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Biomedical subjects

H Kajinuma

Publications and source records attributed to H Kajinuma.

At least 37 records · Page 2Linked to original sources
PubMed1979

Human plasma C-peptide immunoreactivity: its correlation with immunoreactive insulin in diabetes, and chronic liver and renal diseases.

The correlation between plasma C-peptide immunoreactivity (CPR) and immunoreactive insulin (IRI) was investigated during the oral glucose tolerance test in 20 normals, 127 diabetics, and 39 non-diabetics with chronic liver or renal disorders. When all subjects were included, the increment of CPR 30 minutes after glucose load (deltaCPR) correlated well with that of IRI (deltaIRI) (r = 0.66, p less than 0.001), but the return of CPR towards the basal level was delayed as compared with IRI. The positive correlation was also observed between the sum of 6 IRI and that of 6 CPR values during the glucose tolerance test in diabetics and controls (r = 0.53, p less than 0.001). deltaCPR/deltaBS (30 min.) was also well correlated with deltaIRI/deltaBS (30 min.), and was specifically low in diabetics. Insulin-treated maturity-onset diabetics showed low but considerable CPR responses while no CPR responses were observed in insulin-treated juvenile diabetics. In each plasma sample, CPR always exceeded IRI on the molar basis. At fasting CPR/IRI ratio was 15.6 +/- 1.7 (mean +/- SE) in normals and 14.9 +/- 1.3 approximately 16.9 +/- 1.0 in diabetics. In chronic liver diseases IRI response was augmented while CPR response was not different from that of controls, and the molar ratio of CPR/IRI was significantly low (9.5 +/- 1.1). On the contrary, it exceeded that of normals in chronic renal diseases (35.7 +/- 14.9). It is concluded that, first, the plasma CPR response appears to be a valuable indicator of pancreatic B-cell function, and second, it is, nevertheless, modified in chronic liver or renal disorders.

Adolescent↗
PubMed1978

Effect of bombesin infused intrapancreatically on glucagon and insulin secretion.

Synthetic bombesin was infused at a dose of 20 pmoles/kg/min for 10 min into the cranial pancreaticoduodenal artery of anesthetized dogs. Plasma immunoreactive glucagon concentrations in the cranial pancreaticoduodenal vein as well as in the femoral artery were concurrently and slowly elevated. However, the net release of glucagon from the pancreas did not increase significantly during infusion of bombesin. Plasma immunoreactive insulin concentrations in the pancreatic vein were transiently raised, and a delayed rise was noted in arterial plasma IRI. Net release of insulin was significantly augmented during infusion of the tetradecapeptide. Plasma glucose levels did not change after bombesin. These results indicate that the gastrointestinal tetradecapeptide may stimulate secretion of both insulin and gut glucagonlike immunoreactivity in the dog.

Animals↗
PubMed1978

Effect of phentolamine on the somatostatin-induced inhibition of glucagon and insulin secretion.

Synthetic cyclic somatostatin was infused into either the cranial pancreaticoduodenal artery or the femoral vein of anesthetized dogs with or without previous administration of phentolamine. Somatostatin infused into the pancreatic artery at a dose of 50 ng/kg/min for 10 min caused significant decreases in blood flow and plasma basal concentrations of both glucagon and insulin in the cranial pancreaticoduodenal vein, resulting in a profound decline of bihormonal output during the infusion. Arterial plasma glucose was not reduced during the administration of somatostatin in the pancreatic artery. These somatostatin-induced decreases failed to be eliminated by a 0.2 mg/kg injection of phentolamine into the femoral vein followed by a 9-min infusion of this alpha-adrenergic blocker (0.02 mg/kg/min) into the pancreatic artery immediately prior to the somatostatin administration. An inhibition of glucagon and insulin output and a fall of plasma glucose caused by somatostatin (1.7 microgram/min) infused into the femoral vein for 30 min also were not abolished by a prolonged and simultaneous infusion of phentolamine (0.2 mg/min) into the femoral vein over a period of 2 hr. These results indicate that alpha-adrenergic receptor mechanisms do not play a major role in the inhibition of islet glucagon and insulin secretion by somatostatin.

Animals↗
PubMed1978

Degradation and secretion of insulin in hepatic cirrhosis.

To clarify the mechanism of hyperinsulinism of hepatic cirrhosis, plasma insulin and C-peptide levels before and after oral glucose loads were measured in 34 patients with cirrhosis, 15 patients with chronic hepatitis, and 25 normal subjects. While plasma immunoreactive insulin (IRI) levels during oral glucose tolerance testing (OGTT) were significantly increased in cirrhotics, plasma immunoreactive C-peptide (CPR) levels were elevated slightly. The C-peptide to insulin ratio throughout OGTT was significantly smaller in cirrhotics than in normal subjects (P less than 0.01). A decreased hepatic insulin degradation rate has been suggested to one of the main causes of hyperinsulinism in hepatic cirrhosis. The ratio of the difference between basal and 30-min CPR values and basal and 30-min OGTT blood glucose values [delta CPR: delta BS(30)'] as well as the delta IRI: delta BS(30') ratio was significantly decreased in cirrhotics (P less than 0.01). These results indicate that insulin secretion in response to a glycemic stimulus is reduced in cirrhotics. Both the ratios of the sums of six IRS and CPR values of OGTT (sigma CPR: sigma IRI) and delta CPR: delta BS(30') and sigma CPR: sigma BS(30') were found in inverse relationship with indocyanine green retention rate in cirrhotics.

Adult↗
PubMed1978

Comparison of the early time courses of the release of insulin that follow injections of tetragastrin, tolbutamide, xylitol, and glucose into the pancreatic artery of dogs.

The early time courses of insulin release were studied by injecting insulinotropic substances directly into a dog's pancreatic artery. Blood samples from the pancreatic vein were collected every five seconds continuously over 90 seconds and were assayed for their insulin concentrations. Injections were repeated two to five times, with intervals of 30 minutes. Insulin release was stimulated within one minute after injection of each of tetragastrin, tolbutamide, xylitol, and glucose, but the time courses of the release of insulin were different with different stimulants: Tetragastrin and tolbutamide increased insulin release faster than did glucose; xylitol produced a slower insulin release than did glucose. The slower insulin-releasing effects of glucose and xylitol than the other agents would be compatible with the theory that their metabolism is required to cause release of insulin, but it is also possible that the glucoreceptor mechanism may require a longer lag time than the other receptor mechanisms for the perception and transfer of the signal to release insulin.

Animals↗
PubMed1977

Effect of vasoactive intestinal polypeptide infused intrapancreatically on glucagon and insulin secretion.

Synthetic vasoactive intestinal polypeptide (VIP) was infused at a dose of 50 ng/kg/min for 10 min into the cranial pancreaticoduodenal artery in anesthetized dogs. Both mean blood flow and plasma glucagon concentration in the cranial pancreaticoduodenal vein were significantly enhanced during the infusion, indicating a great augmentation in glucagon output. The pancreatic venous plasma concentration of insulin was not significantly raised, but its output increased during the infusion, again due to the increase in plasma flow. Plasma concentration of glucagon in the femoral artery was not significantly augmented, whereas that of insulin was enhanced during VIP infusion. Mean arterial plasma glucose levels rose gradually during the infusion. Intrapancreatic pretreatment with propranolol failed to exert any significant inhibiting effect upon the VIP-induced enhancement in plasma glucose, pancreatic venous blood flow, or bihormonal output. These results suggest that the vasoactive polypeptide of intestinal origin may regulate the function of the endocrine pancreas and that this effect may not be mediated mainly via the beta-adrenergic receptor system.

Animals↗
PubMed1977

Effect of alpha adrenoreceptor stimulants infused intrapancreatically on glucagon and insulin secretion.

To see the effect of alpha adrenergic receptor stimulation upon in vivo basal secretion of glucagon and insulin, phenylephrine and methoxamine were infused at a dose of 236 pmol/kg/min and 2.36 nmol/kg/min, respectively, for 10 min into the cranial pancreaticoduodenal artery in anesthetized dogs. During the infusion of either drug pancreatic venous blood flow was markedly diminished, resulting in a significant decrease of basal output of both glucagon and insulin. Intrapancreatic administration of the stimulants exerted neglible effects on the plasma levels of both hormones in the systemic circulation. Pretreatment with phentolamine abolished the alpha stimulant-induced inhibition of bihormonal output. Under alpha blockade which per se results effectively in a stimulation of insulin release, basal output of glucagon was not significantly augmented. These results suggest that the alpha receptors on the A cell of the islets may be involved in the similar inhibitor mechanism, but less potently than those on the B cell under basal physiological adrenergic control in the canine.

Animals↗
PubMed1975

Demonstration of anti-"a-component" antibody--a possible means to differentiate patients with auto-antibodies to endogenous insulin from insulin-treated patients.

The presence of anti-"a-component" antibody was examined in sera of 4 groups of patients with or without anti-insulin antibody, using 125I-a-component and the polyethylene glycol precipitation method. 125I-a-component crossreacted with insulin antibody. This cross-reactivity was abolished after preincubation of these sera with monocomponent insulin. The specificanti-"a-component" antibody could be estimated in this procedure. After preincubation with monocomponent insulin, significant binding of 125I-a-component was demonstrated in sera of most patients treated with ordinary commercial insulin, but not in sera of 2 hypoglycemic patients suspected of an insulin autoimmune syndrome. Some cases treated with commercial insulin for less than one year and all cases treated with monocomponent insulin for 7-10 months did not have significant anti-"a-component" antibody. The test for the presence of anti-"a-component" antibody is not definitive but if positive it differentiates "auto-antibodies" from the antibodies produced by injections of commercial insulin.

Animals↗
PubMed1975

Effect of splanchnic nerve stimulation on glucagon and insulin output in the dog.

In order to study the role of the sympathetic nerves in the regulation of glucagon and insulin secretion, the distal stump of the left splanchnic nerve was electrically stimulated at the diaphragmatic level in the anesthetized dog under bilateral ligation of the adrenal veins. During stimulation, plasma glucose concentration rose rapidly, and pancreatic vein plasma concentration of glucagon increased along with pancreatic vein blood flow, indicating a greater output of glucagon. Insulin output in pancreatic vein plasma was slowly elevated despite continued stimulation. Pretreatment with propranolol resulted in a decline of the basal output of both glucagon and insulin and in their marked initial fall at the onset of the stimulus. However, glucagon output still showed a vigorous increase during neural stimulation whereas insulin output remained totally suppressed, but showed a rebound rise after cessation of stimulation. Pretreatment with phentolamine evoked an enhancement in both basal output of insulin and its response to splanchnic stimulation, but did not exert any marked effect on glucagon output. Pretreatment with atropine inhibited the basal output of glucagon and insulin, but the response of insulin output to splanchnic stimulation was not suppressed, thus excluding the possibility that activation of aberrant parasympathetic nerve fibers located in the splanchnic nerve would be responsible for the delayed increase in insulin release. The present results indicate that glucagon secretion may be regulated by different receptor mechanisms from those involved in insulin release following sympathetic activation.

Animals↗
PubMed1975

Effects of glucosamine on insulin and glucagon secretion in dogs and ducks.

The effects of infusion of glucosamine on immunoreactive glucagon (IRG) and insulin (IRI) secretion were studied in dogs and ducks. During systemic infusion of glucosamine, hyperglycemia developed and insulin secretion was inhibited in both species. An immediate and sustained elevation of peripheral IRG levels was induced in ducks but a transient rise, detectable only in the pancreatic vein blood, was provoked in dogs. Suppression of insulin release and stimulation of glucagon release may be mediated by the inhibition of glucose utilization in beta- and alpha-cells. The very prompt response of IRG in ducks may imply that glucosamine has a specific stimulating effect on the alpha-cells of ducks. Intrapancreatic administration of glucosamine in dogs, however, failed to elicit the rise of IRG, although insulin secretion was inhibited. Thus, it is suggested that the systemic administration of glucosamine in dogs may stimulate IRG secretion by some indirect effect. In one dog, however, a sustained rise of the pancreatic vein IRG was observed. Thus, the possibility cannot be ruled out that the difference in IRG response to glucosamine in dogs and ducks is quantitative rather than qualitative. Glucagon release by glucosamine may provide an additional factor to the hyperglycemic effect of glucosamine, in addition to its effect to suppress insulin release as well as its direct inhibitory effect on glucose utilization in tissues.

Animals↗