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C Nakanome

Publications and source records attributed to C Nakanome.

At least 19 recordsLinked to original sources
PubMed1990

[The diameter of main pancreatic duct on endoscopic retrograde pancreatography and the appearance of main pancreatic duct on computed tomography: a comparative study].

We have carried out a comparative study of the diameter of main pancreatic duct (MPD) on endoscopic retrograde pancreatography (ERP) with the frequency of detection of MPD by computed tomography (CT) in order to clarify the importance of MPD appearance on CT in the pancreatic and biliary diseases. The normal MPD on ERP was demonstrated by CT in a low frequency. MPD was most frequently observed in the pancreatic body on CT. The dilatation of MPD on ERP was found in both moderate and advanced pancreatitis group. However, the significant demonstration of MPD by CT was found in advanced group alone. We observed that CT finding of dilated duct correlated with that on ERP in advanced group alone.

Cholangiopancreatography, Endoscopic Retrograde↗
PubMed1984

Somatostatinoma syndrome accompanied by overproduction of pancreatic polypeptide.

A case of somatostatin and pancreatic polypeptide (PP) producing tumor of the pancreas is presented. A 65-year-old woman was admitted for the evaluation of the tumor in the right upper quadrant of the abdomen. Clinical abnormalities included diabetic glucose intolerance, pancreatic insufficiency and marked dilatation of gallbladder. Marked high concentration of plasma PP and low levels of plasma insulin and glucagon were observed before operation. Plasma insulin concentrations in response to oral glucose tolerance test and arginine infusion were markedly low. A large quantity of somatostatin (4,300 ng/g ww) as well as PP (1,340 ng/g ww) was detected in the tumor, and somatostatin cells and PP cells were determined by immunofluorescence studies. After operation, pancreatic insufficiency and glucose intolerance were improved, and the patient made a favorable progress.

Aged↗
PubMed1984

Serum group I pepsinogen (PG I) levels and their changes in the healing process of the ulcer in patients with and without unoperated recurrent ulcer.

We measured serum group I pepsinogen (PG I) levels in subjects with endoscopically normal gastric and duodenal mucosa and patients with peptic ulcer. The release mechanism of PG I into blood stream was also investigated. The mean (+/- S.E.) serum PG I level in 136 subjects with endoscopically normal mucosa was 61 +/- 2 ng/ml and the normal range was calculated to be 30-109 ng/ml from the frequency distribution. In the patients with unoperated recurrent duodenal ulcer, the serum PG I levels remained high with the healing process of the ulcer. On the other hand, in the patients with non-recurrent duodenal ulcer and those with recurrent or non-recurrent gastric ulcer, the serum PG I levels decreased with the healing process of the ulcer gradually and significantly from the value in the active stage. These findings suggest that duodenal ulcer patients with high levels of serum PG I throughout the healing process of the ulcer tend to have the recurrence. Therefore, the serial measurements of serum PG I with the healing process will be helpful for the prediction of ulcer recurrence. Administration of atropine caused a significant decrease in serum PG I in the patients with duodenal ulcer, which suggests the vagal control of PG I release in duodenal ulcer patients.

Adolescent↗
PubMed1983

Serum group I pepsinogen levels in patients with peptic ulcer and normal subjects.

Serum group I pepsinogen (PG I) levels were measured by radioimmunoassay in patients with peptic ulcer and normal subjects. The mean (+/-S.E.) serum PG I level in 318 normal subjects was 79 +/- 3 ng/ml. The level in males, 87 +/- 2 ng/ml (n = 246), was significantly higher than in females, 72 +/- 4 ng/ml (n = 72). The serum PG I levels in the patients with gastric ulcer and in those with duodenal ulcer were 91 +/- 7 ng/ml (n = 31) and 117 +/- 10 ng/ml (n = 31), respectively. Both values were significantly higher than the value in the subjects with endoscopically normal mucosa (63 +/- 5 ng/ml). No significant change in serum PG I was observed after subcutaneous injection of tetragastrin or after ingestion of meal. A significant correlation was found between serum PG I and stimulated pepsin output, peak pepsin output, and maximal acid output and peak acid output. These findings suggest that serum PG I may be determined by the chief cell mass.

Adult↗
PubMed1983

Characteristics of decrease of plasma gastrin by glucagon in man.

Exogenously administered glucagon causes a decrease of plasma gastrin concentration, but the mechanism has not been fully elucidated. We measured antral gastrin concentrations and plasma gastrin levels before and during glucagon infusion in nine patients free of gastrointestinal diseases. In addition, we measured plasma gastrin levels in both the renal artery and renal vein in six patients with normal renal function before and during glucagon infusion. Glucagon caused a significant increase of antral gastrin concentration concomitant with a significant decrease of plasma gastrin level and a significant decrease of percent extraction of gastrin in the kidney. These observations suggest that glucagon causes the decrease of plasma gastrin level by inhibiting the release of gastrin from the antrum, but not by accelerating the renal extraction of gastrin.

Adult↗
PubMed1983

Disturbances of the alimentary tract motility and hypermotilinemia in the patients with diabetes mellitus.

Lower esophageal sphincter pressure (LESP), gastric emptying, small bowel transit time and plasma motilin levels were measured in diabetics and normal subjects in order to investigate the disturbances of the alimentary tract motility and the participation of motilin in these motility disorders. Hypermotilinemia was observed in all diabetics with or without autonomic neuropathy. Low response of LESP to tetragastrin found in diabetics with autonomic neuropathy could not be explained by motilin. Gastric emptying was highly correlated with fasting plasma motilin levels and a significantly accelerated gastric emptying observed in diabetics without complications or diabetics with diarrhea was considered to be due to hypermotilinemia. On the contrary, no significant correlation was observed between small bowel transit time and plasma motilin levels, suggesting no participation of endogenous motilin in the regulation of small bowel transit.

Adolescent↗
PubMed1983

Gastric inhibitory polypeptide (GIP) response to an oral glucose load in the patients with diabetes mellitus.

Plasma gastric inhibitory polypeptide (GIP) concentrations following an oral glucose load were measured in 27 diabetics and 10 normal subjects. Plasma GIP concentrations increased significantly from the mean basal value following an oral glucose load in both groups. Diabetics showed significantly higher levels of plasma GIP in association with delayed and diminished peak increases in plasma insulin levels. When diabetics were divided into two groups according to their basal levels of blood glucose, moderate and severe diabetics exhibited more exaggerated increments of plasma GIP than mild diabetics. This exaggerated GIP response to an oral glucose load in proportion to the glucose intolerance indicates a relative failure of the beta cell response to GIP in diabetics and that the mechanism involved in hypersecretion of GIP would be diminution of the inhibition of GIP release caused by insulin in diabetics.

Adult↗
PubMed1983

A 10 year follow-up of diabetes in a rural area of Japan using the 50 g oral glucose tolerance test.

We performed a 10 year follow-up study on diabetics using the 50 g oral glucose tolerance test in a rural area of Japan. In untreated borderline diabetics, high or normal insulin responders became normal for glucose tolerance 10 years later. However, low insulin responders became overt diabetics or remained borderline diabetics. Therefore, insulinogenic index was considered to be one of the most valuable indexes in the prospective investigation of untreated borderline diabetics.

Adult↗
PubMed1982

[The effect of calcium on the release of gastric inhibitory polypeptide (GIP) - with reference to the release of GIP in patients with hyperparathyroidism (author's transl)].

Plasma gastric inhibitory polypeptide (GIP), insulin, glucagon concentrations and blood glucose levels in response to the ingestion of 100 g glucose were measured in 5 patients with hyperparathyroidism in order to elucidate the effect of hypercalcemia on the release of these hormones. In addition, the effect of acute hypercalcemia on the release of these hormones in response to glucose ingestion was investigated in normal subjects. Fasting plasma GIP concentration in patients with hyperparathyroidism was significantly greater than the value in seventeen normal subjects. Significantly higher responses of plasma GIP and insulin were observed after the glucose ingestion in the patients with hyperparathyroidism as compared with the values in the normal subjects, and integrated GIP and insulin responses to the glucose ingestion for 120 min in the patients with hyperparathyroidism were significantly greater than the values in the normal subjects. On the other hand, plasma glucagon concentration after the glucose ingestion in the patients with hyperparathyroidism remained unchanged, although plasma glucagon concentrations after the glucose ingestion decreased significantly from the basal value in the normal subjects. Blood glucose levels after the glucose ingestion in two groups increased significantly from the basal value in the same manner. In nine normal subjects calcium infusion (4 mg/kg bolus injection followed by continuous infusion of 4 mg/kg/hr for 3 hr) caused a significantly high concentration of plasma calcium (11.5 approximately 13.0 mg/dl) from the basal value. Significantly higher responses of plasma GIP and insulin to the glucose ingestion were observed during calcium infusion as compared with the values during saline infusion. On the other hand, plasma glucagon concentration after the glucose ingestion was not significantly changed during calcium infusion in contrast with a significant decrease of plasma glucagon after the glucose ingestion during saline infusion. Consequently, calcium was considered to play a major part in the release of GIP and insulin. The characteristic response of plasma glucagon during calcium infusion was considered, at least in part, to protect the hypoglycemia caused by hyperinsulinemia.

Adult↗
PubMed1982

Release of gastric inhibitory polypeptide (GIP) during calcium infusion and in hyperparathyroidism.

Gastric inhibitory polypeptide (GIP) is a candidate hormone for an incretin which stimulates or potentiates insulin secretion. We elucidated that, in five patients with hyperparathyroidism, GIP and insulin responded remarkably to glucose ingestion, and that hypercalcaemia appeared to have a stimulatory effect on glucose-induced GIP release as well as on insulin release. In nine healthy subjects a 2% calcium solution was continuously infused intravenously and a hypercalcaemic state was maintained. This caused GIP to respond significantly more to glucose ingestion. In spite of GIP being considered an incretin in the normoglycaemic state, GIP does not markedly stimulate insulin secretion. However, in the hypercalcaemic state in healthy subjects, glucose-induced GIP and insulin secretion is significantly greater than in the normocalcaemic state. The potentiated response of insulin to glucose may be caused, in part, by GIP.

Adult↗
PubMed1982

[Motilin].

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Diarrhea↗