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Biomedical subjects

A Ohneda

Publications and source records attributed to A Ohneda.

At least 91 records · Page 5Linked to original sources
PubMed1977

Dietary intake and hyperlipidemia in controlled diabetic outpatients.

Statistical analyses were performed in order to determine the effects of the control of the diabetes as well as the food intake on serum lipid levels of 73 diabetic outpatients. They had had elevated fasting blood glucose levels, mostly complicated by various grades of hyperlipidemia, before the initiation of treatment. Hyperlipidemia was found to be ameliorated in nearly half of those patients after the start of diabetic treatment. However, the elevation of serum triglyceride persisted in 30 per cent of controlled diabetics, and no differences were found in occurrence of hypertriglyceridemia between diet-treatment group, sulfonylurea group, biguanide group, combined group and insulin group. Estimation of diet intake revealed that the controlled hypertriglyceridemic patients consumed slightly (but significantly) greater amounts of sucrose, alcohol, and total calories than the controlled normotriglyceridemic patients. In addition to such inadequate diet consumptions, the tendency to be overweight and the subtle increment of fasting blood glucose levels were also shown to have contributed to hypertriglyceridemia. It is thus concluded that the lipid disorder in controlled diabetic outpatients is the result of multifactorial influences and that well-conducted diet therapy and stricter regulation of blood glucose are essential in the management of posttreatment hyperlipidemia.

Adult↗
PubMed1976

Purification of canine gut glucagon-like immunoreactivity (GLI) and its insulin releasing activity.

In order to clarify the nature of the biological action of gut glucagon-like immunoreactivity (GLI), GLI was extracted from the mucosa of the canine intestine and purified by gel filtration and affinity chromatography. 1500 gm of the mucosa yielded approximately 7 gm of crude extract of GLI. This crude extract was applied to a column packed with Sephadex G-50 or Bio-Gel P-10 and two peaks were obtained, Peak I and II. Each peak was purified with affinity chromatography, bound to gamma-globulin of anti-glucagon rabbit-serum. In this step, the GLI was purified approximately 80 times in comparison with the crude extract. Peak I or Peak II, as well as pancreatic glucagon, was infused successively into the pancreaticoduodenal artery of the anesthetized dogs. When buffer solution or the Peak I GLI was infused, the plasma immunoreactive insulin in the pancreatic vein did not change significantly. In contrast, both the Peak II and pancreatic glucagon promoted insulin secretion from the pancreas. The results obtained in this experiment demonstrate the promotion of insulin release from the pancreas and suggest an important role of gut GLI in the absorption and metabolic processing of nutrients.

Animals↗
PubMed1976

Relationship between insulin secretory function and endogenous hypertriglyceridemia in obese humans with insulin resistance.

Eighteen obese inpatients with insulin resistance revealed by i.v. insulin test and expressed in various grades of hyperinsulinemia and hyperglycemia were examined for plasma lipid levels. A significant positive correlation was found to be present between the plasma triglyceride (TG) level and the insulin response to glucose load. A stepwise multiple regression analysis revealed that the insulin secretory response, the plasma cholesterol level and the relative body weight contributed to the level of plasma TG. No difference was found in the grades of insulin resistance between patients with and without elevated TG. The ratio of sum of plasma insulin values to that of blood glucose values during glucose tolerance test was markedly increased in patients with elevated TG. The patients with relatively blunted insulin response and impaired glucose tolerance curves showed only slight slight hypertriglyceridemia. Endogenous hypertriglyceridemia in obesity seems to be more closely correlated with plasma insulin level, and therefore, with insulin action rather than insulin resistance.

Adult↗
PubMed1976

Insulin and glucagon response in patients with chronic pancreatitis.

The oral glucose tolerance test and arginine infusion test were carried out on 22 patients with chronic pancreatitis and 11 normal control subjects. According to the glucose tolerance curve, the patients were divided into three groups; group I (normal or slightly impaired), group II (mildly diabetic) and group III (moderately diabetic). Markedly impaired insulin responses to oral glucose as well as to arginine infusion were observed in groups II and III. In group I, the mean plasma insulin levels during glucose tolerance test were the same as those in the controls, but the insulin response to arginine was reduced except in two cases. On the other hand, the glucagon levels during arginine infusion test were within the normal range in group I and slightly reduced in the other groups with diabetic glucose tolerance. The ratio of increment area of insulin to that of glucagon during arginine infusion in the patients was slightly decreased in comparison with the controls. Neither insulin nor glucagon response after arginine infusion showed a significant correlation with pancreatic exocrine function. It is concluded that in chronic pancreatitis insulin response to glucose as well as to arginine is markedly decreased, and that glucagon rise after arginine infusion is lowered compared with the controls.

Adolescent↗
PubMed1976

Evidence for a familial form of hypertriglyceridemia as disorders coupled with insulin resistance.

To evaluate the role of insulin in familial hypertriglyceridemia, 34 relatives of the pedigrees of 3 index cases of endogenous hypertriglyceridemia and hepatic steatosis as well as 9 spouses were examined for plasma lipids and responses of blood glucose and plasma insulin during oral glucose tolerance tests. The combined disorders of hypertriglyceridemia and hyperinsulinemia plus glucose intolerance--insulin resistance--were most commonly found among the relatives, which were often accompanied by an impaired liver function. Some relatives showed hyperinsulinemia without hypertriglyceridemia. Obesity was frequent, but its incidence was similar to the controls. Thus, the observed form of familial hypertriglyceridemia was apparently coupled with insulin resistance; and hyperinsulinemia, or insulin resistance by itself, might be a basic genetical trait in this form of lipid disorder.

Adolescent↗
PubMed1975

Hepatic steatosis and the elevated plasma insulin level in patients with endogenous hypertriglyceridemia.

Among 31 nonobese or obese patients with endogenous hypertriglyceridemia, hepatic steatosis was found by histologic examination of the biopsied specimen in 17 patients, and it was severe in six patients, They had no history of excessive alcohol intake. Chemical analysis revealed that the lipid accumulated in the liver was triglyceride. The hypertriglyceridemic patients, with or without histologic steatosis, showed significantly increased responses of both plasma insulin and blood glucose to oral glucose load compared with control subjects. The responses were more exaggerated in the hypertriglyceridemic patients with steatosis than in the hypertriglyceridemic patients without steatosis. Analysis of correlations between five variables (liver triglyceride, plasma insulin, blood glucose, body weight index, and serum triglyceride) was done on 15 subjects whose liver triglyceride values were quantified, and highly significant correlations were found between liver triglyceride and plasma insulin, blood glucose, or body weight index. A step wise multiple regression analysis performed on the five variables with liver triglyceride as the dependent variable revealed that the plasma insulin level was the most closely related variable, and the blood glucose level the next. The prediction equation for liver triglyceride as a function of plasma insulin and blood glucose levels (r = 0.91, p greater than 0.001) accounted for 84 percent of the total variance of liver triglyceride. It was shown that the decay of intravenously injected insulin in plasma was not delayed in the hypertriglyceridemic patients with steatosis, while the insulin sensitivity examined after intravenous insulin injection significantly decreased in the hypertriglyceridemic patients with or without steatosis, thus suggesting that the hyperinsulinemia in the hypertriglyceridemic patients was due to an increased insulin secretion associated with the decrease in the insulin sensitivity. Therefore, the elevated plasma insulin and blood glucose levels--or the insulin insensitivity by itself--might be the essential abnormalities in patients with endogenous hypertriglyceridemia, which, in extreme cases, might lead to massive triglyceride accumulation in the liver.

Adult↗
PubMed1975

Glucagon-induced insulin secretion in normal diabetic subjects.

Eight normal subjects and ten diabetic patients were studied to compare the response of plasma insulin to glucagon with that to glucose and tolbutamide. Oral glucose tolerance test, glucagon test and tolbutamide-glucagon test were performed at intervals of several days. In glucose tolerance test, insulin response was reduced in the patients with severe diabetes. Plasma insulin increased and reached the peak 3 min after glucagon injection (glucagon I) in the normal controls, while plasma insulin response was reduced in diabetic patients, especially in the severe diabetics. In the normal controls plasma insulin rose and reached the peak 6 min after the tolbutamide injection and thereafter fell to the initial level. Glucagon injection following tolbutamide (glucagon II) caused the rise in insulin in the control subjects. In diabetics insulin response to either tolbutamide or glucagon I was reduced. Tolbutamide or glucagon II caused a significant difference in plasma insulin response in all the diabetic groups compared with the normal subjects, while glucose or glucagon I showed a significant increment of plasma insulin between the normal subjects and the severe diabetics. These results suggest that injection of tolbutamide as well as glucagon II provides a definite discrimination of insulin response in diabetics from the normal controls. The usefulness of the tolbutamide-glucagon test in the diagnosis of diabetes mellitus was discussed. -- glucose tolerance test; glucagon test; tolbutamide-glucagon test; plasma insulin.

Administration, Oral↗
PubMed1975

Glucagon response to arginine after treatment of diabetes mellitus.

To investigate the aminogenic glucagon response in diabetes mellitus, arginine infusion tests were carried out on twenty-four diabetic patients before and after treatment. Eleven healthy men served as a control group. Plasma glucagon was measured by radioimmunoassay using an antiserum, G21, specific for pancreatic glucagon. Out of twenty-four patients, five were treated with diet alone, eight with sulfonylurea, and eleven with insulin. In all these diabetic groups, the glucose tolerance improved after treatment for diabetes mellitus, while the insulin response to the glucose did not show any remarkable change. The fasting levels of the plasma glucagon did not differ from that of the normal subjects both before and after treatment. Hyperresponsiveness of the plasma glucagon to arginine infusion was observed in all diabetic groups, in comparison with that of the normal controls. The exaggerated response of the plasma glucagon to arginine was lowered following appropriate treatment in each diabetic group. However, as far as the changes in glucagon area during the arginine test are concerned, the aminogenic hyperresponsiveness of the plasma glucagon was reduced prominently in the diabetic group treated with sulfonylurea. The relationship between the response of glucose and plasma insulin and between glucose and glucagon to arginine was investigated, and the importance of the changes in the insulin:glucagon ratio was emphasized. Moreover, the possibility that long-term administration of a sulfonylurea may reduce an exaggerated glucagon response to arginine was discussed.

Adult↗
PubMed1969

The role of aminogenic glucagon secretion in blood glucose homeostasis.

Hyperaminoacidemia is a powerful stimulus of pancreatic glucagon secretion. These studies were designed to elucidate the role of aminogenic hyperglucagonemia in glucoregulation. Conscious dogs with previously implanted indwelling venous catheters were employed. The results support the view that a role of glucagon is to limit blood glucose decline during hyperaminoacidemia.First, a significant negative correlation between the area of glucagon increment during the 1st 20 min of a 10 amino acid infusion and the maximum fall in glucose concentration was observed. Second, when endogenous glucagon secretion was suppressed by means of a continuous glucose infusion, hyperaminoacidemia induced a maximal glucose decline which averaged 35 mg/100 ml, differing significantly from mean maximal fall of 3 mg/100 ml, which normally occurs in the presence of endogenous hyperglucagonemia. Third, when, during hyperglycemic suppression of endogenous glucagon secretion, 50 mmug of exogenous glucagon/min was infused via the mesenteric vein with the amino acids, the fall in glucose was reduced to an average of 5 mg/100 ml. Similarly when pancreozymin, administered during the combined infusion of glucose and amino acids, overcame glucose suppression of endogenous glucagon secretion, plasma glucose did not fall. Similar results were obtained when aminogenic hyperglucagonemia was prevented by other means. Hyperlipacidemia, induced by infusing a triglyceride emulsion and giving heparin injections, also suppressed aminogenic hyperglucagonemia in two of four experiments; in these two dogs glucose fell 15 and 11 mg/100 ml. In a final group of experiments, the canine pancreas was resected except for the uncinate process, which is virtually devoid of alpha-cells. In two dogs, in which this procedure resulted in zero portal venous glucagon levels, the administration of amino acids and/or pancreozymin resulted in a glucose decline of 14 and 16 mg/100 ml, despite the reduced beta-cell population resulting from the subtotal pancreotectomy. It thus appears that the secretion of pancreatic glucagon during hyperaminoacidemia in association with insulin secretion, serves to limit the decline of glucose concentration.

Amino Acids↗
PubMed1968

Characterization of the responses of circulating glucagon-like immunoreactivity to intraduodenal and intravenous administration of glucose.

The effects of ingested and infused glucose upon circulating glucagon-like immunoreactivity (GLI) were compared in 14 triply catheterized conscious dogs. Within 60 min after the intraduodenal administration of 2 g/kg of glucose, the mean level of glucagon-like immunoreactivity in the vena caval plasma more than doubled, whereas after intravenous infusion of the same dose over a 90 min period no change in the mean vena caval level was observed; during glucose infusion mean glucagon-like immunoreactivity in the pancreatic venous effluent declined, suggesting that hyperglycemia suppresses rather than stimulates pancreatic glucagon secretion. To determine if the rise in glucagon-like immunoreactivity that occurs during glucose absorption was of pancreatic origin, the effect of pancreatectomy performed 1 hr after the intraduodenal administration of glucose was determined. Although circulating insulin disappeared after resection of the pancreas, the level of glucagon-like immunoreactivity continued to rise, establishing its extrapancreatic origin. In other experiments, measurements of Glucagon-like immunoreactivity in plasma obtained simultaneously from pancreaticoduodenal and mesenteric veins and from the vena cava revealed the increment after intraduodenal glucose loading to be greatest in the mesenteric vein in 8 of 12 experiments, favoring the gut as the likely source of the rise. To characterize gut glucagon-like immunoreactivity, acid-alcohol extracts of canine jejunum were compared with similar glucagon-containing extracts of canine pancreas with respect to certain physical and biological properties. On a G-25 Sephadex column the elution volume of the jejunal immunoreactivity was found to be smaller than that of glucagon, which suggested a molecular size at least twice that of pancreatic glucagon. Furthermore, the in vivo and in vitro biological activities of the eluates containing jejunal glucagon-like immunoreactivity appeared to differ from those of eluates containing pancreatic glucagon. The jejunal material lacked hyperglycemic activity when injected endoportally into dogs, was devoid of glycogenolytic activity in the isolated perfused rat liver, and did not increase hepatic 3',5' cyclic adenylate in the perfused liver; however, like glucagon it appeared to stimulate insulin release. It seems quite clear the material in intestinal extracts either is a different substance or a different form from that of true pancreatic glucagon, although it crossreacts in the radioimmunoassay with antibodies to glucagon. It is concluded, (a) that hyperglycemia does not stimulate and probably suppresses the secretion of pancreatic glucagon; (b) that during intestinal absorption of glucose, a rise in glucagon-like immunoreactivity occurs; (c) this immunoreactivity is derived from an extrapancreatic site, probably the gut; (d) that the glucagon-like immunoreactivity extractable from jejunum is not the same as pancreatic glucagon but is a larger molecule devoid of hyperglycemic and glycogenolytic activity, a cross-reactant in radioimmunoassay for glucagon; and (e) that the eluate in which jejunal immunoreactivity is contained can stimulate insulin release in conscious dogs.

Animals↗
PubMed1968

Characterization of response of circulating glucagon to intraduodenal and intravenous administration of amino acids.

Studies were carried out to determine if hyperaminoacidemia stimulates the secretion of pancreatic glucagon, and, if so, to evaluate the effect of endogenous and exogenous pancreozymin and of hyperglycemia upon this response. The intravenous administration to 16 dogs of 1 g/kg of a 10 amino acid mixture over a 60 min period raised amino nitrogen to a mean level of 13.5 mg/100 ml; mean pancreaticoduodenal vein insulin rose from 84 to 459 muU/ml and glucagon from 1.1 to 2.7 mmug/ml. Further augmentation of both insulin and glucagon secretion was achieved during hyperaminoacidemia by infusing pancreozymin. Since endogenous pancreozymin is known to be stimulated by amino acids in the gut, it seemed possible that intraduodenal loading of amino acids would elicit a greater insulin and glucagon response than could be explained by the accompanying hyperaminoacidemia. The intraduodenal administration of 1 g/kg of the amino acid mixture was followed by substantial hyperinsulinemia and hyperglucagonemia, which frequently anticipated the hyperaminoacidemia, and in many of the dogs the ratio of hormone rise to amino nitrogen rise was greater after intraduodenal than after the intravenous route of amino acid administration in the same animal. Intraduodenal administration of amino acids did not cause measurable release of intestinal glucagon-like immunoreactivity into the mesenteric vein plasma. Hyperglycemia induced by constant glucose infusion prevented aminogenic hyperglucagonemia and even suppressed the augmenting action of pancreozymin; sudden termination of the infusion with continued amino acid infusion was associated with a striking rise in glucagon. It is concluded (a) that hyperaminoacidemia stimulates pancreatic glucagon secretion, (b) that aminogenic hyperglucagonemia is augmented by the infusion of pancreozymin, (c) that intraduodenal administration of amino acids stimulates pancreatic glucagon secretion without measurable release of glucagon-like immunoreactivity into the mesenteric vein, and (d) that hyperglycemia prevents aminogenic hyperglucagonemia even during augmentation with pancreozymin. This conclusion suggests that the prevention of hypoglycemia during amino acid-induced insulin secretion may be an important function of glucagon.

Amino Acids↗