The Role of GLP-1 Receptor Expressed in Pancreatic a Cells in Regulating Glucagon Secretion

Diabetes ◽  
2018 ◽  
Vol 67 (Supplement 1) ◽  
pp. 355-OR ◽  
Author(s):  
YANQING ZHANG ◽  
KESHAB R. PARAJULI ◽  
GENEVIEVE E. SMITH ◽  
RAJESH GUPTA ◽  
WEIWEI XU ◽  
...  
Keyword(s):  
Glucagon Secretion ◽  
A Cells

scholarly journals The Difference δ-Cells Make in Glucose Control

Physiology ◽  
2018 ◽  
Vol 33 (6) ◽  
pp. 403-411 ◽  
Author(s):  
Mark O. Huising ◽  
Talitha van der Meulen ◽  
Jessica L. Huang ◽  
Mohammad S. Pourhosseinzadeh ◽  
Glyn M. Noguchi
Keyword(s):  
Glucose Control ◽  
Feedback Loop ◽  
Physiological Role ◽  
Glucagon Secretion ◽  
Negative Feedback Loop ◽  
Β Cells ◽  
Insulin And Glucagon Secretion ◽  
The Difference ◽  
Delta Cells

The role of beta and α-cells to glucose control are established, but the physiological role of δ-cells is poorly understood. Delta-cells are ideally positioned within pancreatic islets to modulate insulin and glucagon secretion at their source. We review the evidence for a negative feedback loop between delta and β-cells that determines the blood glucose set point and suggest that local δ-cell-mediated feedback stabilizes glycemic control.

scholarly journals The role of somatostatin in GLP-1-induced inhibition of glucagon secretion in mice

Diabetologia ◽  
2017 ◽  
Vol 60 (9) ◽  
pp. 1731-1739 ◽  
Author(s):  
Anne Ørgaard ◽  
Jens J. Holst
Keyword(s):  
Glucagon Secretion

Role of glucagon in mediating metabolic effects of epinephrine.

1977 ◽  
Vol 232 (5) ◽  
pp. E464
Author(s):  
E W Chideckel ◽  
C J Goodner ◽  
D J Koerker ◽  
D G Johnson ◽  
J W Ensinck
Keyword(s):  
Maximum Level ◽  
Glucagon Secretion ◽  
Metabolic Effects ◽  
Glucagon Release ◽  
Direct Effects ◽  
Fuel Metabolism ◽  
65 H ◽  
Epinephrine Dose ◽  
Beta Hydroxybutyrate

In order to separate direct effects of epinephrine on fuel metabolism from those mediated by glucagon, epinephrine (0.1 microng/kg-min) was infused for 120 min in 18- and 65-h fasted, nonanesthetized baboons with and without a concomitant somatostatin infusion. At both stages of fasting, epinephrine stimulated glucagon, secretion, and this was blocked by somatostatin. At 18 h, with epinephrine alone, glucose rose early and remained elevated throughout the infusion. In the glycogen-depleted 65-h fasted animals, there was attenuation of the early glucose rise, with glucose reaching a maximum level at 100-120 min. With somatostatin blockade of glucagon release in the 18-h fasted animals, a pattern of attenuated early glucose rise similar to that of the 65-h fasted animals occurred. Somatostatin also inhibited this early glycogenolytic response when the epinephrine dose was increased fivefold. The behavior of FFA, glycerol, and beta-hydroxybutyrate was unchanged by the addition of somatostatin to epinephrine at either stage of fasting. Thus, glucagon mediates the early glycogenolytic response to epinephrine, but not the delayed hyperglycemia and probably not the lipolysis.

scholarly journals Arginine-induced pancreatic hormone secretion during exercise in rats

1996 ◽  
Vol 81 (6) ◽  
pp. 2528-2533 ◽  
Author(s):  
Fethi Trabelsi ◽  
Jean-Marc Lavoie
Keyword(s):  
Hormone Secretion ◽  
Exercise Bout ◽  
Glucagon Secretion ◽  
Sympathoadrenal System ◽  
Control Groups ◽  
Insulin And Glucagon Secretion ◽  
Hormone Responses ◽  
Pancreatic Hormone ◽  
Hepatic Branch

Trabelsi, Fethi, and Jean-Marc Lavoie. Arginine-induced pancreatic hormone secretion during exercise in rats. J. Appl. Physiol. 81(6): 2528–2533, 1996.—The aim of the present investigation was to 1) determine whether arginine-induced pancreatic hormone secretion can be modified during an exercise bout, and 2) verify whether the sectioning of the hepatic branch of the vagus nerve can alter the arginine-induced insulin and glucagon secretion during exercise in rats. To this end, we studied the effects of an intraperitoneal injection of arginine (1 g/kg body mass) during an exercise bout (30 min, 26 m/min, 0% grade) on the pancreatic hormone responses. These effects were determined in one group of sham-operated exercising rats and compared with three control groups: one group of resting rats, one group of saline-injected exercising rats, and one group of hepatic-vagotomized exercising rats. Five minutes after the injection of arginine, significant ( P < 0.05) increases in insulin, glucagon, and C-peptide concentrations were observed in exercising as well as in resting rats. These responses were not, however, altered by the hepatic vagotomy and/or by the exercise bout. It is concluded that arginine is a potent stimulus of pancreatic hormone secretion during exercise, even though the sympathoadrenal system is activated. These results also indicate that a hepatic vagotomy does not seem to influence arginine-induced hormonal pancreatic responses and question the role of the putative hepatic arginoreceptors in the control of the pancreatic hormone secretion during exercise.

scholarly journals Role of 12-lipoxygenase in glucagon secretion from rat pancreatic alpha cells

1998 ◽  
Vol 76 ◽  
pp. 100
Author(s):  
Hiroo Kawajiri ◽  
Na Qiao ◽  
Da-Ming Zhuang ◽  
Tanihiro Yoshimoto ◽  
Miyuki Yamamoto ◽  
...  
Keyword(s):  
Glucagon Secretion ◽  
Alpha Cells ◽  
Pancreatic Alpha Cells ◽  
12 Lipoxygenase

Glucagonotropic and Glucagonostatic Effects of KATP Channel Closure and Potassium Depolarization

Endocrinology ◽  
2020 ◽  
Vol 162 (1) ◽  
Author(s):  
Eike Früh ◽  
Christin Elgert ◽  
Frank Eggert ◽  
Stephan Scherneck ◽  
Ingo Rustenbeck
Keyword(s):  
Insulin Secretion ◽  
Beta Cells ◽  
Katp Channel ◽  
Glucagon Secretion ◽  
Alpha Cells ◽  
High Potassium ◽  
Intrinsic Signal ◽  
Mouse Islets ◽  
Glucagon And Insulin

Abstract The role of depolarization in the inverse glucose-dependence of glucagon secretion was investigated by comparing the effects of KATP channel block and of high potassium. The secretion of glucagon and insulin by perifused mouse islets was simultaneously measured. Lowering glucose raised glucagon secretion before it decreased insulin secretion, suggesting an alpha cell–intrinsic signal recognition. Raising glucose affected glucagon and insulin secretion at the same time. However, depolarization by tolbutamide, gliclazide, or 15 mM KCl increased insulin secretion before the glucagon secretion receded. In contrast to the robust depolarizing effect of arginine and KCl (15 and 40 mM) on single alpha cells, tolbutamide was of variable efficacy. Only when applied before other depolarizing agents had tolbutamide a consistent depolarizing effect and regularly increased the cytosolic Ca2+ concentration. When tested on inside-out patches tolbutamide was as effective on alpha cells as on beta cells. In the presence of 1 µM clonidine, to separate insulinotropic from glucagonotropic effects, both 500 µM tolbutamide and 30 µM gliclazide increased glucagon secretion significantly, but transiently. The additional presence of 15 or 40 mM KCl in contrast led to a marked and lasting increase of the glucagon secretion. The glucagon secretion by SUR1 knockout islets was not increased by tolbutamide, whereas 40 mM KCl was of unchanged efficiency. In conclusion a strong and sustained depolarization is compatible with a marked and lasting glucagon secretion. KATP channel closure in alpha cells is less readily achieved than in beta cells, which may explain the moderate and transient glucagonotropic effect.

scholarly journals Disrupted Leptin Signaling in the Lateral Hypothalamus and Ventral Premammillary Nucleus Alters Insulin and Glucagon Secretion and Protects Against Diet-Induced Obesity

Endocrinology ◽  
2016 ◽  
Vol 157 (7) ◽  
pp. 2671-2685 ◽  
Author(s):  
Heather C. Denroche ◽  
Maria M. Glavas ◽  
Eva Tudurí ◽  
Subashini Karunakaran ◽  
Whitney L. Quong ◽  
...  
Keyword(s):  
Central Nervous System ◽  
Nervous System ◽  
Weight Gain ◽  
Blood Glucose ◽  
Glucagon Secretion ◽  
Hypothalamic Nucleus ◽  
Leptin Signaling ◽  
Glucose Levels ◽  
The Central Nervous System

Leptin signaling in the central nervous system, and particularly the arcuate hypothalamic nucleus, is important for regulating energy and glucose homeostasis. However, the roles of extra-arcuate leptin responsive neurons are less defined. In the current study, we generated mice with widespread inactivation of the long leptin receptor isoform in the central nervous system via Synapsin promoter-driven Cre (Leprflox/flox Syn-cre mice). Within the hypothalamus, leptin signaling was disrupted in the lateral hypothalamic area (LHA) and ventral premammillary nucleus (PMV) but remained intact in the arcuate hypothalamic nucleus and ventromedial hypothalamic nucleus, dorsomedial hypothalamic nucleus, and nucleus of the tractus solitarius. To investigate the role of LHA/PMV neuronal leptin signaling, we examined glucose and energy homeostasis in Leprflox/flox Syn-cre mice and Leprflox/flox littermates under basal and diet-induced obese conditions and tested the role of LHA/PMV neurons in leptin-mediated glucose lowering in streptozotocin-induced diabetes. Leprflox/flox Syn-cre mice did not have altered body weight or blood glucose levels but were hyperinsulinemic and had enhanced glucagon secretion in response to experimental hypoglycemia. Surprisingly, when placed on a high-fat diet, Leprflox/flox Syn-cre mice were protected from weight gain, glucose intolerance, and diet-induced hyperinsulinemia. Peripheral leptin administration lowered blood glucose in streptozotocin-induced diabetic Leprflox/flox Syn-cre mice as effectively as in Leprflox/flox littermate controls. Collectively these findings suggest that leptin signaling in LHA/PMV neurons is not critical for regulating glucose levels but has an indispensable role in the regulation of insulin and glucagon levels and, may promote the development of diet-induced hyperinsulinemia and weight gain.

scholarly journals Enhancement of glucagon secretion from isolated rat islets of Langerhans by phorbol 12-myristate 13-acetate

1986 ◽  
Vol 233 (1) ◽  
pp. 287-289 ◽  
Author(s):  
C S Hii ◽  
J Stutchfield ◽  
S L Howell
Keyword(s):  
Islets Of Langerhans ◽  
Glucagon Secretion ◽  
Glucose Stimulation ◽  
Rat Islets ◽  
Kinase C ◽  
Isolated Rat Islets ◽  
Rat Islets Of Langerhans ◽  
Isolated Rat ◽  
Stimulation Of

The phorbol ester 4 beta-phorbol 12-myristate 13-acetate (PMA), at concentrations of 0.1 microM and above, stimulated secretion of glucagon and of insulin from isolated rat islets of Langerhans incubated in the presence of 5.5 mM-glucose. Stimulation of secretion of both hormones by 1 microM-PMA persisted in the absence of external Ca2+, and could be abolished by incubating the islets at 4 degrees C. These findings suggest a role of protein kinase C in the alpha-cell (and beta-cell) secretory mechanism.

scholarly journals Insulin and Glucagon Impairments in Relation with Islet Cells Morphological Modifications Following Long Term Pancreatic Duct Ligation in the Rabbit – A Model of Non-insulin-dependent Diabete

2001 ◽  
Vol 2 (2) ◽  
pp. 101-112 ◽  
Author(s):  
J. Catala ◽  
M. Daumas ◽  
A. Pham Huu Chanh ◽  
B. Lasserre ◽  
E Hollande
Keyword(s):  
Pancreatic Duct ◽  
Islet Cells ◽  
Rabbit Model ◽  
Fold Increase ◽  
Pancreatic Duct Ligation ◽  
A Cells ◽  
Duct Ligation ◽  
Insulin Dependent

Plasma levels of glucose, insulin and glucagon were measured at various time intervals after pancreatic duct ligation (PDL) in rabbits. Two hyperglycemic periods were observed: one between 15–90 days (peak at 30 days of 15.1 ± 1.2mmol/l, p < 0.01), and the other at 450 days (11.2 ± 0.5 mmol/l, p < 0.02). The first hyperglycemic episode was significantly correlated with both hypoinsulinemia (41.8 ± 8pmol/l, r= –0.94, p < 0.01) and hyperglucagonemia (232 ± 21ng/l, r=0.95, p < 0.01). However, the late hyperglycemic phase (450 days), which was not accompanied by hypoinsulinemia, was observed after the hyperglucagonemia (390 days) produced by abundant immunostained A-cells giving rise to a 3-fold increase in pancreatic glucagon stores. The insulin and glucagon responses to glucose loading at 180, 270 and 450 days reflected the insensitivity of B- and A-cells to glucose. The PDL rabbit model with chronic and severe glycemic disorders due to the predominant role of glucagon mimicked key features of the NIDDM syndrome secondary to exocrine disease.

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