The feeding responses evoked by cholecystokinin are mediated by vagus and splanchnic nerves

Brown, Thelma A.L.; Washington, Martha C.; Metcalf, Shannon A.; Sayegh, Ayman I.

doi:10.1016/j.peptides.2011.06.024

Cited by 21 publications

(11 citation statements)

References 39 publications

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“…There is mounting evidence for the role played by the autonomic nervous system in mediating the effects of hormones in regulating food intake. For example, both vagal and splanchanic nerves are involved in mediating the satiety effects of CCK in rats (32) and a vagal‐mediated mechanism is implicated in the anorectic effects of CCK in goldfish (21). It is possible that the centrally administered nesfatin‐1 and/or ghrelin elicits a vagal efferent mediated response to alter gut mRNA expression.…”

Section: Discussionmentioning

confidence: 99%

Nesfatin‐1 Suppresses Energy Intake, Co‐localises Ghrelin in the Brain and Gut, and Alters Ghrelin, Cholecystokinin and Orexin mRNA Expression in Goldfish

Kerbel

Unniappan

2012

J Neuroendocrinology

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Nesfatin-1 is a novel anorectic peptide encoded in the precursor protein nucleobindin-2 (NUCB2). We recently reported the presence and appetite suppressing effects of nesfatin-1 in goldfish. Nesfatin-1 has been co-localised with ghrelin in the stomach of rats. Whether nesfatin-1 influences other appetite regulatory peptides in goldfish remains unclear. The main objectives of the present study were to investigate whether nesfatin-1 co-localises ghrelin in goldfish, and to test whether exogenous nesfatin-1 influences endogenous ghrelin, cholecystokinin (CCK) and orexin A (OXA). We found co-localisation of nesfatin-1-like and ghrelin-like immunoreactivity in the enteroendocrine cells of the goldfish anterior intestine (J-loop). Furthermore, co-localisation of ghrelin and nesfatin-1 was also observed in the posterior nucleus lateralis tuberis of the goldfish hypothalamus, a brain region implicated in the regulation of food intake. These findings suggest a functional relationship between ghrelin and nesfatin-1 in goldfish. In support of this, i.c.v. administration of goldfish (gf) nesfatin-1 [25 ng/g body weight (BW)], suppressed food intake and the expression of mRNAs encoding preproghrelin, ghrelin receptor (GHS-R 1a-1), CCK and NUCB2 in the forebrain of fed fish, as well as ghrelin and NUCB2 mRNA in the hypothalamus of unfed fish, both at 1 h post-injection. Nesfatin-1 stimulated hypothalamic CCK mRNA expression at 30 min post-injection in fed fish, and inhibited OXA mRNA in the unfed fish hypothalamus 1 h post-injection. Similarly, i.c.v. injections of gfghrelin (1 ng/g BW), although stimulating food intake, suppressed NUCB2 and preproghrelin mRNAs, but not ghrelin receptor mRNA expression in the forebrain. It is also evident that exogenous ghrelin and nesfatin-1 mRNAs encoding these peptides. Our novel results indicate interactions between nesfatin-1 and ghrelin, CCK and orexin, and show that nesfatin-1 acts on other appetite regulatory peptides in a time- and feeding status-dependent, as well as tissue-specific, manner in goldfish.

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Section: Discussionmentioning

confidence: 99%

Nesfatin‐1 Suppresses Energy Intake, Co‐localises Ghrelin in the Brain and Gut, and Alters Ghrelin, Cholecystokinin and Orexin mRNA Expression in Goldfish

Kerbel

Unniappan

2012

J Neuroendocrinology

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“…Sympathetic denervation, or celiacomesenteric ganglionectomy ( n = 11), and sham surgeries ( n = 14) were performed as previously described. 28,29,33 Briefly, the left kidney, cranial mesenteric artery and celiac artery were exposed by blunt dissection of the overlying tissues, and the celiac and mesenteric ganglia were located between the arteries and were removed. Sham celiacomesenteric ganglionectomy surgeries were performed by manipulating the tissue without removal of the celiac or mesenteric ganglia.…”

Section: Methodsmentioning

confidence: 99%

“…PNS denervation, or vagotomy (n ¼ 12), and sham surgeries (n ¼ 15) were performed as previously described. [28][29][30][31][32] Briefly, the dorsal and ventral branches of the subdiaphragmatic vagus were located by blunt dissection of the overlying tissues, isolated, and ligated above the hepatic, celiac, and accessory celiac branches. Each nerve trunk was cut distal to the ligature and above the vagal branches, producing total vagal transection.…”

Section: Surgical Proceduresmentioning

confidence: 99%

Long-term effect of parasympathetic or sympathetic denervation on intestinal epithelial cell proliferation and apoptosis

Davis

Washington

Yaniz

et al. 2017

Exp Biol Med (Maywood)

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This study investigates the long-term effect of autonomic denervation on intestinal epithelial cell turnover, as measured by proliferation, apoptosis, and total cell number. Although previous research has established that autonomic denervation can alter intestinal epithelial turnover under short-term conditions, here we establish for the first time that these changes do not persist long-term when you control for surgical-induced changes in food intake and use targeted denervation procedures. These findings add to the base of knowledge on autonomic control of tissue turnover, highlight the ability of the intestinal epithelium to recover after autonomic injury and reveal possible implications of the use of ANS denervation for disease treatment in humans. AbstractIntestinal epithelial tissue is constantly regenerated as a means to maintain proper tissue function. Previous studies have demonstrated that denervation of the parasympathetic or sympathetic nervous system to the intestine alters this process. However, results are inconsistent between studies, showing both increases and decreases in proliferation after denervation of the parasympathetic or sympathetic. The effect appears to correlate with (1) the timing post-denervation, (2) denervation-induced changes in food intake, (3) the denervation technique used, and (4) which intestinal segment is investigated. Thus, we proposed that parasympathetic or sympathetic denervation does not have an effect on intestinal epithelial regeneration when you (1) evaluate denervation after long-term denervation, (2) control for post-surgical changes in food intake, (3) use minimally invasive surgical techniques and (4) include a segmental analysis. To test this, adult male Sprague Dawley rats underwent parasympathetic denervation via subdiaphragmatic vagotomy, sympathetic denervation via celiacomesenteric ganglionectomy, a parasympathetic denervation sham surgery, or a sympathetic denervation sham surgery. Sham surgery ad libitum-fed groups and sham surgery pair-fed groups were used to control for surgically induced changes in food intake. Three weeks post-surgery, animals were sacrificed and tissue from the duodenum, jejunum, and ileum was excised and immunohistochemically processed to visualize indicators of proliferation (bromodeoxyuridine-positive cells) and apoptosis (caspase-3-positive cells). Results showed no differences between groups in proliferation, apoptosis, or total cell number in any intestinal segment. These results suggest that parasympathetic or sympathetic denervation does not have a significant long-term effect on intestinal epithelial turnover. Thus, intestinal epithelial regeneration is able to recover after autonomic nervous system injury.

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“…CCK-58 has shown qualitatively unique actions on pancreatic secretion [68], and prolonged activation of vagal afferent neurons [33], which might be relevant. Moreover, activation of sympathetic afferents [6] and circumventricular sites at CNS hindbrain level [18, 43] could be involved in the satiety actions by CCK-58.…”

Section: Discussionmentioning

confidence: 99%

CCK-58 elicits both satiety and satiation in rats while CCK-8 elicits only satiation

Overduin¹,

Gibbs²,

Cummings³

et al. 2014

Peptides

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Reduction of food intake by exogenous cholecystokinin (CCK) has been demonstrated primarily for its short molecular form, CCK-8. Mounting evidence, however, implicates CCK-58 as a major physiologically active CCK form, with different neural and exocrine response profiles than CCK-8. In three studies, we compared meal-pattern effects of intraperitoneal injections CCK-8 vs. CCK-58 in undeprived male Sprague-Dawley rats consuming sweetened condensed milk. In study one, rats (N=10) received CCK-8, CCK-58 (0.45, 0.9, 1.8 and 3.6 nmole/kg) or vehicle before a 4-hour test-food presentation. At most doses, both CCK-8 and CCK-58 reduced meal size relative to vehicle. Meal-size reduction prompted a compensatory shortening of the intermeal interval (IMI) after CCK-8, but not after CCK-58, which uniquely increased the satiety ratio (IMI/size of the preceding meal). In the second study, lick patterns were monitored after administration of 0.9nmole/kg CCK-58, CCK-8 or vehicle. Lick cluster size, lick efficiency and interlick-interval distribution remained unaltered compared to vehicle, implying natural satiation, rather than illness, following both CCK forms. In study 3, threshold satiating doses of the two CCK forms were given at 5 and 30 minutes after meal termination, respectively. CCK 58, but not CCK-8 increased the intermeal interval and satiety ratio compared to vehicle. In conclusion, while CCK 58 and CCK-8 both stimulate satiation, thereby reducing meal size, CCK-58 consistently exerts a satiety effect, prolonging IMI. Given the physiological prominence of CCK-58, these results suggest that CCK’s role in food intake regulation may require reexamination.

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The feeding responses evoked by cholecystokinin are mediated by vagus and splanchnic nerves

Cited by 21 publications

References 39 publications

Nesfatin‐1 Suppresses Energy Intake, Co‐localises Ghrelin in the Brain and Gut, and Alters Ghrelin, Cholecystokinin and Orexin mRNA Expression in Goldfish

Nesfatin‐1 Suppresses Energy Intake, Co‐localises Ghrelin in the Brain and Gut, and Alters Ghrelin, Cholecystokinin and Orexin mRNA Expression in Goldfish

Long-term effect of parasympathetic or sympathetic denervation on intestinal epithelial cell proliferation and apoptosis

CCK-58 elicits both satiety and satiation in rats while CCK-8 elicits only satiation

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