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Biomedical subjects

A Ohneda

Publications and source records attributed to A Ohneda.

At least 73 records · Page 4Linked to original sources
PubMed1981

Thickening of basement membrane of muscle capillary in spontaneously diabetic KK mice.

In order to clarify the relationship between the thickening of muscle capillary basement membrane (MCBM) and diabetes mellitus, an experimental study was carried out using spontaneously diabetic KK mice. Glucose tolerance tests and the measurements of the width of MCBM were performed in KK mice and DD mice at the age of one week through 16 months. The KK mice, in general, revealed a less increase in body weight, compared with the control mice. Impaired glucose tolerance in the KK mice was observed at the age of 2 weeks and remained for 12 months. The width of MCBM increased in both KK and DD mice with the aging process until 6 months. Thereafter, however, the KK mice revealed a significant increase of the width of MCBM. In both KK mice and DD mice, significant correlations were observed between age and the width of MCBM. In contrast, there was no significant correlation between glucose intolerance figured out as the sum of blood glucose levels and the width of MCBM. The present study suggests that the thickening of MCBM in the KK mice may occur as an aging phenomenon on the one hand and may develop as the consequence of long-term carbohydrate derangement based on genetic disposition on the other hand.

Aging↗
PubMed1980

Response of extrapancreatic glucagon to glycemic changes.

Since the secretion of pancreatic glucagon is largely influenced by changes in the blood glucose level, the response of extrapancreatic glucagon to glycemic changes was investigated in man and dogs. Neither insulin-induced hypoglycemia nor arginine infusion caused a rise in plasma glucagon in two patients with total pancreatectomy, but plasma glucagon increased transiently in one of the two patients after oral glucose load. Glucose-induced hyperglycemia did not alter plasma glucagon in the portal vein in a group of 4 depancreatized dogs. When blood glucose fell lower than 50 mg/100 ml after insulin infusion in a group of 7 depancreatized dogs, plasma glucagon in the portal vein did not increase significantly. The administration of 2-deoxyglucose did not cause any changes in plasma glucagon in the portal vein in a group of 5 pancreatectomized dogs. After the ligation of the hepatic artery, blood glucose decreased gradually in a group of 5 pancreatectomized dogs with portacaval shunt, but plasma glucagon in the vena cava was not altered significantly. It is concluded from the present study that regulation of extrapancreatic glucagon differs from that of pancreatic glucagon.

Animals↗
PubMed1979

Production of a specific antiserum by synthetic C-terminal fragment of glucagon.

Seven rabbits were immunized with a synthetic C-terminal glucagon fragment [15--29] conjugated with bovine serum albumin by means of glutaraldehyde. Antisera for glucagon were produced in all the animals after six injections of the conjugate. One of them revealed a higher titer antiserum (G42), which did not cross react with gut glucagon-like immunoreactive material, secretin, insulin, gastric inhibitory polypeptide or vasoactive intestinal peptide. From the results of inhibition of 125 I-glucagon in binding with the antiserum by various glucagon-related fragments the immunogenic determinant of the antiserum was proved to be in the C-terminal residue of the glucagon molecule, although peptide [17--29] or [21--29] reacted weakly with the antiserum. The plasma glucagon levels measured by antiserum G 42 during an arginine test in five normal subjects were superposed on those obtained by other antiserum (G21), specific for pancreatic glucagon. Furthermore, a comparable standard curve for glucagon was obtained using antiserum G42, when a labelled p-hydroxyphenylacetylated glucagon fragment [15--29] was employed as a tracer. The present study clearly demonstrated that the C-terminal glucagon fragment could yield a specific antiserum for pancreatic glucagon, supporting the proposal that the C-terminal fragment of glucagon is responsible for such specific antisera. Furthermore, it is concluded that immunoassay for glucagon could be performed using the labelled glucagon fragment as a tracer.

Amino Acid Sequence↗
PubMed1979

Enzyme immunoassay of pancreatic glucagon at the picogram level using beta-D-galactosidase as a label.

An enzyme immunoassay of pancreatic glucagon was established by using E. coli beta-D-galactosidease [EC 3.2.1.23] as a marker. In order to increase the sensitivity of the immunoassay, different peptides obtained from glucagon fragments were used to produce the enzyme conjugate and the immunogen. Antiserum N6E raised against C-terminal fragment peptide (15-29) could be diluted to more than 1 : 100,000 in the assay and was highly specific for pancreatic glucagon. The antiserum reacted well with the C-terminal fragment peptide (21-29) as well as another fragment peptide (15-29) and pancreatic glucagon. The enzyme immunoassay using antiserum N6E and fragment peptide (21-29)-enzyme conjugate could detect as little as 1 to 2 pg of glucagon. The mean recovery of glucagon added to serum specimens was 104% and the coefficients of variation were 3.7-14.5% (within assay) and 9.0-18.5% (between assay).

Escherichia coli↗
PubMed1979

Heterogeneity of plasma insulin and triglyceride levels in obesity demonstrated by family study.

Fifty relatives of 7 families with high prevalence of obesity were investigated and the possibility was shown that there were three forms of familial obesity--normoinsulinemic obesity, hyperinsulinemic obesity and diabetic obesity. In normoinsulinemic obesity, both glucose tolerance and plasma lipids were normal with a few exceptions whereas in hyperinsulinemic obesity, mild glucose intolerance and manifest hyperlipidemia, and in diabetic obesity, blunted insulinogenic index and more advanced glucose intolerance with slight hyperlipidemia existed.

Adolescent↗
PubMed1979

Response of extrapancreatic glucagon to arginine in dogs.

In order to investigate secretion of extrapancreatic glucagon in dogs, plasma glucagon and total immunoreactive glucagon (IRG) in response to arginine were determined with antisera specific and non-specific for pancreatic glucagon, respectively. Only a tiny rise of plasma glucagon was observed in the portal vein following arginine infusion performed immediately after total pancreatectomy in a group of 5 normal dogs. In contrast, total IRG in the portal vein increased significantly after arginine infusion even after pancreatectomy. In alloxan diabetic dogs, arginine infusion after total pancreatectomy caused a rise in plasma glucagon in the portal vein, although not significantly. The response of total IRG to arginine in the portal vein was exaggerated in alloxan diabetic dogs. In a group of one-week post-pancreatectomized animals, plasma glucagon and total IRG increased significantly in response to arginine infusion. Furthermore, in these dogs, response of plasma glucagon and plasma total IRG to arginine infusion was abolished after gastrectomy. From the present results it is concluded that secretion of extrapancreatic glucagon increased in response to arginine infusion in the diabetic state, both alloxan diabetic dogs and one-week post-pancreatectomized dogs. In addition, a rise in extrapancreatic glucagon following arginine infusion in the chronically pancreatectomized dogs almost certainly derived from the stomach, as the rise was abolished by gastrectomy.

Animals↗
PubMed1978

Secondary diabetic retinopathy in chronic pancreatitis.

We found abnormal glucose tolerance curves in 45 of 47 patients with chronic pancreatitis and observed secondary diabetic retinopathy in eight of 45 cases showing slight changes in the fundus. Abnormal glucose tolerance curves were somewhat related to the exocrine dysfunction of the pancreas. Slightly abnormal glucose tolerance curves were observed frequently in patients with chronic pancreatitis, and both insulin and glucagon responses were decreased. We could not explain the cause of the low frequency of secondary diabetic retinopathy in pancreatic diabetes from the results of insulin and glucagon response tests.

Adult↗
PubMed1978

Effect of caerulein upon insulin and glucagon secretion in dogs.

In order to investigate the action of caerulein upon insulin and glucagon secretion, experimental studies were carried out using anesthetized dogs, in which graded doses of caerulein were infused into the pancreatic artery, and insulin and glucagon were measured in the blood obtained from the pancreatic vein. When caerulein was administered at a rate of 15 ng/min, neigher changes of blood glucose in the femoral artery nor plasma levels of insulin or glucagon in the pancreatic vein were prominent. Caerulein infusion at a rate of 120, 240 or 480 ng/min caused a prompt rise of plasma insulin and a delayed increase of plasma glucagon in the pancreatin vein. Blood glucose in the femoral artery increased only with caerulein doses of 240 ng/min or more. A significant increase in pancreatic vein blood flow rate was demonstrated after the infusion of caerulein at a rate of 240 ng/min or more. Neither caerulein-induced insulin secretion nor glucagon secretion was influenced by a simultaneous infusion of glucose. In contrast, caerulein-induced glucagon secretion was exaggreated by a simultaneous arginine infusion. It was concluded from the present experiments that caerulein infusion into the pancreatic artery resulted in increased secretion of insulin and glucagon from the pancreas.

Animals↗
PubMed1978

Abnormal response of pancreatic glucagon to glycemic changes in diabetes mellitus.

In order to determine pancreatic alpha cell function in diabetes mellitus, plasma glucagon responses to either an oral glucose load or insulin-induced hypoglycemia were investigated. Plasma glucagon in 6 normal control subjects fell significantly after the administration of glucose, whereas the levels of plasma glucagon did not decrease after glucose ingestion in patients with diabetes mellitus. In the group with severe diabetes, whose fasting blood glucose exceeded 200 mg/100 ml, the plasma glucagon level rose after glucose administration instead of decreasing. In 6 patients with diabetes mellitus, plasma glucagon did not decrease but rather increased during a glucose tolerance test which was performed after treatment with insulin and/or diet. In 6 control subjects, there was a remarkable rise of plasma glucagon in response to insulin-induced hypoglycemia. In contrast, no significant rise in plasma glucagon was demonstrated in 19 diabetic subjects undergoing intravenous insulin test. Seven patients, in whom an insulin test was repeated after treatment with insulin, sulfonylurea, or diet had a small rise in peak plasma glucagon and an increase in the integrated area under the glucagon response curve. It is concluded that the abnormal glucagon response to changes in blood glucose might be a primary defect in diabetes mellitus.

Adult↗
PubMed1978

Interactions of obesity and glucose-stimulated insulin secretion in familial hypertriglyceridemia.

Plasma lipids and lipoproteins, glucose tolerance, plasma insulin response to glucose load, and liver function were examined in 81 relatives of 12 index cases with primary endogenous hypertriglyceridemia, hyperinsulinemia, and hepatic steatosis, as well as in 90 nonrelatives, including the spouses, as controls. Insulin hypersecretion (with or without glucose intolerance), endogenous hypertriglyceridemia, and abnormal liver function suggesting hepatic steatosis were shown to exist in the relatives mostly in combined fashion. Correlation analysis and stepwise multiple regression analysis revealed that the combined disorder developed on the basis of obesity. The incidence of diabetes mellitus was significantly high in the relatives (14.8 per cent) as compared with the normal Japanese population (3.5 per cent). Although the vertical transmission of the combined disorder was noted in almost all pedigrees, the frequency distribution analysis of insulin response, glucose tolerance, and plasma triglyceride showed the histograms of these variables similarly skewed to the right as compared with those of the controls, with no apparent bimodality. In view of the hitherto suggested role of insulin in triglyceride metabolism, it is concluded that hyperinsulinemia coupled with obesity seems to be the basic trait of this form of familial hypertriglyceridemia and hepatic steatosis, though the mode of transmission remains to be elucidated.

Adolescent↗
PubMed1977

Insulin response to glucose or glucagon in subclinical diabetes previously injected with tolbutamide.

Thirty-one patients with subclinical diabetes, who showed diabetic or impaired glucose tolerance after treatment for diabetes, were investigated in order to clarify the abnormalities of insulin response in diabetes mellitus. These patients showed a delayed response of plasma insulin during oral glucose loading. In the tolbutamide-glucose test, in which glucose loading followed the intravenous tolbutamide injection at a 60-min interval, the insulin level at 90 min was significantly lowered in a group of 20 patients with subclinical diabetes. In the tolbutamide-glucagon test, in which 1 mg of glucagon was injected 60 min after tolbutamide injection, the maximal level of plasma insulin was significantly decreased in a group of 10 subclinical diabetes except for one patient. These results indicate that insulinogenesis and/or release of insulin were decreased even in subclinical diabetes, suggesting that such a defect in islet function might be one of the abnormalities in primary diabetes.

Blood Glucose↗
PubMed1977

Biochemical differences between human malignant and benign insulinoma tissues.

Five cases of malignant insulinoma and 2 cases of benign insulinoma were studied lipid-chemically. Tissues were collected by surgical operation or biopsy under peritoneoscopy. The total lipid was extracted from each tissue, and one part of each total lipid was separated into phospholipid, triglyceride and other lipid fractions by a thin-layer chromatography (TLC) on silica gel. The fatty acid composition and fatty acid content of each lipid fraction were measured by a gas-liquid chromatography (GLC). The most remarkable difference between malignant and benign isulinoma tissues was a higher percentage value of eicosatrienoic acid in the phospholipid of malignant insulinoma tissues when compared with that of non-malignant insulinoma tissues; the values mentioned above distributed between 9.82 and 3.32 in 5 malignant cases, but were 2.89 and 2.57 in 2 benign cases. Those changes in the phospholipid fatty acid composition of malignant insulinoma tissues may represent one of the mechanisms of malignant growth in the malignant neoplastic tissue.

8,11,14-Eicosatrienoic Acid↗
PubMed1977

Changes in glucose tolerance and insulin response in subclinical diabetes after treatment.

In this study, 121 patients who showed diabetic or decreased glucose tolerance and were treated with diet alone for one to fifteen years were investigated as subclinical diabetes. Glucose tolerance in these patients was improved or remained unchanged during the clinical course. Aggravation in glucose tolerance was observed in only seven cases. However, abnormalities in glucose tolerance were still found in 107 cases (88%) of the subclinical diabetes. Insulin response to oral glucose was investigated in 74 patients with subclinical diabetes. Delayed response and/or decreased response in the initial phase were demonstrated in 58 out of 74 patients (79%). No significant difference was observed in the insulinogenic index (ratio of insulin increment/glucose increment) at 30 min between the normal controls and either group with abnormal glucose tolerance. Diabetic retinopathy, including microaneurysm, was detected in 25 out of 109 patients with diabetic glucose tolerance. Abnormal insulin response, delayed and/or decreased, was demonstrated in 13 of 16 patients with diabetic retinopathy (81%). These results indicate the possibility that subclinical diabetes in the present study is a mild type of primary diabetes. In addition, it is suggested that abnormal response of plasma insulin to glucose, delayed and/or decreased, might be one of the prominent findings in diagnosis of diabetes mellitus.

Adult↗