Effects of corticotropin-releasing hormone on insulin and glucagon secretion in mice

1988 ◽  
Vol 117 (1) ◽  
pp. 87-92 ◽  
Author(s):  
Sven Karlsson ◽  
Bo Ahrén
Keyword(s):  
Plasma Levels ◽  
Plasma Insulin ◽  
Glucagon Secretion ◽  
Corticotropin Releasing Hormone ◽  
Releasing Hormone ◽  
Insulin And Glucagon Secretion ◽  
Basal Plasma ◽  
Plasma Insulin Levels ◽  
Dose Levels

Abstract. Besides in the brain, corticotropin-releasing hormone occurs in the pancreas. Therefore, its effects on plasma levels of insulin and glucagon were investigated in vivo in the mouse. At 2 min after CRH injection (0.5–8.0 nmol/kg), plasma insulin was lowered: by 4.0 nmol/kg from 38 ± 4 to 28 ± 2 mU/l (P < 0.05). Plasma insulin was lowered also at 6 min, whereas at 10 min, plasma insulin levels were elevated (P < 0.05). Plasma glucagon levels were slightly lowered (P < 0.05) at 10 min after CRH injection, whereas plasma glucose was slightly elevated (P < 0.05) at 6 min after injection but not at 2 or 10 min. The effects of CRH on the plasma insulin and glucagon response to iv injections of half-maximal dose levels of glucose (2.8 mmol/kg) or the cholinergic agonist carbachol (0.16 μmol/kg) were also investigated. CRH, 4.0 nmol/kg, however, could not influence the plasma insulin or glucagon levels after the iv injection of either glucose or carbachol. Thus, CRH slightly affects basal plasma levels of insulin and glucagon in mice. In contrast, stimulated insulin and glucagon secretions are not affected by CRH. Peripheral CRH may therefore be of slight importance for the regulation of basal plasma levels of insulin and glucagon in the mouse.

ANF inhibits glucose-stimulated insulin secretion in mouse and rat

1988 ◽  
Vol 255 (5) ◽  
pp. E579-E582 ◽  
Author(s):  
B. Ahren
Keyword(s):  
Insulin Secretion ◽  
Atrial Natriuretic Factor ◽  
Plasma Insulin ◽  
Glucagon Secretion ◽  
Insulin Levels ◽  
Atrial Cells ◽  
Insulin And Glucagon Secretion ◽  
Plasma Insulin Levels ◽  
Glucose Stimulated Insulin Secretion ◽  
Dose Levels

Atrial natriuretic factor (ANF) is synthesized in atrial cells and was recently demonstrated to also occur within islet glucagon cells. Therefore, we investigated the possible effects of synthetic rat ANF-(1-28) on basal and stimulated insulin and glucagon secretion in the mouse and on glucose-induced insulin secretion in the rat. We found that ANF did not affect basal levels of insulin, glucagon, or glucose when injected intravenously at dose levels between 0.25 and 4.0 nmol/kg in mice. However, when injected together with glucose (2.8 mmol/kg), ANF (4.0 nmol/kg) inhibited the increase in plasma insulin levels by 40%, from 114 +/- 8 microU/ml in controls to 81 +/- 8 microU/ml (P less than 0.01). Likewise, the increase in plasma insulin levels during an intravenous infusion of glucose in rats (10 mg/min) was significantly reduced by ANF (100 pmol.kg-1.min-1; P less than 0.001). In contrast, the increase in plasma levels of insulin and glucagon after the intravenous injection of the cholinergic agonist carbachol in mice (0.16 mumol/kg) was not significantly affected by ANF. We conclude that ANF inhibits glucose-stimulated insulin secretion in the mouse and the rat. The peptide may therefore be a modulator of insulin secretion.

In vivo action of a new octadecaneuropeptide antagonist on neuropeptide Y and corticotropin-releasing hormone mRNA levels in rat

2005 ◽  
Vol 141 (2) ◽  
pp. 156-160 ◽  
Author(s):  
V. Compère ◽  
S. Li ◽  
J. Leprince ◽  
M.C. Tonon ◽  
H. Vaudry ◽  
...  
Keyword(s):  
Neuropeptide Y ◽  
Mrna Levels ◽  
Corticotropin Releasing Hormone ◽  
Releasing Hormone

Effects of PACAP1–27 on the canine endocrine pancreas in vivo: interaction with cholinergic mechanism

2003 ◽  
Vol 81 (7) ◽  
pp. 720-729 ◽  
Author(s):  
Nobuharu Yamaguchi ◽  
Tamar Rita Minassian ◽  
Sanae Yamaguchi
Keyword(s):  
Endocrine Pancreas ◽  
Venous Blood ◽  
Insulin Response ◽  
Glucagon Secretion ◽  
Venous Blood Flow ◽  
Dependent Manner ◽  
Cholinergic Mechanism ◽  
Insulin And Glucagon Secretion ◽  
Anesthetized Dogs

The aim of the present study was to characterize the effects of pituitary adenylate cyclase activating polypeptide (PACAP) on the endocrine pancreas in anesthetized dogs. PACAP1–27 and a PACAP receptor (PAC1) blocker, PACAP6–27, were locally administered to the pancreas. PACAP1–27 (0.005–5 μg) increased basal insulin and glucagon secretion in a dose-dependent manner. PACAP6–27 (200 μg) blocked the glucagon response to PACAP1–27 (0.5 μg) by about 80%, while the insulin response remained unchanged. With a higher dose of PACAP6–27 (500 μg), both responses to PACAP1–27 were inhibited by more than 80%. In the presence of atropine with an equivalent dose (128.2 μg) of PACAP6–27 (500 μg) on a molar basis, the insulin response to PACAP1–27 was diminished by about 20%, while the glucagon response was enhanced by about 80%. The PACAP1–27-induced increase in pancreatic venous blood flow was blocked by PACAP6–27 but not by atropine. The study suggests that the endocrine secretagogue effect of PACAP1–27 is primarily mediated by the PAC1 receptor, and that PACAP1–27 may interact with muscarinic receptor function in PACAP-induced insulin and glucagon secretion in the canine pancreas in vivo.Key words: atropine, PACAP, PAC1, muscarinic, interaction.

scholarly journals Effects of corticotropin-releasing hormone on locus coeruleus neurons in vivo: a microdialysis study using a novel bilateral approach

2001 ◽  
pp. 359-363 ◽  
Author(s):  
S Asbach ◽  
C Schulz ◽  
H Lehnert
Keyword(s):  
Locus Coeruleus ◽  
Fused Silica ◽  
Corticotropin Releasing Hormone ◽  
Release Of Noradrenaline ◽  
Releasing Hormone ◽  
Significant Prolongation ◽  
Bilateral Approach ◽  
Microdialysis Study ◽  
Na Release

OBJECTIVE: Stress-induced release of noradrenaline (NA) from locus coeruleus (LC) neurons is mainly regulated by corticotropin-releasing hormone (CRH). Tyrosine is a precursor of NA and plays an intriguing role in the regulation of NA release. DESIGN: We studied the effects of injecting CRH into the LC using a novel bilateral approach which relies on the mainly ipsilateral projections of LC neurons allowing stimulation of one hemisphere while using the other as control. To analyze the modification of the CRH effect, tyrosine was given intraperitoneally. A combination of CRH and its antagonist d-Phe was administered for validation of the specificity of CRH effects. METHODS: Wistar rats were used in all experiments. Injections were made through fused silica capillaries implanted into both LCs and microdialysis samples were collected bilaterally from the prefrontal cortex (PFM) every 20 min for 1 h before and 3 h after injections. The effects of LC stimulation were investigated by determining 3-methoxy-4-hydroxyphenylglycol (MHPG) in the dialysates. RESULTS: Following CRH injection into one LC and contralateral infusion of artificial cerebrospinal fluid (aCSF), MHPG levels, which are indicative of NA release, increased only in the ipsilateral PFM. These effects were blocked by d-Phe. Simultaneous administration of tyrosine i.p. led to a significant prolongation of MHPG release. CONCLUSIONS: These data provide the first physiological evidence of unilateral LC projections with the bilateral stimulation design proving to be a very valuable tool for the study of LC firing rate, to decrease number of animals and time expenditure. Prolongation of MHPG release after tyrosine supplementation is most likely due to increased NA synthesis.

Sign in / Sign up

Export Citation Format

Share Document