scholarly journals Evaluation of Antidiabetic Effects of the Traditional Medicinal PlantGynostemma pentaphyllumand the Possible Mechanisms of Insulin Release

2015 ◽  
Vol 2015 ◽  
pp. 1-7 ◽  
Author(s):  
Ezarul Faradianna Lokman ◽  
Harvest F. Gu ◽  
Wan Nazaimoon Wan Mohamud ◽  
Claes-Göran Östenson
Keyword(s):  
Glucose Tolerance ◽  
Insulin Release ◽  
Pertussis Toxin ◽  
Plasma Insulin ◽  
Insulin Response ◽  
Gk Rat ◽  
Insulin Levels ◽  
Gk Rats ◽  
Plasma Insulin Levels ◽  
Antidiabetic Effects

Aims. To evaluate the antidiabetic effects ofGynostemma pentaphyllum(GP) in Goto-Kakizaki (GK) rat, an animal model of type 2 diabetes, and to investigate the mechanisms of insulin release.Methods. Oral glucose tolerance test was performed and plasma insulin levels were measured.Results. An oral treatment withGP(0.3 g/kg of body weight daily) for two weeks in GK rats improved glucose tolerance versus placebo group (P<0.01). Plasma insulin levels were significantly increased in theGP-treated group. The insulin release fromGP-treated GK rats was 1.9-fold higher as compared to the control group (P<0.001).GPstimulated insulin release in isolated GK rat islets at high glucose. Opening of ATP-sensitive potassium (K-ATP) channels by diazoxide and inhibition of calcium channels by nifedipine significantly decreased insulin response toGP. Furthermore, the protein kinase A (PKA) inhibitor H89 decreased the insulin response toGP(P<0.05). In addition,GP-induced insulin secretion was decreased after preincubation of GK islets with pertussis toxin to inhibit exocytoticGeproteins (P<0.05).Conclusion.The antidiabetic effect ofGPis associated with the stimulation of insulin release from the islets.GP-induced insulin release is partly mediated via K-ATP and L-type Ca2+channels, the PKA system and also dependent on pertussis toxin sensitiveGe-protein.

Endocrine pancreatic morphology and function in exocrine insufficiency in rats

1987 ◽  
Vol 253 (2) ◽  
pp. G139-G145
Author(s):  
B. Goke ◽  
K. Elsebach ◽  
W. Hausmann ◽  
M. Schaar ◽  
R. Arnold ◽  
...  
Keyword(s):  
Oleic Acid ◽  
Glucose Tolerance ◽  
Insulin Release ◽  
Plasma Insulin ◽  
Insulin Response ◽  
Serum Glucose ◽  
Relative Distribution ◽  
Perfused Pancreas ◽  
Insulin Levels ◽  
Plasma Insulin Levels

Exocrine pancreatic insufficiency was induced in rats by injection of oleic acid into the pancreatic duct. Six weeks after a single injection of 50 microliters oleic acid, the exocrine tissue was reduced by 98%. The islets of Langerhans remained intact and showed no changes in the relative distribution of beta-, alpha-, D-, and PP-cells. In rats fed ad libitum, plasma insulin levels and pancreatic insulin content did not differ between oleic acid-treated animals and controls. The dynamic insulin response was evaluated in the isolated perfused pancreas. The biphasic pattern of insulin release after stimulation by glucose was preserved. The half-maximal (10 mM) glucose-induced insulin release was reduced to 49% after onset of exocrine atrophy. After stimulation of insulin secretion by a maximal glucose load (20 mM), the insulin output from the perfused pancreas was reduced to 56%. A reduction in insulin release to 24% occurred with respect to the arginine (15 + 10 mM glucose)-stimulated secretion. To evaluate the significance of these findings in intact animals, glucose tolerance tests were performed. There were no differences between oleic acid-, saline-, or untreated animals with respect to serum glucose or plasma insulin levels during the oral glucose tolerance test. The insulin response after intravenous glucose in oleic acid-treated rats was not statistically different from controls. Nevertheless, the serum glucose levels in rats with exocrine atrophy were above controls, indicating a slight impairment of glucose tolerance.

scholarly journals The possible mechanisms by which phanoside stimulates insulin secretion from rat islets

2007 ◽  
Vol 192 (2) ◽  
pp. 389-394 ◽  
Author(s):  
Nguyen Khanh Hoa ◽  
Åke Norberg ◽  
Rannar Sillard ◽  
Dao Van Phan ◽  
Nguyen Duy Thuan ◽  
...  
Keyword(s):  
Insulin Secretion ◽  
B Cells ◽  
Pancreatic Islets ◽  
Insulin Release ◽  
Pertussis Toxin ◽  
Insulin Response ◽  
Gk Rat ◽  
Isolated Pancreatic Islets ◽  
Gk Rats ◽  
Rat Islets

We recently showed that phanoside, a gypenoside isolated from the plant Gynostemma pentaphyllum, stimulates insulin secretion from rat pancreatic islets. To study the mechanisms by which phanoside stimulates insulin secretion. Isolated pancreatic islets of normal Wistar (W) rats and spontaneously diabetic Goto-Kakizaki (GK) rats were batch incubated or perifused. At both 3.3 and 16.7 mM glucose, phanoside stimulated insulin secretion several fold in both W and diabetic GK rat islets. In perifusion of W islets, phanoside (75 and 150 μM) dose dependently increased insulin secretion that returned to basal levels when phanoside was omitted. When W rat islets were incubated at 3.3 mM glucose with 150 μM phanoside and 0.25 mM diazoxide to keep K-ATP channels open, insulin secretion was similar to that in islets incubated in 150 μM phanoside alone. At 16.7 mM glucose, phanoside-stimulated insulin secretion was reduced in the presence of 0.25 mM diazoxide (P<0.01). In W islets depolarized by 50 mM KCl and with diazoxide, phanoside stimulated insulin release twofold at 3.3 mM glucose but did not further increase the release at 16.7 mM glucose. When using nimodipine to block L-type Ca2+ channels in B-cells, phanoside-induced insulin secretion was unaffected at 3.3 mM glucose but decreased at 16.7 mM glucose (P<0.01). Pretreatment of islets with pertussis toxin to inhibit exocytotic Ge-protein did not affect insulin response to 150 μM phanoside. Phanoside stimulated insulin secretion from Wand GK rat islets. This effect seems to be exerted distal to K-ATP channels and L-type Ca2+ channels, which is on the exocytotic machinery of the B-cells.

Interactions of cold exposure and starvation on glucose tolerance and insulin response

1983 ◽  
Vol 245 (6) ◽  
pp. E575-E581 ◽  
Author(s):  
A. L. Vallerand ◽  
J. Lupien ◽  
L. J. Bukowiecki
Keyword(s):  
Glucose Tolerance ◽  
Cold Acclimation ◽  
Cold Exposure ◽  
Plasma Insulin ◽  
Insulin Response ◽  
Insulinogenic Index ◽  
Intravenous Glucose ◽  
Peripheral Tissues ◽  
Insulin Levels ◽  
Plasma Insulin Levels

The metabolic interactions of cold exposure, cold acclimation, and starvation on glucose tolerance and plasma insulin levels were studied in precannulated, unrestrained, and unanesthetized rats. Cold exposure (48 h at 5 degrees C) significantly reduced the insulin response to intravenous glucose injection (P less than 0.01) while improving glucose tolerance (P less than 0.01). Starvation (48 h at 25 degrees C) also reduced the insulin response (P less than 0.01) but did not significantly alter glucose tolerance. “Accelerated starvation” induced by starving rats for 48 h at 5 degrees C dramatically reduced both basal and glucose-stimulated insulin levels while even improving glucose tolerance, resulting in a 15-fold reduction in the insulinogenic index. Cold acclimation (3 wk at 5 degrees C) induced essentially the same alterations as cold exposure. Approximately reversed changes were observed when cold-acclimated rats were returned to a warm environment for 15–18 h. Results from these studies indicate that 1) cold exposure and starvation, but not cold acclimation, act synergistically in decreasing the sensitivity and/or the capacity of pancreatic islets for secreting insulin in response to glucose stimulation; 2) glucose tolerance and possibly insulin sensitivity of peripheral tissues are enhanced by cold exposure and starvation, although glucose tolerance is improved by cold exposure only, not by starvation; 3) an improved glucose tolerance with barely detectable plasma insulin levels was obtained in cold-starved rats under normal physiological conditions.

scholarly journals Glucose Tolerance and Insulin Release in Malnourished Rats

1976 ◽  
Vol 50 (3) ◽  
pp. 153-163 ◽  
Author(s):  
C. Weinkove ◽  
E. A. Weinkove ◽  
B. L. Pimstone
Keyword(s):  
Blood Glucose ◽  
Glucose Tolerance ◽  
Insulin Release ◽  
Glucose Concentration ◽  
Plasma Insulin ◽  
Blood Glucose Concentration ◽  
Protein Energy Malnutrition ◽  
Insulin Response ◽  
Intravenous Glucose ◽  
Protein Energy

1. Young Wistar rats were used as an experimental model to determine the effects of protein-energy malnutrition on glucose tolerance and insulin release. 2. Malnourished rats presented some of the features commonly found in human protein-energy malnutrition, such as failure to gain weight, hypoalbuminaemia, fatty infiltration of the liver and intolerance of oral and intravenous glucose loads. 3. The rate of disappearance of glucose from the gut lumen was greater in the malnourished rats but there was no significant difference in portal blood glucose concentration between normal and malnourished rats 5 and 10 min after an oral glucose load. 4. Insulin resistance was not thought to be the cause of the glucose intolerance in the malnourished animals since these rats had a low fasting plasma insulin concentration with a normal fasting blood glucose concentration and no impairment in their hypoglycaemic response to exogenous insulin administration. Furthermore, fasting malnourished rats were unable to correct the insulin-induced hypoglycaemia despite high concentrations of hepatic glycogen. 5. Malnourished rats had lower peak plasma insulin concentrations than normal control animals after provocation with oral and intravenous glucose, intravenous tolbutamide and intravenous glucose plus aminophyllin. This was not due to a reduction in the insulin content of the pancreas or potassium deficiency. Healthy weanling rats, like the older malnourished rats, had a diminished insulin response to intravenous glucose and intravenous tolbutamide. However, their insulin response to stimulation with intravenous glucose plus aminophyllin far exceeded that of the malnourished rats. Thus the impairment of insulin release demonstrated in the malnourished rats cannot be ascribed to a ‘functional immaturity’ of the pancreas.

GLUCOSE TOLERANCE, PLASMA INSULIN LEVELS AND INSULIN SENSITIVITY IN ELDERLY PATIENTS

1979 ◽  
Vol 8 (2) ◽  
pp. 65-74 ◽  
Author(s):  
W. S. SOERJODIBROTO ◽  
C. R. C. HEARD ◽  
A. N. EXTON-SMITH
Keyword(s):  
Insulin Sensitivity ◽  
Glucose Tolerance ◽  
Elderly Patients ◽  
Plasma Insulin ◽  
Insulin Levels ◽  
Plasma Insulin Levels

scholarly journals Anti-Diabetic Potential of the Leaves of Anisomeles malabarica in Streptozotocin Induced Diabetic Rats

2017 ◽  
Vol 43 (4) ◽  
pp. 1689-1702 ◽  
Author(s):  
Peddanna Kotha ◽  
Kameswara Rao Badri ◽  
Ramya Nagalapuram ◽  
Rajasekhar Allagadda ◽  
Appa Rao Chippada
Keyword(s):  
Diabetes Mellitus ◽  
Glucose Tolerance ◽  
Ethyl Acetate ◽  
Plasma Insulin ◽  
Ethyl Acetate Extract ◽  
Glycosylated Hemoglobin ◽  
Diabetic Rats ◽  
Active Fraction ◽  
Insulin Levels ◽  
Plasma Insulin Levels

Background/Aims: Diabetes mellitus is a pandemic metabolic disorder that is affecting a majority of populations in recent years. There is a requirement for new drugs that are safer and cheaper due to the side effects associated with the available medications. Methods: We investigated the anti-diabetic activity of leaves of Anisomeles malabarica following bioactivity guided fractionation. The different solvent (hexane, ethyl acetate, methanol and water) extracts of A. malabarica leaves were used in acute treatment studies to evaluate and identify the active fraction. The ethyl acetate extract was subjected to further fractionation using silica gel column chromatography and the compounds were identified by LC-SRM/MS and GC-MS. Additional chronic treatment studies were carried out using this active fraction (AMAF) for 30 days in experimental diabetic rats. Fasting blood glucose (FBG), glycosylated hemoglobin (HbA1c), plasma insulin levels and glucose tolerance were measured along with insulin resistance/sensitivity indicators (HOMA-IR, HOMA-β and QUICKI) to assess the beneficial effects of A. malabarica in the management of diabetes mellitus. Results: Among the different solvent extracts tested, ethyl acetate extract showed maximum (66%) anti-hyperglycemic activity. The hexane and ethyl acetate (1: 1) fraction that has maximum anti-diabetic activity was identified as active fraction of A. malabarica (AMAF). The FBG, HbA1c, plasma insulin levels and insulin sensitivity/resistance indicators such as glucose tolerance, HOMA-IR, HOMA-β and QUICKI were significantly improved to near normal in diabetic rats treated with AMAF. Further, we identified key flavonoids and fatty acids as the anti-diabetic active principles from the AMAF of A. malabarica leaves. Conclusion: The results of our study suggest that Anisomeles malabarica has potential anti-diabetic activity in STZ induced diabetic rats.

Nucleus ambiguus stimulation increases plasma insulin levels in the rat

1981 ◽  
Vol 241 (1) ◽  
pp. E22-E27 ◽  
Author(s):  
D. A. Bereiter ◽  
H. R. Berthoud ◽  
M. Brunsmann ◽  
B. Jeanrenaud
Keyword(s):  
Electrical Stimulation ◽  
Insulin Release ◽  
Plasma Insulin ◽  
Inhibitory Effect ◽  
Nucleus Ambiguus ◽  
Male Rats ◽  
Insulin Levels ◽  
Adrenergic Antagonist ◽  
Cervical Vagotomy ◽  
Plasma Insulin Levels

The ventral lateral brainstem has been explored for sites that facilitate insulin release unilaterally, using electrical stimulation techniques in male rats anesthetized with alpha-chloralose/urethane. Stimulation in the region of nucleus ambiguus (amb) produced a rapid rise (by 1 min) in plasma insulin levels, whereas stimulation of brainstem regions further than 500 micrometers from amb had no consistent effect on insulin levels. The amb-induced rise in insulin was markedly exaggerated by the alpha-adrenergic antagonist, phentolamine, and was greatly diminished by bilateral cervical vagotomy or atropine pretreatment. These results strongly suggest that the amb is one source of vagal motoneurons that facilitate insulin secretion. However, amb electrical stimulation alone also activated an apparent sympathetic efferent output whose inhibitory effect on insulin release could be blocked by phentolamine.

Alterations in body fat stores and plasma insulin levels with daily intervals of heat exposure in Holtzman rats

1993 ◽  
Vol 265 (5) ◽  
pp. R1109-R1114 ◽  
Author(s):  
C. J. De Souza ◽  
A. H. Meier
Keyword(s):  
Glucose Tolerance ◽  
Ambient Temperature ◽  
Body Fat ◽  
Plasma Glucose ◽  
Plasma Insulin ◽  
Time Of Day ◽  
Light Onset ◽  
Insulin Levels ◽  
Fat Stores ◽  
Plasma Insulin Levels

The ability of timed daily increases in ambient temperature (from 22 +/- 1 degree C to 40 +/- 1 degree C for 2 h) to alter body fat stores, blood lipid levels, and insulin resistance were tested in male Holtzman rats. Of the six times of day tested only temperature pulses administered 16 h after light onset consistently decreased body weights, retroperitoneal fat stores, and plasma insulin levels. Subsequently, temperature pulses were administered either 0 (TP0) or 16 (TP16) h after light onset (light-dark 12:12 h). While no differences were observed between the TP0 group and the constant temperature (22 degrees C) controls, decreases in body weight gain, food consumption, retroperitoneal fat stores, and plasma concentrations of insulin, cholesterol, and triglycerides were consistently observed in the TP16 group. Although changes in plasma glucose during an oral glucose tolerance test were similar when the two treatment groups were compared with their respective controls, glucose tolerance was achieved with less insulin in the TP16 animals than in their respective controls. Insulin effectiveness was greater in the TP16 group as indicated by a decrease in plasma glucose, after insulin injection, that was of greater magnitude and longer duration than in controls. Hence, timed daily increases in ambient temperature may decrease obesity in part by decreasing plasma insulin levels apparently as a consequence of increased tissue sensitivity to insulin (greater glucose tolerance and less insulin intolerance). Because the treatment is effective only at a particular time of day the findings support a role for circadian neuroendocrine interactions in the regulation of these metabolic states.

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