INTRAPANCREATIC REGULATION OF HORMONE SECRETION IN THE DOMESTIC FOWL, GALLUS DOMESTICUS

1978 ◽  
Vol 76 (3) ◽  
pp. 449-459 ◽  
Author(s):  
R. L. HAZELWOOD ◽  
D. R. LANGSLOW
Keyword(s):  
Uric Acid ◽  
Gastric Juice ◽  
Free Acid ◽  
Hormone Secretion ◽  
Volume Flow ◽  
Endocrine Regulation ◽  
Hormone Release ◽  
Endocrine Secretion ◽  
Temporal Basis ◽  
Chicken Pancreas

The intrapancreatic endocrine regulation of hormone secretion by the chicken pancreas was studied. Fasted adult male chickens were prepared surgically for the collection of 'gastric' juice and blood samples from the femoral artery. Avian hormone preparations of insulin, glucagon and pancreatic polypeptide (APP) were injected at doses of 50 μg hormone/ kg body wt. Immunoassays of insulin, glucagon and APP were carried out on plasma, as were analyses for glucose, uric acid and free fatty acids (FFA). Gastric juice was analysed for volume flow and total protein, free acid and pepsin concentrations. Injection of insulin decreased all gastric parameters markedly (in contrast to its effect in mammals) and also increased the concentrations of FFA, glucagon (a bimodal response) and uric acid. The increases in levels of FFA, glucagon and uric acid occurred as early as 2·5 min after injection and considerably before significant hypoglycaemia was induced (15–30 min). Injection of glucagon caused a modest decrease in the volume of gastric secretion, but had little other effect except for a small increase in the amount of pepsin released. At 2·5 min, glucagon gave rise to a significant increase in the levels of insulin and FFA in the plasma, and after 15 min the levels of glucose and uric acid had also increased. A progressive decrease in the concentration of APP in the plasma was observed, which was greatest after 15 min and was 28% below control values. In all respects, APP was a powerful avian gastric secretogogue, but had no effect on the concentrations of plasma glucose and insulin. Whereas APP decreased the concentration of FFA in the plasma immediately, the peptide increased both the total and pancreatic levels of immunoreactive glucagon by 50% within 2·5 min, and this increase was even greater at 15 min. Collectively, the results obtained indicate, on a temporal basis, that intrapancreatic regulation of endocrine secretion occurs in Aves and that the release phenomena produce an immediate response. Subsequent or secondary hormone release may occur in response to peripheral metabolic events, especially those requiring homeostatic corrective measures.

scholarly journals Effect of the Natural Sweetener Xylitol on Gut Hormone Secretion and Gastric Emptying in Humans: A Pilot Dose-Ranging Study

Nutrients ◽  
2021 ◽  
Vol 13 (1) ◽  
pp. 174
Author(s):  
Anne Christin Meyer-Gerspach ◽  
Jürgen Drewe ◽  
Wout Verbeure ◽  
Carel W. le Roux ◽  
Ludmilla Dellatorre-Teixeira ◽  
...  
Keyword(s):  
Uric Acid ◽  
Gastric Emptying ◽  
Blood Lipids ◽  
Tap Water ◽  
Hormone Secretion ◽  
Gastrointestinal Symptoms ◽  
Gut Hormones ◽  
Double Blind ◽  
Gut Hormone ◽  
Dose Dependent

Sugar consumption is associated with a whole range of negative health effects and should be reduced and the natural sweetener xylitol might be helpful in achieving this goal. The present study was conducted as a randomized, placebo-controlled, double-blind, cross-over trial. Twelve healthy, lean volunteers received intragastric solutions with 7, 17 or 35 g xylitol or tap water on four separate days. We examined effects on: gut hormones, glucose, insulin, glucagon, uric acid, lipid profile, as well as gastric emptying rates, appetite-related sensations and gastrointestinal symptoms. We found: (i) a dose-dependent stimulation of cholecystokinin (CCK), active glucagon-like peptide-1 (aGLP-1), peptide tyrosine tyrosine (PYY)-release, and decelerated gastric emptying rates, (ii) a dose-dependent increase in blood glucose and insulin, (iii) no effect on motilin, glucagon, or glucose-dependent insulinotropic peptide (GIP)-release, (iv) no effect on blood lipids, but a rise in uric acid, and (v) increased bowel sounds as only side effects. In conclusion, low doses of xylitol stimulate the secretion of gut hormones and induce a deceleration in gastric emptying rates. There is no effect on blood lipids and only little effect on plasma glucose and insulin. This combination of properties (low-glycemic sweetener which stimulates satiation hormone release) makes xylitol an attractive candidate for sugar replacement.

scholarly journals Hyponatremia in visceral leishmaniasis

2010 ◽  
Vol 52 (5) ◽  
pp. 253-258 ◽  
Author(s):  
Frederico A. Lima Verde ◽  
Francisco A.A. Lima Verde ◽  
Francisco José V. Veronese ◽  
Augusto S. Neto ◽  
Galdino Fuc ◽  
...  
Keyword(s):  
Uric Acid ◽  
Visceral Leishmaniasis ◽  
Antidiuretic Hormone ◽  
Hormone Secretion ◽  
Extracellular Volume ◽  
Urine Osmolality ◽  
Control Group ◽  
Volume Depletion ◽  
Antidiuretic Hormone Secretion ◽  
Kala Azar

There are few reports linking hyponatremia and visceral leishmaniasis (kala-azar). This is a study of 55 consecutive kala-azar patients and 20 normal individuals as a control group. Hyponatremia and serum hypo-osmolality were detected in 100% of kala-azar patients. High first morning urine osmolality (750.0 ± 52.0 vs. 894.5 ± 30.0mOsm/kg H2O, p < 0.05), and high 24-hour urine osmolality (426.0 ± 167.0 vs. 514.6 ± 132.0 mOsm/kg H2O, p < 0.05) demonstrated persistent antidiuretic hormone secretion. Urinary sodium was high (82.3 ± 44.2 vs.110.3 ± 34.7 mEq/L, p < 0.05). Low seric uric acid occurred in 61.8% of patients and increased fractional urinary uric acid excretion was detected in 74.5% of them. Increased glomerular filtration rate was present in 25.4% of patients. There was no evidence of extracellular volume depletion. Normal plasma ADH levels were observed in kala-azar patients. No endocrine or renal dysfunction was detected. It is possible that most hyponatremic kala-azar patients present the syndrome of inappropriate antidiuretic hormone secretion.

Comparative nephron function in reptiles, birds, and mammals

1980 ◽  
Vol 239 (3) ◽  
pp. R197-R213 ◽  
Author(s):  
W. H. Dantzler ◽  
E. J. Braun
Keyword(s):  
Uric Acid ◽  
Antidiuretic Hormone ◽  
Flow Rate ◽  
Volume Flow Rate ◽  
Urine Volume ◽  
Volume Flow ◽  
Acid Urine ◽  
Collecting Ducts ◽  
Tubular Absorption ◽  
Similarities And Differences

Volume and osmolarity of urine produced by kidneys of reptiles, birds, and mammals depend on anatomic relationships among nephrons, epithelial permeability to water controlled by antidiuretic hormone, and, for reptiles and birds, probably on volume flow rate through collecting ducts and excretion of uric acid. Urine volume and volume flow rate through collecting ducts in reptiles and birds depend on number of filtering nephrons controlled by antidiuretic hormone. Mammalian nephrons do not filter intermittently but control of nephron filtration rates in all three vertebrate classes may have important similarities and differences. Uric acid excretion by birds and many reptiles permits excretion of inorganic cations in excess of amounts permitted by osmolarity of urine. This process may require tubular absorption of water without sodium. Such absorption, which has been found in reptilian proximal tubules, may be very important for osmoregulation in all birds and uricotelic reptiles and may provide insight into the mechanism of fluid absorption in mammals. Urea excretion in mammals may be important for enhancing concentrating ability. Much more must be learned about these processes, but similarities and differences among them in the three vertebrate classes may help illuminate details of each.

Functional dedifferentiation of parathyroid cells results both from a defective regulation and action of cytoplasmic Ca2+

1986 ◽  
Vol 6 (12) ◽  
pp. 1057-1063 ◽  
Author(s):  
Peter Nygren
Keyword(s):  
Parathyroid Hormone ◽  
Inhibitory Action ◽  
Monolayer Culture ◽  
Hormone Secretion ◽  
Dose Effect ◽  
Parathyroid Cell ◽  
Hormone Release ◽  
Parathyroid Adenomas ◽  
Small Inhibition

Monolayer culture of bovine parathyroid cells for 24 hours resulted in a right-shift of the dose-effect relationships for Ca2+-inhibition of parathyroid hormone (PTH) release and the dependence of the cytoplasmic Ca2+ concentration (Ca2+) on extracellular Ca2+ as well as in a less suppressible hormone release. After 4 days of culture, hormone secretion was almost non-suppressible and Cai2+ increased poorly in response to a rise in extracelluiar Ca2+. Ionomycin, a Ca2+ ionophore, raised Cai2+, but there was only a small inhibition of PTH release and the correlation between Cai2+ and secretion was weak. A deteriorated Cai2+ regulation and a decreased inhibitory action of cytoplasmic Ca2+ on PTH release were also found in ceils from human parathyroid adenomas. Functional dedifferentiation of the parathyroid cell thus results from both defective regulation and action of cytoplasmic Ca2+.

Evidence for calcium inactivation during hormone release in the rat neurohypophysis

1976 ◽  
Vol 65 (3) ◽  
pp. 669-683
Author(s):  
J. J. Nordmann
Keyword(s):  
Hormone Secretion ◽  
Calcium Ionophore ◽  
High Rate ◽  
Hormone Release ◽  
45Ca Uptake ◽  
High K ◽  
K Concentration ◽  
The Relationship ◽  
Internal Calcium

1. A study has been made of the relationship between 45Ca uptake into and hormone release from isolated rat neurohypophyses incubated in vitro. 2. Hormone secretion is triggered by high-K (56 mM) but long exposure to the stimulus does not generate a maintained release of hormone. 3. When hormone release began to wane, addition of Ba of La increased hormone output which suggests that the decline in output did not result from depletion of the neurosecretory granules at the nerve terminals. 4. 45Ca uptake is enhanced in the presence of high-K concentration, but the initial high rate declines during long exposure to the potassium stimulus with a time constant similar to that of the decline in hormone release. 5. After a period of incubation in a K-rich, calcium-free medium, addition of calcium to the medium induced hormone release. The magnitude of this release was dependent on the time of exposure to excess potassium. 6. After inactivation of secretion, mobilization of internal calcium by means of a calcium ionophore increased hormone release.

Effect of epoxyeicosatrienoic acids on growth hormone release from somatotrophs

1989 ◽  
Vol 256 (2) ◽  
pp. E221-E226 ◽  
Author(s):  
G. D. Snyder ◽  
P. Yadagiri ◽  
J. R. Falck
Keyword(s):  
Growth Hormone ◽  
Arachidonic Acid ◽  
Hormone Secretion ◽  
Growth Hormone Secretion ◽  
Epoxyeicosatrienoic Acids ◽  
Hormone Release ◽  
Growth Hormone Release ◽  
Growth Hormone Releasing Hormone ◽  
Epoxyeicosatrienoic Acid ◽  
Releasing Hormone

Growth hormone secretion was stimulated in vitro by products of arachidonic acid epoxygenase, the epoxyeicosatrienoic acids. 5,6-Epoxyeicosatrienoic and 14,15-epoxyeicosatrienoic acid stimulated growth hormone release from an enriched population of somatotrophs (approximately 85%) by twofold. Inhibition of arachidonic acid metabolism by indomethacin did not affect growth hormone-releasing hormone stimulation of growth hormone release. In contrast, pretreatment of somatotrophs with an 11,12-isonitrile analogue of arachidonic acid that inhibits arachidonic acid epoxygenase, resulted in a 20-25% inhibition of growth hormone-releasing hormone-stimulated growth hormone release. 14,15-Epoxyeicosatrienoic acid stimulated a concentration-dependent increase (twofold) in the cytoplasmic concentration of adenosine 3',5'-cyclic monophosphate (cAMP) in the somatotrophs. 14,15-Epoxyeicosatrienoic acid also rapidly increased the intracellular free calcium concentration in somatotrophs from resting levels (approximately 80 nM) to greater than 250 nM. Growth hormone-releasing hormone increased the free intracellular calcium to 160-180 nM. Preincubation of somatotrophs with somatostatin inhibited growth hormone-releasing hormone-stimulated growth hormone secretion, cAMP accumulation, and 14,15-epoxyeicosatrienoic acid stimulated cAMP accumulation. These data are suggestive that the epoxyeicosatrienoic acids may have a role in the secretion of growth hormone.

Fasting gastric content of the squirrel monkey (Saimiri sciurea)

1963 ◽  
Vol 204 (4) ◽  
pp. 681-685 ◽  
Author(s):  
D. A. Brodie ◽  
R. W. Marshall
Keyword(s):  
Gastric Juice ◽  
Squirrel Monkey ◽  
Acid Concentration ◽  
Gastric Content ◽  
Free Acid ◽  
Squirrel Monkeys ◽  
Total Acid ◽  
Significant Fall ◽  
Gastric Contents ◽  
Saimiri Sciurea

Free acid was found in the fasting gastric contents of each of 13 squirrel monkeys studied. A comparison of gastric contents from unrestrained and restrained monkeys indicated that restraint significantly increased the free acid concentration. Over a 24-hr period, there was a decrease in volume, free acid and total acid concentration, and pepsin value of the gastric juice. Histamine (0.1 mg/kg hr, subcutaneously) produced a significant increase in free acid and total acid concentration, while the volume and pepsin values were not changed. Methacholine, at cumulative doses of 1.0 and 2.0 mg/kg, subcutaneously, produced a significant decrease in free and total acid concentration while the volume was not altered. Atropine, in cumulative doses of 8, 16, and 48 mg/kg, intraperitoneally, produced a significant fall in volume of gastric juice collected. However, free acid concentration was reduced only at the highest dose and total acid concentration was not changed by any of the doses tested.

Bombesin and nutrients independently and additively regulate hormone release from GIP/Ins cells

2005 ◽  
Vol 288 (1) ◽  
pp. E208-E215 ◽  
Author(s):  
Lin Li ◽  
Burton M. Wice
Keyword(s):  
Hormone Secretion ◽  
Dominant Negative ◽  
Enteric Neurons ◽  
Cell Physiology ◽  
Hormone Release ◽  
Ampk Signaling ◽  
K Cells ◽  
Diet Induced Obesity ◽  
Gip Release

Glucose-dependent insulinotropic polypeptide (GIP) regulates glucose homeostasis and high-fat diet-induced obesity and insulin resistance. Therefore, elucidating the mechanisms that regulate GIP release is important. GIP is produced by K cells, a specific subtype of small intestinal enteroendocrine (EE) cell. Bombesin-like peptides produced by enteric neurons and luminal nutrients stimulate GIP release in vivo. We previously showed that PMA, bombesin, meat hydrolysate, glyceraldehyde, and methylpyruvate increase hormone release from a GIP-producing EE cell line (GIP/Ins cells). Here we demonstrate that bombesin and nutrients additively stimulate hormone release from GIP/Ins cells. In various cell systems, bombesin and PMA regulate cell physiology by activating PKD signaling in a PKC-dependent fashion, whereas nutrients regulate cell physiology by inhibiting AMPK signaling. Western blot analyses of GIP/Ins cells using antibodies specific for activated and/or phosphorylated forms of PKD and AMPK and one substrate for each kinase revealed that bombesin and PMA, but not nutrients, activated PKC, but not PKD. Conversely, nutrients, but not bombesin or PMA, inhibited AMPK activity. Pharmacological studies showed that PKC inhibition blocked bombesin- and PMA-stimulated hormone release, but AMPK activation failed to suppress nutrient-stimulated hormone secretion. Forced expression of constitutively active vs. dominant negative PKDs or AMPKs failed to perturb bombesin- or nutrient-stimulated hormone release. Thus, in GIP/Ins cells, PKC regulates bombesin-stimulated hormone release, whereas nutrients may control hormone release by regulating the activity of AMPK-related kinases, rather than AMPK itself. These results strongly suggest that K cells in vivo independently respond to neuronal vs. nutritional stimuli via two distinct signaling pathways.

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