Stimulation of intestinal apolipoprotein A-IV by lipid is independent of capsaicin-sensitive afferent signals

1997 ◽  
Vol 273 (3) ◽  
pp. R981-R990 ◽  
Author(s):  
T. J. Kalogeris ◽  
F. Monroe ◽  
P. Tso

We tested the hypothesis that stimulation of synthesis and secretion of intestinal apolipoprotein A-IV (apo A-IV) by intestinally infused lipid is mediated by capsaicin-sensitive afferent signals. Vehicle or capsaicin (125 mg/kg) was systemically administered to rats; then the effects of intestinal infusion of lipid emulsions on lymph lipid and apo A-IV transport were determined in rats equipped with duodenal infusion cannulas and mesenteric lymph fistulas. Capsaicin treatment did not significantly affect lymph outputs of triglyceride, phospholipid, and apo A-IV during duodenal infusion of triglyceride emulsion. In separate studies the effect of capsaicin treatment on ileal lipid-elicited stimulation of intestinal mucosal apo A-IV synthesis was also examined. Ileal lipid infusion increased apo A-IV synthesis in distal ileum, proximal jejunum, and jejunal Thirty-Vella fistulas; this finding was unaffected by capsaicin pretreatment. However, capsaicin treatment significantly attenuated the inhibitory effects of duodenal acid and fat on gastric emptying. These results do not support a role for capsaicin-sensitive, sensory afferent nerves in the stimulation of intestinal apo A-IV by dietary lipid.

1999 ◽  
Vol 277 (5) ◽  
pp. G1081-G1087 ◽  
Author(s):  
Theodore J. Kalogeris ◽  
V. Roger Holden ◽  
Patrick Tso

We examined the role of vagal innervation in lipid-stimulated increases in expression and synthesis of intestinal apolipoprotein A-IV (apoA-IV). In rats with duodenal cannulas and superior mesenteric lymph fistulas given duodenal infusions of lipid emulsion, vagotomy had no effect on either intestinal lipid transport, lymphatic apoA-IV output, or jejunal mucosal apoA-IV synthesis. In rats with jejunal Thiry-Vella fistulas, ileal lipid infusion elicited a twofold stimulation of apoA-IV synthesis without affecting apoA-IV mRNA levels; vagotomy blocked this increase in apoA-IV synthesis. Direct perfusion of jejunal Thiry-Vella fistulas produced 2- to 2.5-fold increases in both apoA-IV synthesis and mRNA levels in the Thiry-Vella segment; these effects were not influenced by vagal denervation. These results suggest two mechanisms whereby lipid stimulates intestinal apoA-IV production: 1) a vagal-dependent stimulation of jejunal apoA-IV synthesis by distal gut lipid that is independent of changes in apoA-IV mRNA levels and 2) a direct stimulatory effect of proximal gut lipid on both synthesis and mRNA levels of jejunal apoA-IV that is independent of vagal innervation.


1996 ◽  
Vol 270 (2) ◽  
pp. G277-G286 ◽  
Author(s):  
T. J. Kalogeris ◽  
T. Tsuchiya ◽  
K. Fukagawa ◽  
R. Wolf ◽  
P. Tso

Biosynthesis of apolipoprotein A-IV (apo A-IV) is stimulated by dietary lipid, but the precise mechanisms involved are not clearly understood. Using an intestinally infused rat model, we compared the effect of delivery of lipid into different intestinal sites on mucosal synthesis of apo A-IV in the jejunum and ileum to determine 1) the effect of lipid delivered to one region of the intestine on apo A-IV synthesis in another region of the gut, and 2) whether any such effect is dependent on the presence of lipid in the latter region. Duodenal infusion of triolein emulsion (40 mumol/h) increased jejunal apo A-IV synthesis and mRNA levels by two- to threefold but had no effect on ileal apo A-IV synthesis or mRNA abundance. Ileal infusion of lipid emulsion containing monoolein (20 mumol/h) + oleic acid (40 mumol/h) stimulated apo A-IV synthesis in both ileum and proximal jejunum. Retrograde (orad) transport of ileally infused lipid was not a likely explanation for the ileal effect on jejunal apo A-IV synthesis, because there was negligible luminal and mucosal recovery of [14C]oleic acid in the jejunum after ileal infusion. Total bile diversion did not block the effect of ileal lipid on jejunal apo A-IV synthesis. Ileal, but not duodenal, lipid infusion stimulated apo A-IV synthesis in a jejunal Thiry-Vella fistula, and perfusion of an ileal Thiry-Vella fistula marginally stimulated proximal jejunal apo A-IV synthesis. Thus administration of lipid to the distal gut produces an increase in mucosal synthesis of apo A-IV in both proximal and distal gut. This effect appears to be independent of direct jejunal presence of lipid, suggesting that lipid in the distal intestine may elicit a signal capable of stimulating jejunal synthesis of apo A-IV.


1982 ◽  
Vol 243 (6) ◽  
pp. E499-E504
Author(s):  
N. S. Krieger ◽  
P. H. Stern

The cardiotonic agent amrinone has been postulated to directly affect Na-Ca exchange. Because stimulated bone resorption has been proposed to require Na-Ca exchange, we examined the effects of amrinone on bone. Amrinone inhibited release of Ca from neonatal mouse calvaria in organ culture stimulated by parathyroid hormone (PTH), 1,25-dihydroxyvitamin d3, or prostaglandin E2. Inhibition was dose dependent and maximal at 2 X 10(-4) M. The effect of amrinone differed from the inhibitory effects of calcitonin, ouabain, or nigericin in that 1) 6-h exposure to amrinone alone prevented the effect of subsequently added PTH; 2) amrinone was only partially effective if added after resorption was initiated by 24-h treatment with PTH; 3) coincubation with amrinone and PTH during the first 48 h of culture allowed for a response to PTH after amrinone was removed; no such protection by a stimulator occurred with ouabain or nigericin. Also submaximal concentrations of amrinone plus calcitonin, ouabain, or nigericin gave greater than additive inhibition of Ca release. Amrinone had no effect on basal bone cAMP or on the acute stimulation of cAMP by PTH. The results suggest that amrinone could have a more direct interaction with the pathway involved in stimulated bone resorption than the other inhibitors.


It was shown in an earlier paper (7) that if maximal stimulation of either of two different afferent nerves can reflexly excite fractions of a given flexor muscle, there are generally, within the aggregate of neurones which innervate that muscle, motoneurones which can be caused to discharge by either afferent (i. e., motoneurones common to both fractions). The relationship which two such afferents bear to a common motoneurone was shown, by the isometric method of recording contraction, to be such that the activation of one afferent, at a speed sufficient to cause a maximal motor tetanus when trans­mitted to the muscle fibres, caused exclusion of any added mechanical effect when the other afferent was excited concurrently. This default in mechanical effect was called “occlusion.” Occlusion may conceivably be due to total exclusion of the effect of one afferent pathway on the common motoneurone by the activity of the other; but facilitation of the effect of one path by the activation of the other when the stimuli were minimal suggests that, in some circumstances at least, the effect of each could augment and summate with th at of the other at the place of convergence of two afferent pathways. Further investigation, using the action currents of the muscle as indication of the nerve impulses discharged by the motoneurone units, has now given some information regarding the effect of impulses arriving at the locus of convergence by one afferent path when the unit common to both is already discharging in response to impulses arriving by the other afferent path. Our method has been to excite both afferent nerves in overlapping sequence by series of break shocks at a rapid rate and to examine the action currents of the resulting reflex for evidence of the appearance of the rhythm of the second series in the discharge caused by the first when the two series are both reaching the motoneurone.


Biochemistry ◽  
1997 ◽  
Vol 36 (32) ◽  
pp. 9816-9825 ◽  
Author(s):  
Takashi Kawano ◽  
Hideki Hakamata ◽  
Takao Ohta ◽  
Yi Ding ◽  
Masaki Yoshida ◽  
...  

1983 ◽  
Vol 61 (10) ◽  
pp. 1149-1155 ◽  
Author(s):  
J. A. Armour

Afferent stimulation of one thoracic cardiopulmonary nerve generated compound action potentials in the efferent axons of other ipsilateral cardiopulmonary nerves in dogs, 14 days after their thoracic autonomic ganglia had been decentralized. The compound action potentials were influenced by the frequency of activation and (in 5 of 12 dogs) by pharmacological autonomic blocking agents (hexamethonium, atropine, phentolamine, and propranolol). Moreover, they were abolished transiently when chymotrypsin was injected locally into the ganglia, and extendedly when manganese was injected. Thus, synapses that can be activated by stimulation of afferent nerves exist in chronically decentralized thoracic autonomic nerves and ganglia. It is proposed that regulation of the heart and lungs occurs in part via thoracic autonomic neural elements independent of the central nervous system.


2000 ◽  
Vol 151 (1) ◽  
pp. 185
Author(s):  
T. Sloane ◽  
D. Sviridov ◽  
L. Pyle ◽  
R.T. Dean ◽  
W. Jessup ◽  
...  

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