ABSTRACT
Objective To investigate correlation between vitamin D and glucose metabolism,lipid metabolism, insulin resistance,early secretory function of pancreatic islets in postmenopausal women with type 2 diabetes. Methods 115 postmenopausal women with type 2 diabetes were selected as observation group.115 postmenopausal women without type 2 diabetes were selected in hospital at same period as control group.All patients received detection of vitamin D,glucose metabolism,lipid metabolism,insulin resistance,early secretory function of pancreatic islets. Correlation between vitamin D and glucose metabolism,lipid metabolism,insulin resistance,early secretory function of pancreatic islets were analyzed.Results Fasting blood glucose,postprandial 2h blood glucose,glycosylated hemoglobin, body mass index,total cholesterol,triglyceride,low density lipoprotein cholesterol,insulin resistance index in the observation group were higher than the control group [(8.5 ±1.2)mmol/L vs (5.1 ±0.6)mmol/L,(13.4 ± 1.5)mmol/L vs (7.8 ±0.7)mmol/L,(8.7 ±1.1)% vs (5.6 ±0.5)%,(25.7 ±1.0)kg/m2 vs (22.3 ±0.4)kg/m2 , (5.6 ±0.7)mmol/L vs (4.5 ±0.4)mmol/L,(2.3 ±0.5)mmol/L vs (1.7 ±0.3)mmol/L,(3.5 ±0.6)mmol/L vs (2.2 ±0.4)mmol/L,(3.6 ±0.5)vs (2.5 ±0.4),t =9.667,10.179,8.535,4.524,5.443,6.529,8.909,7.406, all P <0.05].High density lipoprotein cholesterol,insulin first secretion phase peak factor,pancreatic islet βcell function index,fasting insulin,vitamin D in the observation group were lower than the control group [(1.0 ± 0.2)mmol/L vs (1.2 ±0.3)mmol/L,(5.2 ±1.3)vs (8.4 ±1.6),(135.8 ±11.7)vs (194.3 ±19.2),(4.1 ± 0.9)IU /mL vs (10.8 ±0.6)IU /mL,(10.8 ±2.1)ng/L vs (27.4 ±3.8)ng/L,t =5.087,9.153,7.370,10.414, 18.371,all P <0.05].Vitamin D was significantly negatively correlated with fasting blood glucose,postprandial 2h blood glucose,glycosylated hemoglobin,body mass index,total cholesterol,triglyceride,low density lipoprotein choles-terol,insulin resistance index(r =-0.537,-0.512,-0.469,-0.387,-0.325,-0.316,-0.372,-0.457,all P <0.05).Vitamin D were significantly positively correlated with high density lipoprotein cholesterol,insulin first secretion phase peak factor,pancreatic islet βcell function index,fasting insulin(r =0.351,0.418,0.674,0.316,all P <0.05).Conclusion Vitamin D deficiency in postmenopausal women with type 2 diabetes may be involved in glucose -lipid metabolism and insulin resistance,but also may be one of the reasons leading to decreasing of early secretory function of pancreatic βcells.
ABSTRACT
In the previous studies, we found that endurance training increased pancreatic weight, protein content, and enzyme activity with hypertrophied acinar cells in rats. The purpose of the present study was to investigate the effect of endurance training on pancreatic exocrine response to CCK in rats. Female F344 rats were divided into control (C, n=6) and endurance training (T, n=6) groups. The trained rats were exercised for 60 min on a treadmill (final speed, 35 m/min), 5 days a week, for 8 weeks. Food intake in both groups was matched. On the final day of the experiment, the rats were anesthetized after an overnight fast and prepared with cannulae into the pancreatic duct. After 1-h basal collection with 0.9% NaCl (7.5 ml/kg body weight/h) injected intravenously, CCK-8 (0.06μg/kg body weight/h) was injected intravenously and pancreatic secretions were collected for the additional three 1-h periods. Final body weight in the T group was slightly, but not significantly, lower than in the C group (C : 145±6, T : 137±8 g). Pancreatic wet weight in the T group was significantly higher than in the C group (C : 4.14±0.16, T : 4.71±0.18 mg/g BW). CCK-stimulated pancreatic juice secretion was not significantly changed. There were significant increases in pancreatic protein and amylase secretions with CCK administration. CCK-stimulated pancreatic protein and amylase secretions were significant higher in the T group than in the C group. Total pancreatic protein secretion with CCK administration during 3 hours were significant higher in the T group than in the C group (C : 2.52±1.92, T : 5.11±1.50 mg/3 h). Total amylase secretion with CCK administration during 3 hours were also significant higher in the T group than in the C group (C : 0.69±0.43, T : 1.12±0.37 U/3 h). These results suggest that the endurance training increased pancreatic exocrine secretion response to CCK. CCK may play an important role in exercise-induced enhancement of the exocrine pancreas.
ABSTRACT
To clarify the roles of gonadal steroids on pancreatic exocrine secretion, effects of progesterone and estradiol-17beta on spontaneous and secretagogue-induced exocrine response of isolated perfused rat pancreas were investigated. Intra-arterial infusion of progesterone resulted in significant increase of the spontaneous pancreatic fluid and amylase secretion dose-dependently. However, estradiol-17beta did not exert any influence on spontaneous pancreatic exocrine secretion. Exogenous secretin, cholecystokinin (CCK), and acetylcholine markedly stimulated pancreatic fluid and amylase secretion. Progesterone initially enhanced secretin-induced amylase secretion, but this stimulatory response declined thereafter to basal value. Moreover, secretin-induced fluid secretion was not affected by infusion of progesterone. Therefore, initial increase of secretion-induced amylase secretion by progesterone seems to be a non-specific action by washout effect of secretin. Estradiol-17beta failed to change the secretin-induced fluid and amylase secretion. Both progesterone and estradiol-17beta did not exert any influence on CCK-induced fluid and amylase secretion. Acetylcholine-induced exocrine secretion of isolated perfused pancreas also was not affected by intra-arterial infusion of progesterone or estradiol-17beta. It is concluded from the above results that progesterone could enhance the spontaneous pancreatic fluid and amylase secretion of isolated perfused rat pancreas through non-genomic short- term action, and that these effects could be masked by more potent stimulants such as secretin, CCK, and acetylcholine.
Subject(s)
Animals , Rats , Acetylcholine , Amylases , Cholecystokinin , Estradiol , Gonads , Infusions, Intra-Arterial , Masks , Pancreas , Progesterone , Secretin , SteroidsABSTRACT
A role of endogenous somatostatin in pancreatic exocrine secretion induced by intrapancreatic cholinergic activation was studied in the isolated rat pancreas perfused with modified Krebs-Henseleit solution. Intrapancreatic neurons were activated by electrical field stimulation (EFS: 15 V, 2 msec and 8 Hz). Pancreatic exocrine secretion, including volume flow and amylase output, and release of somatostatin from the pancreas were respectively determined. Somatostatin cells in the islet were stained with an immunoperoxidase method. EFS significantly increased pancreatic volume flow and amylase output, which were reduced by atropine by 59% and 78%, respectively. Intraarterial infusion of either pertussis toxin or a somatostatin antagonist resulted in a further increase in the EFS-evoked pancreatic secretion. EFS also further elevated exocrine secretion in the pancreas treated with cysteamine, which was completely restored by intraarterial infusion of somatostatin. EFS significantly increased not only the number of immunoreactive somatostatin cells in the islet but also the concentration of immunoreactive somatostatin in portal effluent. It is concluded from the above results that intrapancreatic cholinergic activation elevates pancreatic exocrine secretion as well as release of endogenous somatostatin. Endogenous somatostatin exerts an inhibitory influence on exocrine secretion induced by intrapancreatic cholinergic activation via the islet-acinar portal system in the isolated pancreas of the rat.