PubMed Health⌕ Search

Biomedical subjects

A Niki

Publications and source records attributed to A Niki.

At least 19 recordsLinked to original sources
PubMed1989

Insulin release by D-glucose anomers in a non-insulin-dependent diabetes rat model.

The alpha anomer of D-glucose is more potent than the beta anomer in stimulating insulin release. We have studied the effects of D-glucose anomers on insulin release from the perfused pancreas isolated from a rat model of non-insulin-dependent diabetes (NIDD) induced by streptozotocin injection at 2 days of age. Insulin release from the pancreas of the diabetic rat in response to 10 mM alpha-D-glucose was markedly impaired, while insulin response to the same concentration of beta-D-glucose was only slightly reduced as compared to that in the control pancreas. Thus, the pancreatic B cell of the diabetic rat did not discriminate between the alpha and beta anomers of D-glucose. Insulin release induced by 5 mM D-glyceraldehyde was decreased in the diabetic pancreas, while insulin release induced by 0.15 mg/ml tolbutamide did not differ from that in the control pancreas. Glucose oxidation in the islets isolated from the diabetic pancreas was not lower than that in comparable control islets. Treatment of the diabetic pancreas with 5 microM forskolin or 0.15 mg/ml tolbutamide did not restore its defective discrimination between the two anomers, although forskolin potentiated insulin release more markedly in the diabetic pancreas. The findings may provide some insight into the pathophysiology of the pancreatic B cell in NIDD.

Animals↗
PubMed1989

Receptors of paraneurons, with special reference to glucoreceptors.

Among glucose-recognizing paraneurons, the gustatory cell is believed to have a glucoreceptor, while the pancreatic B cell is thought to metabolize glucose for signal production for insulin release. To investigate whether a common mechanism of glucose recognition exists among these cells, we have studied the interaction of the anomers of glucose or its derivative, known as a sugar taste inhibitor, with the pancreatic B cell of normal and diabetic rats. Inhibitors of the sugar taste response inhibited glucose-induced insulin release in various manners. A non-specific inhibitor, dibucaine, impaired not only the insulin response to glucose but also the ability to discriminate the anomers of glucose, without inhibiting glucose oxidation in the islets. Dibucaine also inhibited insulin release induced by a non-glucose secretagogue, tolbutamide. The alpha anomer, but not the beta anomer, of p-nitrophenyl-D-glucopyranoside, a specific-competitive inhibitor of sugar taste response, inhibited glucose-induced insulin release, but did not inhibit insulin release induced by non-glucose secretagogues or glucose oxidation. The pancreatic B cell of a non-insulin-dependent diabetes (NIDD) rat model, the NSZ rat, exhibited low insulin response to glucose and did not discriminate between the two anomers of glucose. The diabetic B cell responded to non-glucose secretagogues to the same extent as the control. Glucose oxidation in the diabetic islets was not impaired. These findings, together with previous ones, suggest that the gustatory and pancreatic B cells have a common glucose recognition site, which has a steric preference for the alpha anomer and is impaired in NIDD.

Animals↗
PubMed1988

Insulin release by glucose anomers in a rat model of non-insulin-dependent diabetes.

The effects of the alpha and beta anomers of D-glucose on insulin release were studied in a rat model of non-insulin-dependent diabetes, which was induced by streptozotocin injection at 2 days of age. Glucose tolerance of the streptozotocin-treated rats at 8-10 weeks of age was mildly diabetic. Insulin release from the isolated perfused pancreas of the diabetic rats in response to 10 mmol/l alpha-D-glucose was markedly impaired, while insulin response to 10 mmol/l beta-D-glucose in the diabetic pancreas was only slightly reduced as compared to that in the control pancreas.

Animals↗
PubMed1988

Possible involvement of diacylglycerol-activated, Ca2+-dependent protein kinase in glucose memory of the rat pancreatic B-cell.

Exposure to high concentrations of glucose potentiates insulin release from the pancreatic B-cell stimulated by various secretagogues after an interval under basal condition. We studied the role of diacylglycerol-activated, Ca2+-dependent protein kinase (protein kinase C) in this priming effect of glucose in rat pancreatic islets, using 12-O-tetradecanoyl phorbol-13-acetate (TPA), 1-(5-isoquinolinesulfonyl)-2-methylpiperazine (H-7),N-(2-guanidinoethyl)-5-isoquinolinesulfonamide (HA-1004) and forskolin. The priming effect of glucose was mimicked by 10 nmol/l of TPA, an activator of protein kinase C, but not by 5 mumol/l of forskolin, which increases cAMP via activating adenylate cyclase. When pancreatic islets were exposed to glucose (10 mmol/l) together with 50 mumol/l of H-7, an inhibitor of protein kinase C, the secretory response to glucose (10 mmol/l) after a 30-min interval was significantly reduced compared with that in the islets previously exposed to 10 mmol/l glucose alone. In contrast, this was not the case for HA-1004, its inhibitory activity against protein kinase C being less potent than H-7. These findings suggest that protein kinase C may play an important role in the priming effect of glucose on the pancreatic B-cell.

1-(5-Isoquinolinesulfonyl)-2-Methylpiperazine↗
PubMed1985

Insulin release independent of a rise in cytosolic free Ca2+ by forskolin and phorbol ester.

The role of cytosolic free Ca2+ in insulin release was evaluated using isolated rat pancreatic islets permeabilized with digitonin and incubated in Ca-EGTA buffers to fix free Ca2+ concentration at arbitrary levels. Ca2+ induced insulin release in a concentration-dependent manner with the threshold being between 0.1 and 1 microM. The hormone release was increased by forskolin and 12-O-tetradecanoyl phorbol-13-acetate (TPA), a potent activator of adenylate cyclase and that of protein kinase C, respectively. The findings suggest that activation of both protein kinase A and protein kinase C modulate insulin release without a concomitant increase in cytosolic free Ca2+.

Animals↗
PubMed1978

Effect of alpha-D-mannose and equilibrated D-mannose of insulin release.

The effects on insulin release of alpha-D-mannose and equilibrated D-mannose were studied in the isolated perfused rat pancreas. Although phosphomannose isomerase, in contrast to phosphoglucose isomerase, is stereospecific for beta-D-mannose-6-phosphate, the alpha anomer of D-mannose (2 mg/ml) was significantly more effective than equilibrated D-mannose in stimulating insulin release. The finding does not seem to accord with the view that the signal for hexose-induced insulin release arises from the glycolytic pathway, and suggests the existence of the stereospecific glucoreceptor(s) on the pancreatic B-cell membrane.

Animals↗
PubMed1976

Interaction of alloxan and anomers of D-glucose on glucose-induced insulin secretion and biosynthesis in vitro.

The direct effects of alloxan on glucose-induced insulin secretion and biosynthesis and the interaction of alloxan and D-glucose anomers were studied in vitro by use of isolated islets from rat pancreas. Islets were pretreated by incubation for five minutes in media containing alloxan (0.2 mg./ml.) alone or alloxan with either the alpha or beta anomer of D-glucose (3 mg./ml.). After washing, batches of five islets were incubated in the medium supplemented with glucose (1.8 mg./ml.) for 60 minutes to observe insulin secretion and for 90 minutes to observe insulin biosynthesis. Prior exposure to alloxan alone produced marked inhibition of subsequent glucose-induced insulin secretion and biosynthesis. A significantly greater protection against these inhibitory effects of alloxan was observed by using the alpha anomer of D-glucose than the beta anomer. The anomeric preference of D-glucose for protecting islet cells from the inhibitory effect of alloxan on glucose-induced insulin secretion and biosynthesis was similar to that for triggering insulin secretion. Possible mechanisms of the inhibitory effect of alloxan and the protective effect of D-glucose anomers in connection with those of other sugars are discussed. It is suggested that a glucoreceptor, stereospecific to the alpha anomer of D-glucose, may exist for both insulin secretion and biosynthesis.

Alloxan↗
PubMed1975

Uptake of radioactive D-glucose anomers by pancreatic islets.

Isolated rat islets were incubated in media containing either the alpha or beta anomer of D-[1-3H]glucose for 5 min at 37 degrees. The amounts of the two anomers incorporated were determined using L-[1-14C]glucose as an extracellular space marker. The incorporation of beta-D-glucose was about twice that of alpha-D-glucose. Our previous and present results suggest that the two anomers of D-glucose each have a preferential function in pancreatic beta cells; alpha-D-glucose stimulates insulin secretion, and beta-D-glucose is transported into the cells.

Animals↗
PubMed1974

Insulin secretion by anomers of d-glucose.

Isolated rat islets were incubated for 5 minutes in the media containing either the alpha or beta anomer of D-glucose (2 milligrams per milliliter). The amounts of secreted insulin and changes of anomers ratio were concomitantly determined. In spite of rapid mutarotation, significantly greater stimulation of insulin secretion was observed by alpha-D-glucose as compared with beta-D-glucose.

Animals↗
PubMed1973

[Proinsulin].

Explore the source record for details and available documents.

Amino Acid Sequence↗