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Biomedical subjects

A Ohneda

Publications and source records attributed to A Ohneda.

At least 55 records · Page 3Linked to original sources
PubMed1984

Response of extrapancreatic immunoreactive glucagon to intraluminal nutrients in pancreatectomized dogs.

To investigate the response of extrapancreatic glucagon to intraluminal stimuli, nutrients were administered to normal and pancreatectomized dogs through a stomach tube in a fully conscious state after an overnight fast. Plasma immunoreactive glucagon was determined with antisera specific and nonspecific to glucagon and was designated as IRG and total IRG, respectively. Oral glucose load elicited a decrease in plasma IRG and a remarkable rise of plasma total IRG in a group of 6 pancreatectomized dogs, as in the control dogs. When arginine was given, both plasma IRG and total IRG significantly increased in a group of 5 pancreatectomized dogs, while only total IRG rose significantly in the normal control dogs. Butter load did not reveal any changes in plasma IRG and total IRG in a group of 5 pancreatectomized dogs, whereas only total IRG increased in the normal control dogs. It is concluded that extrapancreatic glucagon responds to intraluminal administration of nutrients, as pancreatic glucagon does. In addition, gut glucagon-like immunoreactivity increased following glucose or arginine ingestion in pancreatectomized dogs. Furthermore, the failure in response of plasma IRG and total IRG to butter load in pancreatectomized animals suggests that its intraluminal hydrolysis is important in the secretion of extrapancreatic immunoreactive glucagon.

Animals↗
PubMed1984

Characterization of response of gut GLI to fat ingestion in dogs.

Previous study from our laboratory demonstrated that an increased release of gut glucagon-like immunoreactivity (GLI) following triglyceride digestion was not observed in pancreatectomized dogs. Therefore, in order to clarify the response of gut GLI to triglyceride ingestion, experimental study was carried out in normal and pancreatectomized dogs. When butter was administered to pancreatectomized dogs in combination with pancreatic enzymes, plasma glucagon (IRG) measured by specific antiserum did not change significantly but plasma triglyceride as well as plasma total immunoreactive glucagon (total IRG) measured by nonspecific antiserum increased. Oral administration of glycerol induced no significant increase in plasma IRG but elicited a moderate increase of plasma total IRG. Gastric instillation of palmitic acid induced a remarkable rise of plasma total IRG in normal dogs, whereas plasma IRG did not reveal any changes. Oral administration of triglyceride of medium chain fatty acid, tricaprylin, did not promote any rise of plasma IRG but a slight increase of plasma total IRG. From the present experiment, it is concluded that hydrolysis of triglyceride and its metabolites are important in the release of gut GLI following fat ingestion. Among its metabolites, long chain fatty acid and glycerol promote the GLI secretion, whereas medium chain fatty acid does not.

Animals↗
PubMed1984

Influence of vagotomy upon GIP release in patients with peptic ulcer.

Twenty-two vagotomized peptic ulcer patients were studied on the influence of vagotomy on the release of GIP. Moreover, the relationship between acid output and GIP release was analyzed. These patients underwent one of the three types of operation; truncal vagotomy with pyloroplasty (TV + P) selective vagotomy with pyloroplasty (SV + P) and selective vagotomy with antrectomy (SV + A). Before and after surgery, a gastric juice study and an oral glucose tolerance test were performed on separate days. Maximum acid output in response to tetragastrin correlated significantly with integrated GIP response after oral glucose loading. In the SV + P group, the response of GIP was slightly greater after surgery. In the SV + A group, the integrated GIP response diminished postoperatively, although, after surgery, GIP reached its peak sooner. The integrated GIP response was greater in the SV + P group than in the TV + P group. The response of GIP was less in the SV + A group than in the SV + P group. These changes were insignificant. In conclusion, it is presumed that GIP release is affected by gastric acid, gastric emptying time, intestinal transit time and vagal nerve action.

Adult↗
PubMed1983

Effect of endogenous gastric inhibitory polypeptide (GIP) on the removal of triacylglycerol in dogs.

In order to clarify the effect of endogenous gastric inhibitory polypeptide (GIP) upon lipid metabolism, the removal of intravenously administered triacylglycerol was investigated following an oral glucose or galactose load in dogs. After an overnight fast, the triacylglycerol emulsion was infused at a constant rate of 1 ml/min for 90 min, and glucose, galactose or tap water was orally administered at 30 min. Blood glucose increased after the glucose load but it did not change following the galactose load or water ingestion. Plasma insulin increased after the glucose load but did not change after galactose or tap water ingestion. Plasma glucagon did not show any discernible change in the three experimental groups. Plasma GIP increased following the glucose or galactose load to 4360 or 1653 pg/ml, respectively. Plasma triacylglycerol increased to the same levels at 30 min in the three experimental groups. The peak levels of plasma triacylglycerol and integrated plasma triacylglycerol for 150 min did not differ in the three groups. Moreover, there was no difference in the removal rate of plasma triacylglycerol following the withdrawal of the fat emulsion. It is concluded from the present study that endogenously released GIP does not elicit any effect upon triacylglycerol removal.

Animals↗
PubMed1983

Response of gastric inhibitory polypeptide (GIP) to oral administration of nutrients in normal and pancreatectomized dogs.

In order to clarify the response of plasma gastric inhibitory polypeptide (GIP) to various nutrients and to investigate the relationship between the pancreas and GIP secretion, an experimental study was performed using normal and pancreatectomized dogs. Oral administration of glucose (2 g/kg) or butter (2 g/kg) resulted in an increase of plasma GIP in five normal dogs. In contrast, oral administration of arginine (1 g/kg) did not produce any discernible changes in plasma GIP in normal dogs. In a group of nine pancreatectomized dogs, the fasting level of plasma GIP did not differ from that of the control group. Furthermore, glucose ingestion in the pancreatectomized group resulted in the same pattern and the same degree of change in plasma GIP as it did in the normal controls. In contrast, plasma GIP did not change at all following fat loading in the pancreatectomized group. However, butter with pancreatic enzymes elicited a significant rise of plasma GIP in the pancreatectomized dogs. The present study indicates that plasma GIP increases following oral administration of glucose or fat but not arginine. Furthermore, it is demonstrated that GIP secretion following fat ingestion occurs only after fat digestion by pancreatic enzymes. In addition, the findings observed in the present study do not support the existence of feedback effect of insulin on GIP secretion.

Animals↗
PubMed1983

Measurement of glucagon in human plasma by enzyme immunoassay.

In order to investigate the validity of an enzyme immunoassay for glucagon, the glucagon levels of human plasma were determined by both enzyme immunoassay (EIA) and radioimmunoassay (RIA). After a glucose load, plasma glucagon measured by both EIA and RIA fell in 12 normal subjects. The glucagon levels measured by both assays during glucose tolerance test showed good agreement in a group of 10 patients. After arginine infusion, plasma glucagon increased in 6 normal subjects and 3 patients and glucagon values measured by EIA correlated well with those by RIA. The present study demonstrates correlation between glucagon levels measured by RIA and EIA and indicates the usefulness of EIA for determining glucagon in human plasma.

Colonic Neoplasms↗
PubMed1983

Effects of Ca antagonists, nifedipine, niludipine and verapamil, on endocrine function of the pancreas.

To study the effects of two Ca antagonists, nifedipine and niludipine, on insulin and glucagon secretion, experiments were performed using an in situ local circulation of the canine pancreas. The test drugs were injected into the pancreatic artery in three graded doses (5, 10 and 100 nmoles/kg) during arginine infusion, and blood samples were taken from the pancreatic vein. Verapamil, 10, 100 and 1,000 nmoles/kg, administered in the same way, was used as a control drug. Nifedipine, 5 to 100 nmoles/kg, decreased plasma insulin (IRI) and increased plasma glucagon (IRG) in the pancreatic vein, but caused no marked changes of blood glucose levels in five dogs. Niludipine, 5 to 100 nmoles/kg, injected into the pancreatic artery of 5 dogs, did not change blood glucose levels, but decreased slightly plasma IRI in the pancreatic vein and increased plasma IRG. Verapamil administered to 5 dogs caused no remarkable change of blood glucose or plasma IRG but decreased plasma IRI slightly. The maximum secretion of insulin was significantly lowered by nifedipine and niludipine, and that of pancreatic glucagon markedly increased by niludipine. The experiments revealed that Ca antagonists inhibit insulin secretion, and increase glucagon, and proved that calcium plays an important role in the A cell function of the pancreas.

Animals↗
PubMed1983

Response of extrapancreatic glucagon to glycemic changes under chronic insulin deficiency in dogs.

Since the secretion of pancreatic glucagon is largely influenced by the changes in the blood glucose level, the response of extrapancreatic glucagon was investigated in totally pancreatectomized dogs under chronic insulin deficiency. Insulin-induced hypoglycemia did not alter plasma glucagon in the portal vein in a group of 5 pancreatectomized dogs, but the decrease of the blood glucose was small, by 70 mg/100 ml, in spite of a large amount of insulin. The administration of 2-deoxyglucose did not cause any changes in plasma glucagon in the portal vein in a group of 6 pancreatectomized dogs. Glucose-induced hyperglycemia, both transient and continuous, did not cause any changes in plasma glucagon in the portal vein, although blood glucose was significantly elevated. It is concluded that regulation of extrapancreatic glucagon differs from that of pancreatic glucagon.

Animals↗
PubMed1983

Factors influencing the development of diabetic vascular complications.

In order to elucidate the factors influencing the development of diabetic vascular complications, a retrospective clinical study was carried out in 255 patients, who had been treated in our diabetes clinic for more than 10 years. The patients were divided into three groups according to their retinal lesions: group A, 89, had no retinal lesions; group B, 118, Scott I and II; and group C, 48, Scott III or more advanced lesions. Although there were no significant differences in body weight or age at onset of diabetes between the three groups, the severity of the disease at the first visit and the method of treatment were regarded as important factors in the development of vascular complications. Hypertension, albuminuria and hypercholesterolemia were observed more often in group C than groups A and B, while there was no difference in EKG abnormalities between the three groups. No significant difference was demonstrated concerning control of blood glucose, incidence of hypoglycemia, urinary glucose and ketone bodies, serum triglyceride, hemoglobin A1c, beta-N-acetylglucosaminidase or serum lipoperoxide. These results suggest that the complicated mechanism involved in the development of vascular complications should be investigated and a long-term dynamic observation should be carried out.

Acetylglucosaminidase↗
PubMed1982

Effects of cold exposure on insulin and glucagon secretion in sheep.

The effectiveness of cold exposure on the secretion of insulin and glucagon were examined using five adult sheep. Endocrine responses were studied in a warm environment and after cold exposure (0 C) from 4-19 days. Compared to levels at room temperature, basal plasma glucose levels were elevated during cold exposure, but basal levels of plasma insulin and glucagon were unchanged. Cold exposure significantly decreased the early insulin response to a primed iv infusion of glucose. Plasma glucose and glucagon levels during glucose infusion were unaffected by cold exposure. The decrease in plasma glucose after iv insulin injection (0.2 U/kg BW) was greater during cold exposure than at room temperature. Butyrate injection (0.625 mmol/kg, iv) resulted in a significantly lower secretion of both insulin and glucagon in the cold than in the warm environment. The glucagon response to arginine infusion (0.5 g/kg over 30 min, iv) was elevated by cold exposure, whereas the insulin response to arginine tended to be reduced. Propranolol infusion (20 micrograms/kg . min, iv) caused a slight inhibition of insulin secretion in the cold environment, but did not affect glucagon levels in either the cold or warm environment. Phentolamine infusion (20 micrograms/kg . min, iv) inhibited glucagon secretion, particularly in the cold environment, and caused a markedly greater stimulation of insulin secretion in the cold. It is concluded that cold exposure insufficient to cause hypothermia decreases insulin secretion in response to a variety of stimuli. Effects of cold on glucagon secretion depend upon the stimulating agent used.

Animals↗
PubMed1982

Insulin response to glucagon with or without tolbutamide in normal and diabetic subjects.

In order to investigate insulin response to glucagon, eight normal subjects and thirty diabetic patients were studied. According to fasting blood glucose, diabetic patients were classified into three groups; mild, moderate and severe. An oral glucose tolerance test, a glucagon test and a tolbutamide-glucagon test were performed at intervals of several days. In the glucose tolerance test, insulin response was reduced in the patients with moderate or severe diabetes. Plasma insulin increased and reached a peak 3 min after glucagon injection (glucagon 1) in the normal controls (66.1 +/- 9.9 microunits/ml), while plasma insulin response to glucagon 1 was reduced in the three diabetic groups (35.8 +/- 7.3, 33.2 +/- 9.7 and 22.9 +/- 5.0 microunits/ml, respectively). In the normal subjects glucagon injected 60 min after tolbutamide (glucagon 2) caused a rise in insulin (72.0 +/- 4.9 microunits/ml). In the diabetic groups, glucagon 2 caused a reduced response of plasma insulin (38.6 +/- 8.9, 49.5 +/- 17.4 and 34.8 +/- 11.3 microunits/ml, respectively). Glucagon with or without tolbutamide produced a far greater maximal response of plasma insulin in all the diabetic groups than in the normal subjects, while glucose produced a not significantly different increment of plasma insulin between the normal subjects and the mild diabetics. The present study demonstrates the glucagon injection with or without tolbutamide could clearly discriminate the insulin response in diabetics from that in normal subjects.

Adult↗
PubMed1982

Plasma insulin response to various secretagogues in insulinoma.

Since the development of radioimmunoassay for insulin, the diagnosis of insulinoma has been made easily. However, it has been assumed that insulinoma is heterogenous in the histological structure as well as in clinical findings. Therefore, the present study was performed to investigate the insulin response to various stimuli and to evaluate the various insulin response tests in 19 patients with insulinoma. The fasting blood glucose was 19 to 90 mg/100 ml in insulinoma and 81 +/- 5 (mean +/- S.D.) mg/100 ml in normal controls. Plasma insulin (IRI) in insulinoma ranged from 10 to 255 microU/ml, while in the control it was 14 +/- 9 microU/ml. However, insulin/blood glucose ratio increased in insulinoma (0.2-11.2) compared with the normal control (0.18 +/- 0.11). In oral glucose tolerance tests, plasma IRI increased and reached peak levels of 48-244 microU/ml, remaining elevated in most cases. In the intravenous tolbutamide test, plasma IRI increased conspicuously to 82-1,330 microU/ml and hypoglycemic coma was provoked in 54%. Plasma IRI was elevated in the intravenous glucagon test and reached the peak levels of 85-400 microU/ml, which exceeded those of the control group. Plasma IRI increased to more than 100 microU/ml after arginine infusion and formed bizarre curves. There were no correlations between plasma IRI response to various stimuli and malignancy, type of B-granule or insulin content of insulinoma tumors. It is concluded that fasting plasma IRI, insulin/glucose ratio, tolbutamide test and glucagon test are highly valuable for the diagnosis of insulinoma.

Adenoma, Islet Cell↗
PubMed1982

Evaluation of new criteria for diagnosis of diabetes mellitus based on follow-up study of borderline diabetes.

In order to evaluate the validity of recently proposed criteria for diagnosis of diabetes mellitus, a retrospective study was performed in 315 patients with borderline diabetes, who were selected from approximately 4,000 outpatients under treatment for more than three years. They were divided into two groups, BI and BII, according to the 2-hr blood glucose level in the 50 g glucose tolerance test (GTT): BI between 100 and 135 mg/100 ml and BII between 135 and 195 mg/100 ml. In group BI, glucose tolerance was deteriorated in 38 of 75 patients (51%) and converted to diabetes mellitus in 21 patients (28%). In group BII, 78 among 232 patients (34%) developed diabetes mellitus. Furthermore, in 85% of the 99 cases of the conversion to diabetes mellitus from borderline diabetes, it occurred within 5 years. Diabetic retinopathy was observed in 25 of 72 patients (35%) in group BI and in 60 of 212 patients (28%) in group BII. More than two thirds of the patients with diabetic retinopathy observed in the borderline diabetes developed their retinopathy within 5 years. Normal insulin response during GTT was proved only in 21% and 17% among groups BI and BII, respectively. These results indicate that the patients with borderline diabetes BI as well as BII, are closely related with diabetes mellitus, and that the patients with impaired glucose tolerance should be treated with diet restriction as in diabetes mellitus.

Adult↗
PubMed1982

Analysis of insulin secretion based on changes in plasma insulin and C-peptide in man.

In order to clarify the mechanism of insulin secretion, responses of insulin (IRI) and C-peptide (CPR) in plasma to various stimuli were investigated in normal subjects and patients with diabetes mellitus, liver cirrhosis, chronic nephritis or insulinoma. The response of plasma IRI and CPR to oral glucose load was less marked in the mild and moderate diabetes groups than in the normal controls. Neither IRI nor CPR in the severe diabetes group responded to oral glucose. The patients with liver cirrhosis revealed an exaggerated and delayed response of IRI and CPR, and a lowered CPR/IRI ratio, indicating a remarkable response of IRI to glucose. In contrast, the patients with chronic nephritis showed a prominent rise of CPR alone. In the insulinoma patients, both plasma IRI and CPR increased after glucose load. In the response to glucose, there was approximately 30-min lag time between the peaks of IRI and CPR in the normal controls and the patients with various diseases. Following arginine infusion, plasma IRI and CPR increased in the normal subjects and the patients with moderate diabetes. In the normal subjects, plasma IRI reached a peak at 6 min and 3 min in response to tolbutamide and glucagon, respectively, which elicit an abrupt and sharp rise of insulin from B-cells. However, diabetic patients showed a minimal change in plasma IRI and CPR, whereas there was an exaggerated response of plasma IRI and CPR in insulinoma patients. In analysis of responses of plasma IRI and CPR to tolbutamide or glucagon, there was a lag time longer than 10 min in the normal subjects. The present study confirms the concurrent release of C-peptide from the B-cells in the secretion of insulin. In addition, it was suggested that insulin and C-peptide are mainly handled in the liver and the kidney, respectively. Furthermore, a longer lag time between the peaks of IRI and CPR in response to tolbutamide or glucagon did not necessarily indicate a simultaneous release of insulin and C-peptide from the B-cell, but a delayed release of the latter.

Adult↗
PubMed1981

Glucagon in spontaneously diabetic KK mice.

In order to investigate the relationship between the development of diabetes mellitus and glucagon, experimental studies were performed in genetically diabetic mice (KKA gamma and KK B1) and in C57 mice of various ages. In the KK mice, the fasting plasma glucose increased during the aging process and reached the maximum at 14 weeks. The fasting plasma insulin in the KK mice was significantly elevated during the aging process and continued to increase till 20 weeks of age. In contrast, an increase in the fasting plasma glucagon was observed only at the age of 4 weeks, although the plasma glucagon increased during the aging process. The content of the insulin in the pancreas of the KK mice was significantly higher than that of the C57 mice, continuing to increase during the aging process. the glucagon content of the pancreas increased during the aging process but no significant difference was observed between the KK mice and the control mice. The total immunoreactive glucagon in the jejunum measured by non-specific antiserum was slightly reduced in the KK mice at the age of 14 weeks, compared with the C57 mice. There was no difference in the glucagon content of the stomach between the KK mice and the C57 mice of various ages. The KK mice at 14 weeks showed an elevated plasma glucagon 30 min after glucose injection, compared with the C57 mice, which indicates a reduced suppression of glucagon in response to hyperglycemia in the KK mice. The plasma glucagon in the KK mice 30 min after arginine was slightly higher than in the control mice, although not significantly so. From these results it was concluded that the KK mice revealed an elevation of fasting plasma glucagon in the early stage of diabetes mellitus and a decrease in glucose-induced glucagon suppression at 14 weeks and that diabetes mellitus in the KK mice derived mainly from insulin resistance associated with hyperinsulinemia.

Animals↗