BACKGROUND The possible existence of an acini–islet–acinar(AIA)reflex,involving mutual amylase and insulin interactions,was investigated in the current acute experiment on pigs.AIM To confirm the existence of an AIA...BACKGROUND The possible existence of an acini–islet–acinar(AIA)reflex,involving mutual amylase and insulin interactions,was investigated in the current acute experiment on pigs.AIM To confirm the existence of an AIA reflex and justify the placement of the exocrine and endocrine pancreatic components within the same organ.METHODS The study was performed on six pigs under general anesthesia.An intravenous glucose tolerance test was performed,with a bolus infusion of 50%glucose to the jugular vein,while amylase(5000 U/kg)or vehicle intrapancreatic infusions were administered via the pancreaticoduodenalis cranialis artery during 30 min with a 1 mL/min flow rate.RESULTS The amylase infusion to pancreatic arterial circulation inhibited and delayed the insulin release peak which is usually associated with the highest value of blood glucose and is typically observed at 15 min after glucose infusion,for>1 h.The intrapancreatic infusion of the vehicle(saline)did not have any effect on the time frame of insulin release.Infusion of 1%bovine serum albumin changed the insulin release curve dramatically and prolonged the high range of insulin secretion,far beyond the glucose peak.CONCLUSION Intrapancreatic arterial infusion of amylase interrupted the integrated glucose–insulin interactions.This confirms an AIA reflex and justifies placement of the exocrine and endocrine pancreatic components within the same organ.展开更多
To investigate the effects of cadmium exposure on insulin expression in rats. Methods Eighteen adult SD rats were administered cadmium subcutaneously （0.5, 1.0, and 2.0 mg/kg bw）. The effects on endocrine of pancrea...To investigate the effects of cadmium exposure on insulin expression in rats. Methods Eighteen adult SD rats were administered cadmium subcutaneously （0.5, 1.0, and 2.0 mg/kg bw）. The effects on endocrine of pancreas were assessed. The levels of cadmium and zinc in pancreas, blood and urine glucose, serum insulin and urine NAG （N-acyetyl-β-glucosaminidase） were determined. The gene expressions of metallothionein （MT） and insulin were also measured, and the oral glucose tolerance tests （OGTT） were carried out. Results The contents of cadmium in pancreas in cadmium-treated rats were higher than that in the control group, which was associated with slight increase of zinc in pancreas. Cadmium-exposed rats （1.0 and 2.0 mg/kg bw） demonstrated a marked glucose intolerance. But the levels of serum insulin did not change significantly after cadmium administration, and the UNAG had no change in Cd-treated group. The gene expression of insulin decreased in 1.0 and 2.0 mg/kg bw cadmium-exposed groups, compared with the control group. The expression of MT-I was higher in the groups exposed to 1.0 and 2.0 mg/kg bw cadmium while the expression of MT-II was higher in the group exposed to 2.0 mg/kg bw cadmium. Conclusions Cadmium may be accumulated in the pancreas, resulting in the change of the expression of insulin, MT-I and MT-Ⅱ genes. Cadmium can influence the biosynthesis of insulin, but does not induce the release of insulin. The dysfunction of pancreas occurs earlier than that of kidney after administration of cadmium.展开更多
The nature of the binding site(s) involved in the insulin secretory activity of imidazoline compo- unds remains unclear. An imidazoline I2 binding site (I2BS) has been neglected since the classic I2 ligand, idazoxan, ...The nature of the binding site(s) involved in the insulin secretory activity of imidazoline compo- unds remains unclear. An imidazoline I2 binding site (I2BS) has been neglected since the classic I2 ligand, idazoxan, does not release insulin. Using the rabbit as an appropriate model for the study of this type of binding sites, we have tried to re-evaluate the effects of idazoxan, the selective I2 compound BU 224, and efaroxan on insulin secretion. Mimicking efaroxan, idazoxan and BU 224 potentiated insulin release from perifused islets in the presence of 8 mM glucose. In static incubation, insulin secretion induced by idazoxan and BU 224 exhibited both dose and glucose dependencies. ATP-sensitive K+ (KATP) channel blockade, though at a different site from the SUR1 receptor, with subsequent Ca2+ entry, mediates the insulin releasing effect of the three ligands. However, additional MAO independent intracellular steps in stimulus- secretion coupling linked to PKA and PKC activation are only involved in the effect of BU 224. Therefore, both an I2 related binding site at the channel level shared by the three ligands and a putative I3-intracellularly located binding site stimulated by BU 224 would be mediating insulin release by these compounds. In vivo experiments reassess the abilities of idazoxan and BU 224 to enhance glucose-induced insulin secretion and to elicit a modest blood glucose lowering response.展开更多
The aim of this study was to examine the inhibitory effect of acute oral chlorogenic acid (CGA) ingestion on increases in blood glucose levels following glucose tolerance testing. Ten healthy male adults (age: 25.9 &#...The aim of this study was to examine the inhibitory effect of acute oral chlorogenic acid (CGA) ingestion on increases in blood glucose levels following glucose tolerance testing. Ten healthy male adults (age: 25.9 ± 5.4 years) participated in the study. Blood samples were collected from the antecubital vein of subjects following overnight fasting. After a 120-min rest, they were administered 75 g glucose and chlorogenic acid or placebo. The amount of chlorogenic acid administered (in the form of capsules) to the subjects was 0.1g per body mass. In addition, only capsules were ingested in placebo ingestion conditions. Blood samples were collected 4 times during the 120-min rest period at intervals of 30 min. Serum insulin and plasma glucose levels were analyzed. Serum insulin levels increased significantly at 30 min after glucose ingestion, and fixed until 120 min in both conditions. Plasma glucose level increased significantly at 30 min after glucose ingestion, followed by a slow decrease. In addition, no significant difference was found between the conditions in each parameter. In conclusion, acute oral chlorogenic acid ingestion may not inhibition blood glucose increase following glucose tolerance.展开更多
文摘BACKGROUND The possible existence of an acini–islet–acinar(AIA)reflex,involving mutual amylase and insulin interactions,was investigated in the current acute experiment on pigs.AIM To confirm the existence of an AIA reflex and justify the placement of the exocrine and endocrine pancreatic components within the same organ.METHODS The study was performed on six pigs under general anesthesia.An intravenous glucose tolerance test was performed,with a bolus infusion of 50%glucose to the jugular vein,while amylase(5000 U/kg)or vehicle intrapancreatic infusions were administered via the pancreaticoduodenalis cranialis artery during 30 min with a 1 mL/min flow rate.RESULTS The amylase infusion to pancreatic arterial circulation inhibited and delayed the insulin release peak which is usually associated with the highest value of blood glucose and is typically observed at 15 min after glucose infusion,for>1 h.The intrapancreatic infusion of the vehicle(saline)did not have any effect on the time frame of insulin release.Infusion of 1%bovine serum albumin changed the insulin release curve dramatically and prolonged the high range of insulin secretion,far beyond the glucose peak.CONCLUSION Intrapancreatic arterial infusion of amylase interrupted the integrated glucose–insulin interactions.This confirms an AIA reflex and justifies placement of the exocrine and endocrine pancreatic components within the same organ.
基金This study was supported by 973 Program of China (2002 CB 512905).
文摘To investigate the effects of cadmium exposure on insulin expression in rats. Methods Eighteen adult SD rats were administered cadmium subcutaneously （0.5, 1.0, and 2.0 mg/kg bw）. The effects on endocrine of pancreas were assessed. The levels of cadmium and zinc in pancreas, blood and urine glucose, serum insulin and urine NAG （N-acyetyl-β-glucosaminidase） were determined. The gene expressions of metallothionein （MT） and insulin were also measured, and the oral glucose tolerance tests （OGTT） were carried out. Results The contents of cadmium in pancreas in cadmium-treated rats were higher than that in the control group, which was associated with slight increase of zinc in pancreas. Cadmium-exposed rats （1.0 and 2.0 mg/kg bw） demonstrated a marked glucose intolerance. But the levels of serum insulin did not change significantly after cadmium administration, and the UNAG had no change in Cd-treated group. The gene expression of insulin decreased in 1.0 and 2.0 mg/kg bw cadmium-exposed groups, compared with the control group. The expression of MT-I was higher in the groups exposed to 1.0 and 2.0 mg/kg bw cadmium while the expression of MT-II was higher in the group exposed to 2.0 mg/kg bw cadmium. Conclusions Cadmium may be accumulated in the pancreas, resulting in the change of the expression of insulin, MT-I and MT-Ⅱ genes. Cadmium can influence the biosynthesis of insulin, but does not induce the release of insulin. The dysfunction of pancreas occurs earlier than that of kidney after administration of cadmium.
文摘The nature of the binding site(s) involved in the insulin secretory activity of imidazoline compo- unds remains unclear. An imidazoline I2 binding site (I2BS) has been neglected since the classic I2 ligand, idazoxan, does not release insulin. Using the rabbit as an appropriate model for the study of this type of binding sites, we have tried to re-evaluate the effects of idazoxan, the selective I2 compound BU 224, and efaroxan on insulin secretion. Mimicking efaroxan, idazoxan and BU 224 potentiated insulin release from perifused islets in the presence of 8 mM glucose. In static incubation, insulin secretion induced by idazoxan and BU 224 exhibited both dose and glucose dependencies. ATP-sensitive K+ (KATP) channel blockade, though at a different site from the SUR1 receptor, with subsequent Ca2+ entry, mediates the insulin releasing effect of the three ligands. However, additional MAO independent intracellular steps in stimulus- secretion coupling linked to PKA and PKC activation are only involved in the effect of BU 224. Therefore, both an I2 related binding site at the channel level shared by the three ligands and a putative I3-intracellularly located binding site stimulated by BU 224 would be mediating insulin release by these compounds. In vivo experiments reassess the abilities of idazoxan and BU 224 to enhance glucose-induced insulin secretion and to elicit a modest blood glucose lowering response.
文摘The aim of this study was to examine the inhibitory effect of acute oral chlorogenic acid (CGA) ingestion on increases in blood glucose levels following glucose tolerance testing. Ten healthy male adults (age: 25.9 ± 5.4 years) participated in the study. Blood samples were collected from the antecubital vein of subjects following overnight fasting. After a 120-min rest, they were administered 75 g glucose and chlorogenic acid or placebo. The amount of chlorogenic acid administered (in the form of capsules) to the subjects was 0.1g per body mass. In addition, only capsules were ingested in placebo ingestion conditions. Blood samples were collected 4 times during the 120-min rest period at intervals of 30 min. Serum insulin and plasma glucose levels were analyzed. Serum insulin levels increased significantly at 30 min after glucose ingestion, and fixed until 120 min in both conditions. Plasma glucose level increased significantly at 30 min after glucose ingestion, followed by a slow decrease. In addition, no significant difference was found between the conditions in each parameter. In conclusion, acute oral chlorogenic acid ingestion may not inhibition blood glucose increase following glucose tolerance.
