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.

Adaptive changes in insulin and glucagon secretion during cold acclimation in the rat

1986 ◽  
Vol 250 (6) ◽  
pp. E669-E676 ◽  
Author(s):  
C. I. Edwards ◽  
R. J. Howland
Keyword(s):  
Cold Acclimation ◽  
Cold Exposure ◽  
Hormone Secretion ◽  
Glucagon Secretion ◽  
Molar Ratio ◽  
Adaptive Process ◽  
Insulin And Glucagon Secretion ◽  
Pancreatic Hormone

Arginine-stimulated insulin and glucagon outputs from isolated perfused pancreata of warm-acclimated and 2-, 4-, and 6-wk cold-acclimated rats (4 degrees C) were determined to assess whether observed changes in these parameters were a result of cold exposure per se or a part of the adaptive process of cold acclimation. Progressive and sequential changes were seen in both insulin and glucagon outputs. At 2 wk cold acclimation, glucagon rose and insulin output tended to fall, at 4 wk, glucagon output remained elevated and insulin output was further reduced, and at 6 wk, glucagon output had returned to control levels, whereas insulin output was substantially further reduced. These changes resulted in reduction of the insulin-to-glucagon molar ratio of the total arginine-induced output from 7.27 +/- 1.76 (SE) in the warm acclimate to 2.31 +/- 0.79 (SE) at 2 wk, 1.42 +/- 0.29 (SE) at 4 wk, and 1.26 +/- 0.21 (SE) at 6 wk cold acclimation. The data do not provide in vitro support for the hypothesis that changes in pancreatic hormone secretion in vivo are a consequence of cold exposure and not cold acclimation.

Insulin and glucagon secretion from isolated islets of Langerhans. The effects of calcium ionophores

1975 ◽  
Vol 150 (1) ◽  
pp. 88-96 ◽  
Author(s):  
J P Ashby ◽  
R N Speake
Keyword(s):  
Islets Of Langerhans ◽  
Hormone Secretion ◽  
Glucagon Secretion ◽  
Ionophore A23187 ◽  
Glucagon Release ◽  
Membrane Function ◽  
Isolated Islets Of Langerhans ◽  
Insulin And Glucagon Secretion ◽  
Perifused Islets

The role of Ca2+ in the secretion of insulin and glucagon was investigated by studying the effects of Ca2+ ionophores on hormone secretion from isolated perifused islets of Langerhans. Ionophore X537A (100 μM), which binds alkaline earth cations and also complexes some univalent cations, caused a rapid transient increase in insulin and glucagon secretion which was not dependent on the presence of Ca2+ in the perifusion medium. Ionophore A23187 (100 μM), which specifically binds bivalent cations at neutral pH values, similarly increased insulin secretion in complete and Ca2+-free medium, but only stimulated glucagon release in the presence of extracellular Ca2+. Since the stimulatory effects of both ionophores were associated with an increased Ca2+ flux in the islets, these experiments support the hypothesis that Ca2+ may trigger the release of insulin and suggest that it is also involved in the secretion of glucagon. The basal rate of both insulin and glucagon release was significantly increased when Ca2+ was omitted from the perifusion medium, but it is proposed that this finding may be due to adverse effects on cell-membrane function under these conditions.

Somatostatin, insulin, and glucagon secretion from isolated perfused pancreas of obese rats

1981 ◽  
Vol 241 (2) ◽  
pp. E146-E150
Author(s):  
S. Seino ◽  
Y. Seino ◽  
J. Takemura ◽  
K. Tsuda ◽  
H. Kuzuya ◽  
...  
Keyword(s):  
Hormone Secretion ◽  
Glucagon Secretion ◽  
Ventromedial Hypothalamus ◽  
Perfused Pancreas ◽  
Isolated Perfused Pancreas ◽  
Insulin And Glucagon Secretion ◽  
Perfusion Experiment ◽  
Pancreatic Hormone ◽  
And Control

A comparison of the somatostatin with the insulin and glucagon secretions in hypothalamic obesity and genetic obesity was made using the isolated perfused pancreas of rats. In our perfusion experiment, the somatostatin response to 19 mM arginine in the presence of 4.4 mM glucose was significantly greater in both ventromedial hypothalamus (VMH)-lesioned and Zucker fa/fa rats than in their controls, as was the perfusate insulin. The perfusate arginine-stimulated glucagon secretion appeared no different in obese and control rats. Because hyperinsulinemia in vivo and hyperresponses to arginine of perfusate insulin and somatostatin were observed in both VMH-lesioned and Zucker fa/fa rats, whereas the perfusate glucagon secretion in the presence of 4.4 mM glucose was unchanged by obesity, the secretory behavior of some pancreatic hormones seems similar in VMH-lesioned and Zucker fa/fa rats in certain conditions. These results suggest that some abnormalities of pancreatic hormone secretion may be caused by a mechanism common to obesity, whether caused experimentally or genetically.

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 Free-fatty acid receptor 4 inhibitory signaling in delta cells regulates islet hormone secretion in mice

2020 ◽  
Author(s):  
Marine L. Croze ◽  
Marcus F. Flisher ◽  
Arthur Guillaume ◽  
Caroline Tremblay ◽  
Glyn M. Noguchi ◽  
...  
Keyword(s):  
Fatty Acid ◽  
Free Fatty Acid ◽  
Glucose Tolerance ◽  
Hormone Secretion ◽  
Glucagon Secretion ◽  
Compound A ◽  
Acid Receptor ◽  
Somatostatin Secretion ◽  
Insulin And Glucagon Secretion ◽  
Free Fatty Acid Receptor

ABSTRACTObjectiveMaintenance of glucose homeostasis requires the precise regulation of hormone secretion from the endocrine pancreas. Free-fatty acid receptor 4 (FFAR4/GPR120) is a G protein-coupled receptor whose activation in islets of Langerhans promotes insulin and glucagon secretion and inhibits somatostatin secretion. However, the contribution of individual islet cell types (α, β, and δ cells) to the insulinotropic and glucagonotropic effects of GPR120 remains unclear. As gpr120 mRNA is enriched in somatostatin-secreting δ cells, we hypothesized that GPR120 activation stimulates insulin and glucagon secretion via inhibition of somatostatin release.MethodsGlucose tolerance tests were performed in mice after administration of the selective GPR120 agonist Compound A. Insulin, glucagon and somatostatin secretion were measured in static incubations of isolated mouse islets in response to endogenous (ω-3 polyunsaturated fatty acids) and/or pharmacological (Compound A and AZ-13581837) GPR120 agonists. The effect of Compound A on hormone secretion was tested further in islets isolated from mice with global or somatostatin cell-specific knockout of gpr120. Gpr120 expression was assessed in pancreatic section by RNA in situ hybridization and immunohistochemistry. Cyclic AMP (cAMP) and calcium dynamics in response to pharmacological GPR120 agonists were measured specifically in α, β and δ cells in intact islets using cAMPER and GCaMP6 reporter mice, respectively.ResultsAcute exposure to Compound A increased glucose tolerance and circulating insulin and glucagon levels in vivo. Endogenous and/or pharmacological and GPR120 agonists reduced somatostatin secretion in isolated islets and concomitantly demonstrated dose-dependent potentiation of glucose-stimulated insulin secretion and arginine-stimulated glucagon secretion. GPR120 was enriched in δ cells and pharmacological GPR120 agonists reduced cAMP and calcium levels in δ cells, but increased these signals in α and β cells. Compound A-mediated inhibition of somatostatin secretion was insensitive to pertussis toxin. The effect of Compound A on hormone secretion was completely absent in islets from mice with either global or somatostatin cell-specific deletion of gpr120 and was partially reduced upon blockade of somatostatin receptor signaling by cyclosomatostatin.ConclusionsInhibitory GPR120 signaling in δ cells contributes to both insulin and glucagon secretion in part via mitigating somatostatin release.

Cholinergic regulation of fuel-induced hormone secretion and respiration of SUR1−/− mouse islets

2006 ◽  
Vol 291 (3) ◽  
pp. E525-E535 ◽  
Author(s):  
Nicolai M. Doliba ◽  
Wei Qin ◽  
Marko Z. Vatamaniuk ◽  
Carol W. Buettger ◽  
Heather W. Collins ◽  
...  
Keyword(s):  
Insulin Release ◽  
High Glucose ◽  
Hormone Secretion ◽  
Glucagon Secretion ◽  
Insulin And Glucagon Secretion ◽  
Intracellular Ca ◽  
Mouse Islets ◽  
Endocrine Factors ◽  
Glucose Responsiveness

Neural and endocrine factors (i.e., Ach and GLP-1) restore defective glucose-stimulated insulin release in pancreatic islets lacking sulfonylurea type 1 receptors (SUR1−/−) (Doliba NM, Qin W, Vatamaniuk MZ, Li C, Zelent D, Najafi H, Buettger CW, Collins HW, Carr RD, Magnuson MA, and Matschinsky FM. Am J Physiol Endocrinol Metab 286: E834–E843, 2004). The goal of the present study was to assess fuel-induced respiration in SUR1−/− islets and to correlate it with changes in intracellular Ca2+, insulin, and glucagon secretion. By use of a method based on O2 quenching of phosphorescence, the O2 consumption rate (OCR) of isolated islets was measured online in a perifusion system. Basal insulin release (IR) was 7–10 times higher in SUR1−/− compared with control (CON) islets, but the OCR was comparable. The effect of high glucose (16.7 mM) on IR and OCR was markedly reduced in SUR1−/− islets compared with CON. Ach (0.5 μM) in the presence of 16.7 mM glucose caused a large burst of IR in CON and SUR1−/− islets with minor changes in OCR in both groups of islets. In SUR1−/− islets, high glucose failed to inhibit glucagon secretion during stimulation with amino acids or Ach. We conclude that 1) reduced glucose responsiveness of SUR1−/− islets may be in part due to impaired energetics, as evidenced by significant decrease in glucose-stimulated OCR; 2) elevated intracellular Ca2+ levels may contribute to altered insulin and glucagon secretion in SUR1−/− islets; and 3) The amplitudes of the changes in OCR during glucose and Ach stimulation do not correlate with IR in normal and SUR1−/− islets suggesting that the energy requirements for exocytosis are minor compared with other ATP-consuming reactions.

scholarly journals SUN-266 Protein Induced Pancreatic Hormone Secretion Is Modulated by Vagal CaSR

2020 ◽  
Vol 4 (Supplement_1) ◽  
Author(s):  
Mariana Norton ◽  
Simon C Cork ◽  
Aldara Martin Alonso ◽  
Anna G Roberts ◽  
Yateen S Patel ◽  
...  
Keyword(s):  
Amino Acids ◽  
Amino Acid ◽  
Hormone Secretion ◽  
Sensory Information ◽  
Glucagon Secretion ◽  
Vagal Afferents ◽  
Acid Uptake

Abstract The existence of a vago-vagal entero-pancreatic pathway, where sensory information from the gut can signal via vagal afferents to the brain to mediate changes in pancreatic function, has been recognised for over a century, and investigated extensively with regards to pancreatic exocrine secretions. However, the role of such pathways in pancreatic endocrine secretions has received less attention. The secretion of insulin and glucagon in response to protein and amino acids is conserved across species. This effect is thought to promote amino acid uptake into tissues without concomitant hypoglycaemia. We found that the essential amino acid L-Phenylalanine potently stimulates glucagon secretion, even when administered directly into the gut at small doses unlikely to significantly raise systematic levels. Administration of L-Phenylalanine also increased neuronal activation in the rat and mouse dorsal vagal complex, the central nervous system region directly innervated by vagal afferents. L-Phenylalanine modulates the activity of the calcium sensing receptor (CaSR), a nutrient sensor more commonly known for its role in calcium homeostasis, but which is thought to also act as a sensor of aromatic amino acids. Interestingly, the CaSR is one of the few nutrient sensors expressed in vagal afferents and in vitro calcium imaging revealed CaSR synthetic agonists activate subpopulations of vagal afferents. The role of CaSR in vivo was investigated further by selectively knocking down the CaSR in vagal afferents. Briefly, CaSR floxed mice were bilaterally injected directly into the nodose ganglion, where the cell bodies of vagal afferents are located, with a cre expressing adeno-associated virus. CaSR knockdown did not interfere with normal food intake, nor the vagal-dependent anorectic effects of cholecystokinin, or of L-Phenylalanine. However, it did blunt protein-induced glucagon secretion, suggesting involvement of the CaSR in the vagus nerve in protein sensing and glucose homeostasis. Future studies are required to determine the importance of vagal CaSR in protein induced pancreatic endocrine secretions, and the possibility of exploiting this circuit to develop new anti-diabetic therapies.

Chemical specificity of short-chain fatty acids in stimulating insulin and glucagon secretion in sheep

1994 ◽  
Vol 267 (2) ◽  
pp. E234-E241 ◽  
Author(s):  
H. Mineo ◽  
Y. Hashizume ◽  
Y. Hanaki ◽  
K. Murata ◽  
H. Maeda ◽  
...  
Keyword(s):  
Fatty Acids ◽  
Butyric Acid ◽  
Hormone Secretion ◽  
Glucagon Secretion ◽  
Hydrocarbon Chain ◽  
Short Chain Fatty Acids ◽  
Short Chain ◽  
Response Curves ◽  
Insulin And Glucagon Secretion ◽  
Chain Fatty Acids

The chemical specificity and structural requirements of short-chain fatty acids (SCFAs) in stimulating pancreatic endocrine responses was investigated in conscious sheep. Normal SCFAs with one to eight carbons were injected intravenously at seven doses of 39-2,500 mumol/kg body wt. The isomers or derivatives of SCFAs were administered at 625 mumol/kg body wt. Analysis of dose-response curves showed that n-butyric acid (4 carbons in the molecule) was most effective for both insulin and glucagon secretion among the normal SCFAs tested. In addition, one carboxylic group was absolutely required, since hormone secretion was significantly reduced or abolished with compounds in which the carboxylic element was replaced by other groups and with dicarboxylic acids. The form of the hydrocarbon chain (branched, cyclic, or benzoic ring) also affected hormone secretory activity. Most of the compounds that replaced hydrogen in the hydrocarbon chain by other groups at various positions reduced or abolished the hormone secretory effect obtained by n-butyric acid. In conclusion, a monocarboxylic acid with several numbers of hydrocarbons was required for insulin or glucagon secretion. These results suggest that the pancreatic endocrine system can recognize the chemical structure of SCFAs in detail and induce hormone secretion in sheep.

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