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Biomedical subjects

Y Kai

Publications and source records attributed to Y Kai.

At least 199 records · Page 11Linked to original sources
PubMed1978

Secondary diabetic retinopathy in chronic pancreatitis.

We found abnormal glucose tolerance curves in 45 of 47 patients with chronic pancreatitis and observed secondary diabetic retinopathy in eight of 45 cases showing slight changes in the fundus. Abnormal glucose tolerance curves were somewhat related to the exocrine dysfunction of the pancreas. Slightly abnormal glucose tolerance curves were observed frequently in patients with chronic pancreatitis, and both insulin and glucagon responses were decreased. We could not explain the cause of the low frequency of secondary diabetic retinopathy in pancreatic diabetes from the results of insulin and glucagon response tests.

Adult↗
PubMed1978

Effect of caerulein upon insulin and glucagon secretion in dogs.

In order to investigate the action of caerulein upon insulin and glucagon secretion, experimental studies were carried out using anesthetized dogs, in which graded doses of caerulein were infused into the pancreatic artery, and insulin and glucagon were measured in the blood obtained from the pancreatic vein. When caerulein was administered at a rate of 15 ng/min, neigher changes of blood glucose in the femoral artery nor plasma levels of insulin or glucagon in the pancreatic vein were prominent. Caerulein infusion at a rate of 120, 240 or 480 ng/min caused a prompt rise of plasma insulin and a delayed increase of plasma glucagon in the pancreatin vein. Blood glucose in the femoral artery increased only with caerulein doses of 240 ng/min or more. A significant increase in pancreatic vein blood flow rate was demonstrated after the infusion of caerulein at a rate of 240 ng/min or more. Neither caerulein-induced insulin secretion nor glucagon secretion was influenced by a simultaneous infusion of glucose. In contrast, caerulein-induced glucagon secretion was exaggreated by a simultaneous arginine infusion. It was concluded from the present experiments that caerulein infusion into the pancreatic artery resulted in increased secretion of insulin and glucagon from the pancreas.

Animals↗
PubMed1978

Abnormal response of pancreatic glucagon to glycemic changes in diabetes mellitus.

In order to determine pancreatic alpha cell function in diabetes mellitus, plasma glucagon responses to either an oral glucose load or insulin-induced hypoglycemia were investigated. Plasma glucagon in 6 normal control subjects fell significantly after the administration of glucose, whereas the levels of plasma glucagon did not decrease after glucose ingestion in patients with diabetes mellitus. In the group with severe diabetes, whose fasting blood glucose exceeded 200 mg/100 ml, the plasma glucagon level rose after glucose administration instead of decreasing. In 6 patients with diabetes mellitus, plasma glucagon did not decrease but rather increased during a glucose tolerance test which was performed after treatment with insulin and/or diet. In 6 control subjects, there was a remarkable rise of plasma glucagon in response to insulin-induced hypoglycemia. In contrast, no significant rise in plasma glucagon was demonstrated in 19 diabetic subjects undergoing intravenous insulin test. Seven patients, in whom an insulin test was repeated after treatment with insulin, sulfonylurea, or diet had a small rise in peak plasma glucagon and an increase in the integrated area under the glucagon response curve. It is concluded that the abnormal glucagon response to changes in blood glucose might be a primary defect in diabetes mellitus.

Adult↗
PubMed1977

Heterogeneity of extractable gut glucagon-like immunoreactivity (GLI) and its lipolytic activity.

Gut glucagon-like immunoreactivity (GLI) was extracted from the mucosa of the canine intestine and was separated into two peaks by gel filtration; Peak I (7,000 daltons) and Peak II (3,500 daltons). These two peaks were purified by means of affinity chromatography using an anti-glucagon antibody as a ligand substance. These purified gut GLIs were not composed of single component, when applied to ion exchange chromatography. These partially purified Peak I and Peak II showed lipolytic activities, though very weak in potency, in vitro on the rat fat tissue at pharmacologically high concentration (5 ng eq/ml in final). It was concluded that gut GLI, even though purified, showed heterogeneity and that gut GLI revealed lipolytic activity although weak in potency compared with pancreatic glucagon.

Adipose Tissue↗
PubMed1977

Structure-activity relationships of gastrointestinal hormones: motilin, GIP, and [27-TYR]CCK-PZ.

The docosapeptide and the tritetracontapeptide corresponding to the entire amino acid sequence of porcine motilin and gastric inhibitory peptide were synthesized, and in addition, an unsulfated form of cholecystokinin-pancreozymin (CCK-PZ) was prepared to cast some light on the structure-activity relationships of these gastrointestinal hormones. In a series of motilin peptides, elimination of the pentapeptide from the amino terminus decreased the activity (in vitro contraction of rabbit duodenal muscle) to 1/250 of the whole molecule, and subsequent removal of the tripeptide Thr-Tyr-Gly resulted in the complete loss of its effects, In a series of gastric inhibitory peptides, two fragments corresponding to positions 1 to 28 and 26 to 43 were both inactive. However, the nonacosapeptide (15 to 43) retained one-fourth of the activity of the tritetracontapeptide (suppression of the gastric acid secretion stimulated by tetragastrin in Heidenhain pouch dogs). Synthetic [27-Tyr]CCK-PZ exhibited 1/250 of the activity of natural CCK-PZ (amylase release from rat pancreas). This compound was smoothly and efficiently labeled with 125I (specific activity 200 to 250 muc per mug).

Amino Acid Sequence↗
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

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↗