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Biomedical subjects

T Kanatsuna

Publications and source records attributed to T Kanatsuna.

At least 37 records · Page 2Linked to original sources
PubMed1987

Somatostatin suppresses plasma aldosterone concentration in a case of Bartter's syndrome.

The study was conducted to examine the effect of somatostatin on activated renin-angiotensin-aldosterone system in a case of Bartter's syndrome. After 60 minutes of 500 micrograms of somatostatin infusion, the plasma aldosterone concentration was reduced from the basal level of 250 pg/ml to 140 pg/ml, whereas plasma renin activity remained at the basal level. This result suggests that somatostatin may specifically inhibit aldosterone secretion in Bartter's syndrome and the agent can be applied to a treatment of this syndrome.

Adrenocorticotropic Hormone↗
PubMed1986

Elevated serum CA19-9 levels in poorly controlled diabetic patients.

Serum CA19-9 levels were measured in 60 diabetic patients and 40 healthy volunteers. Serum CA19-9 concentration was correlated with hemoglobin A1 (HbA1) (r = 0.4368 P less than 0.005) and fasting plasma glucose levels (r = 0.3410 P less than 0.01). None of the 40 healthy subjects showed elevated CA19-9 concentrations over 37 units/ml as the upper normal value. The percentage of positive serum CA19-9 levels in poorly controlled patients (fasting plasma glucose greater than 200 mg/dl or HbA1 greater than 13%) and moderately to well controlled patients was 50% and 10%, respectively. No correlation was found between the level of CA19-9 and those total cholesterol, and triglycerides, or the duration of diabetes. In patients who had diabetic retinopathy or persistent proteinuria, the CA19-9 concentration was significantly elevated when compared with those without these complications. It has been shown that patients with adenocarcinoma of the gastrointestinal tract have high plasma CA19-9 levels and those who have benign disease have normal CA19-9 levels. Even though diabetes mellitus is not a malignant disease, serum CA19-9 levels were increased in diabetic patients. These results indicate that HbA1 and fasting plasma glucose should be examined in patients with high CA19-9 levels.

Adult↗
PubMed1986

Defect of the first-phase insulin secretion to glucose stimulation in the perfused pancreas of the nonobese diabetic (NOD) mouse.

To investigate the development of impaired insulin secretion in type I diabetes mellitus, the pancreata of ICR and NOD mice (10-50 wk of age) were perfused. According to insulin responses to 30 mM glucose and to 19 mM arginine, we classified the NOD mice into four groups: those having normal insulin secretion to glucose and to arginine similar to that of control ICR mice (group 1); those with a defect in the first-phase insulin secretion to glucose stimulation but with almost normal insulin secretion to arginine, total insulin release to glucose being significantly smaller than that of group 1 (group 2); those having only a small insulin response to either stimulus, but a fasting plasma glucose level still within the normal range (group 3); and those being overtly diabetic, showing no insulin response to either stimulus (group 4). The severity of insulitis and insulin concentration of the pancreas in each group of NOD mice was well correlated with the insulin release from the perfused pancreas. These results indicate that the initial sign of B-cell damage in NOD mice is a defect of the first phase of glucose-induced insulin secretion, which is followed by a total loss of ability to respond to glucose or arginine stimulation.

Animals↗
PubMed1985

Reduced norepinephrine turnover in brown adipose tissue of pre-obese mice treated with monosodium-L-glutamate.

Norepinephrine (NE) turnover, an index of sympathetic nervous system (SNS) activity, was measured in interscapular brown adipose tissue (IBAT), heart and pancreas of 3-weeks-old pre-obese monosodium-L-glutamate (MSG) mice and at 6-weeks-old mildly obese MSG mice. In IBAT, rates of NE turnover were slower not only in 3-weeks-old MSG mice but also in older obese MSG mice than in their saline controls. In heart, rates of NE turnover were slower in 6-weeks-old mildly obese MSG mice, but not in pre-obese MSG mice. No significant difference in NE turnover in pancreas was observed at either age. The low NE turnover in IBAT of MSG-treated mice prior to the onset of gross obesity suggests that low SNS activity may be an initial contributor to their high energy efficiency and resultant obesity.

Adipose Tissue, Brown↗
PubMed1985

Insulin release from column-perifused isolated islets of uremic rats.

In order to examine the insulin secretion in chronic renal failure, isolated pancreatic islets either from uremic rats or from control rats were mixed into a short column of Bio-Gel P-2 polyacrylamide beads and perifused. Uremic rats had higher concentrations of blood urea nitrogen, serum creatinine, and immunoreactive insulin and lower concentration of plasma 1,25-(OH)2D3 than control rats. Although the basal insulin release in the presence of 5.0 mM glucose showed no difference between uremic and control rats, the initial insulin release in the presence of 16.2 mM glucose was significantly lower (p less than 0.05) in uremic than in controls rats. The insulin content in islets was not different between both groups. These findings suggest that there might be impairment of the initial insulin secretion without changes of insulin content in pancreatic islets in uremia.

Animals↗
PubMed1985

Effects of aspartame on diabetic rats and diabetic patients.

The effects of aspartame (L-aspartyl-L-phenylalanine methyl ester) on plasma glucose and insulin levels were investigated in diabetic rats and patients with non-insulin-dependent diabetes mellitus. The oral administration of 0.45 mg aspartame per 100g body weight, which is equivalent to 150 mg of glucose in sweetness, to streptozotocin-induced diabetic rats had no effect on the plasma glucose or insulin levels. Also, 225 mg oral aspartame loading, which is equivalent to 75 g of glucose in sweetness, to patients with non-insulin-dependent diabetes mellitus did not increase plasma glucose or insulin levels, although 75 g of oral glucose loading increased plasma glucose and insulin levels in diabetic patients as expected. Aspartame ingestion for three days at a dose of 24-48 mg per day and the intake of snacks flavored with 240 mg of aspartame also did not increase fasting plasma glucose levels. These results suggest that acute administration of aspartame has no influence on plasma glucose or insulin levels in diabetic rats and patients with non-insulin-dependent diabetes mellitus.

Adult↗
PubMed1985

Effects of nifedipine on insulin secretion and glucose metabolism in rats and in hypertensive type 2 (non-insulin dependent) diabetics.

The effects of nifedipine (Adalat) on glucose metabolism and insulin release were studied in rats and in patients with type 2 diabetes mellitus complicated with hypertension. 1. In rats, 2.5-50 micrograms/kg of intravenous nifedipine reduced glucose tolerance and insulin release after intravenous glucose in a dose related fashion, although fasting blood sugar and insulin were not affected at 50 micrograms/kg of nifedipine. 2. Daily 20 to 60 mg of oral nifedipine for 12-75 weeks to 14 type 2 diabetics with hypertension did not affect their fasting blood glucose or hemoglobin A1. Mean glucose tolerance curve after the treatment was significantly ameliorated, although insulin response during the oral glucose loading did not show any significant change. Those results suggest firstly that there may be a difference in insulinopenic effect of nifedipine between the species, and secondly that long-term administration of nifedipine produced no adverse influence on glucose metabolism in type 2 diabetics.

Aged↗
PubMed1984

Concentrated loss of insulin secretion in Wistar rats with normal glucose tolerance.

Rats with decreased insulin response and with normal glucose tolerance were concentrated by repeated selective breeding of normal Wistar rats with low insulinogenic index. In general, the mean insulinogenic index of the inbred offsprings showed a tendency to decrease more than their parents generation. Thus mean insulinogenic indices in second (F2), third (F3) and fourth (F4) generations were significantly reduced more than the normal rats without glucose intolerance. Pancreatic islets from the F3 and F4 rats lost partially their ability to release insulin at 20 mM glucose in vitro. It is suggested that a defect responsible for the decreased insulin response in the F2, F3 and F4 rats resulted from a loss of the ability to secrete insulin in each islet, and that this defect was concentrated by repeated selective breeding of normal Wistar rats.

Animals↗
PubMed1984

Islet-activating protein (IAP)-induced adrenergic modulation of pancreatic A and B cell in dogs.

Islet-activating protein (IAP) is a substance purified from the culture medium of Bordetella pertussis, and its main action is characterized by the enhancement of secretory response to glucose and other stimuli in pancreatic islet. In this experiment, the effect of IAP on epinephrine-induced secretion of immunoreactive insulin (IRI) and glucagon (IRG) was investigated in normal dogs. Epinephrine suppressed IRI secretion and it had a little increment to IRG secretion in control group, while IRI and IRG secretions were significantly increased by epinephrine in IAP pretreated group. Using beta-blocker (Propranolol) with epinephrine, these increments of IRI and IRG secretions in IAP pretreated group were abolished. However, using alpha-blocker (Phentolamine) with epinephrine, these secretions of IRI and IRG in IAP pretreated group were much more increased than epinephrine alone induced secretions. Blood glucose levels were lower in IAP pretreated group than in control group throughout the loading tests in all of the experiments. These findings suggest that (1) IAP decreases blood glucose level and (2) IAP enhances epinephrine-induced secretion of insulin and glucagon by acceleration of beta-adrenergic effect and by reduction of alpha-adrenergic suppression in dogs.

Animals↗
PubMed1983

Immunoglobulin from insulin-dependent diabetic children inhibits glucose-induced insulin release.

Immunoglobulin was separated from islet cell antibody positive plasma of six children with newly diagnosed insulin-dependent (type I) diabetes mellitus. The dynamics of insulin release in response to glucose and partially purified antibodies were determined in dispersed rat islet cells perifused on small columns of Biogel P-2 beads. After perifusion at 5.5 mmol/L D-glucose in the presence of healthy control immunoglobulin, the rate of insulin release increased in a biphasic manner after stimulation with 30 mmol/L D-glucose. In cells exposed to diabetic immunoglobulin, 30 mmol/L D-glucose had little, if any, effect on insulin release. These results suggest that islet cell antibodies in insulin-dependent diabetes may interfere with the insulin release mechanisms in the pancreatic B-cells.

Adolescent↗