should be used with caution. Plasma exchange is a treatment to be tried. It is important to note that spontaneous remission may occur more than half a year after the onset of insulin resistant diabetes.

Adult↗