Differential effects of selective vagotomy and tropisetron in aminoprivic feeding

Dixon, Kimberly D.; Williams, Fred E.; Wiggins, Raymond L.; Pavelka, Jason; Lucente, James; Bellinger, Larry L.; Gietzen, Dorothy W.

doi:10.1152/ajpregu.2000.279.3.r997

Cited by 20 publications

(17 citation statements)

References 30 publications

Supporting

Mentioning

Contrasting

Unclassified

Order By: Relevance

“…Subdiaphragmatic vagotomy was performed using a modified technique previously described by Dixon et al (17). Briefly, rats were fasted for 14 h before vagotomy.…”

Section: Vagotomymentioning

confidence: 99%

Autonomic involvement in the permanent metabolic programming of hyperinsulinemia in the high-carbohydrate rat model

Mitrani¹,

Srinivasan²,

Dodds³

et al. 2007

American Journal of Physiology-Endocrinology and Metabolism

View full text Add to dashboard Cite

Mitrani P, Srinivasan M, Dodds C, Patel MS. Autonomic involvement in the permanent metabolic programming of hyperinsulinemia in the high-carbohydrate rat model. Am J Physiol Endocrinol Metab 292: E1364 -E1377, 2007. First published January 16, 2007; doi:10.1152/ajpendo.00672.2006.-Exposure to a high-carbohydrate (HC) milk formula during the suckling period results in permanent metabolic programming of hyperinsulinemia in HC rats. Previous studies have shown that hyperinsulinemia in HC rats involves a programmed hyperresponsiveness to glucose. However, the immediate onset and persistence of enhanced insulin secretion throughout life suggests a role for numerous factors that control insulin secretion. Present in vivo and in vitro studies have shown a role for altered autonomic activity, including increased parasympathetic and decreased sympathetic activities, in the maintenance of hyperinsulinemia in 100-day-old HC rats. HC rats were shown to be more sensitive to cholinergic-induced potentiation of glucose-stimulated insulin secretion (GSIS) in response to acetylcholine and showed increased sensitivity to blockade of cholinergic-induced insulin secretion by the muscarinic-type 3 receptor-specific antagonist 4-diphenylacetoxy-Nmethylpiperidine. In addition, HC rats were less sensitive to adrenergic-induced inhibition of insulin secretion by oxymetazoline, whereas treatment with yohimbine resulted in increased GSIS. Furthermore, HC rats showed greater reductions in plasma insulin levels after vagotomy, as well as an attenuation of yohimbine-induced potentiation of GSIS, suggesting that yohimbine-mediated changes are mediated by parasympathetic activity. Changes in autonomic regulation of GSIS are supported by increased mRNA levels of the parasympathetic signaling molecules muscarinic-type 3 receptor, phospholipase C␤1, and protein kinase C-␣ and decreased levels of ␣ 2a-adrenergic receptors in islets from adult HC rats. In conclusion, metabolic programming of hyperinsulinemia throughout adulthood of HC rats involves changes in autonomic activity in response to the HC dietary intervention in the suckling period.high-carbohydrate milk formula; parasympathetic nervous system; and sympathetic nervous system STUDIES OF THE RISING PREVALENCE of obesity, type 2 diabetes mellitus (48), and metabolic syndrome (19) suggest that the origins of these growing epidemics involve an acquired susceptibility to altered nutritional environments during critical periods of early development, including both the fetal and neonatal periods (9,47). This vulnerability manifests as a metabolic programming phenomenon in which a stimulus or insult during critical periods of organogenesis in early life induces permanent alterations in the development and function of affected organs at the cellular, biochemical, and molecular levels to increase the chance of survival in altered nutritional environments (52). These adaptations result in an increased susceptibility to metabolic diseases in adulthood, including obesity, type 2 diabetes mellitus, an...

show abstract

“…Subdiaphragmatic vagotomy was performed using a modified technique previously described by Dixon et al (17). Briefly, rats were fasted for 14 h before vagotomy.…”

Section: Vagotomymentioning

confidence: 99%

Autonomic involvement in the permanent metabolic programming of hyperinsulinemia in the high-carbohydrate rat model

Mitrani¹,

Srinivasan²,

Dodds³

et al. 2007

American Journal of Physiology-Endocrinology and Metabolism

View full text Add to dashboard Cite

show abstract

“…This receptor class has been shown to be involved in mediating GI functions such as gastric emptying, pancreatic secretion, and colonic transit (29,61,80) and have also been shown to be involved in the control of intake under a variety of feeding paradigms. For instance, 5-HT 3 receptors mediate anorectic responses to dietary amino acid deficiency (1,2,19), as well as peripheral CCK administration (17,38,39). There is also some preliminary data demonstrating that 5-HT 3 receptors mediate suppression of intake following intestinal preloads of a nutritionally complete meal (7).…”

mentioning

confidence: 99%

Serotonin-type 3 receptors mediate intestinal Polycose- and glucose-induced suppression of intake

Savastano¹,

Carelle²,

Covașă³

2005

American Journal of Physiology-Regulatory, Integrative and Comp

View full text Add to dashboard Cite

Savastano, David M., Melissa Carelle, and Mihai Covasa. Serotonin-type 3 receptors mediate intestinal Polycose-and glucoseinduced suppression of intake. Am J Physiol Regul Integr Comp Physiol 288: R1499 -R1508, 2005. First published February 17, 2005 doi:10.1152/ajpregu.00745.2004.-Ondansetron, a selective serotonin-type 3 (5-HT3) receptor antagonist, was used to test the hypothesis that duodenal infusion of isosmotic solutions of Polycose or its hydrolytic product glucose suppressed intake through 5-HT3 receptors. Polycose suppressed sucrose intake across both concentrations infused (132 mM, 7.6 Ϯ 0.6 ml; 263 mM, 2.3 Ϯ 0.5 ml), compared with intake under control conditions (12.6 Ϯ 0.3 ml, P Ͻ0.001). Pretreatment with 1.0 mg/kg ondansetron attenuated reduction of sucrose intake induced only by the highest concentration of Polycose (4.6 Ϯ 0.8 ml, P ϭ 0.004). Dose-response testing revealed that suppression of food intake by 263 mM Polycose was equally attenuated by ondansetron administered at 1.0, 2.0, and 5.0 mg/kg but not when given at 0.125, 0.25, and 0.5 mg/kg. Acarbose, an ␣-glucosidase inhibitor, attenuated Polycose-induced suppression of food intake, and pretreatment with 1.0 mg/kg ondansetron had no further effect. Suppression of intake after 990 mM glucose but not mannitol infusion was attenuated by pretreatment with 1.0 mg/kg ondansetron. The competitive SGLT1 inhibitor, phloridzin, had no effect on 60-min 990 mM glucose-induced suppression of intake or the ability of ondansetron to attenuate this suppression of intake. Conversely, glucoseinduced suppression of intake was attenuated by phloridzin at earlier time points and further attenuated when rats were pretreated with 1.0 mg/kg ondansetron. Ondansetron administration alone had no effect on intake at any dose tested. We conclude that 5-HT 3 receptors participate in the inhibition of food intake by intraduodenal infusion of carbohydrate solutions through a posthydrolytic, preabsorptive mechanism. nutrient absorption; food intake; satiation THE PRESENCE OF NUTRIENTS in the intestine elicits signals essential to feedback control of ingestion. Considerable advances have been made in understanding the mechanisms by which nutrients in the intestine suppress intake in a number of species (30, 33), including rats (42, 51, 53) and humans (74). For example, it is well documented that intestinal carbohydrates reduce food intake in a dose-responsive manner (53, 76) by preabsorptive (63, 78) as well as postabsorptive (71) factors, largely through vagal afferent pathways (78, 79). However, the complete mechanism(s) by which intestinal oligosaccharides or monosaccharides is perceived to elicit negative feedback control of intake is not known. Administration of the ␣-glucosidase inhibitor, acarbose, attenuates reduction of food intake and c-Fos-immunoreactivity by maltotriose (62, 63). Moreover, inhibition of sodium-dependent glucose transporter 1 (SGLT 1 ) by intestinal phloridzin infusion fails to attenuate suppression of food intake and vagal afferent activation...

show abstract

“…Arising from each trunk is a branch of the celiac vagus nerve that courses to the pancreas (43). These nerves were either transected [designated celiac vagotomy (CVX); n ϭ 11] or simply exposed (sham surgery; n ϭ 12) using the criteria of Dixon et al (9), and then the animal was sutured and subjected to standard postoperative care, including warming, eye ointment, and buprenorphene analgesia. Age-matched, untouched rats (n ϭ 7) served as additional controls for comparison.…”

Section: Methodsmentioning

confidence: 99%

Vagal control of pancreatic β-cell proliferation

Lausier

Diaz

Roskens

et al. 2010

American Journal of Physiology-Endocrinology and Metabolism

View full text Add to dashboard Cite

The physiological mechanisms that preserve pancreatic ␤-cell mass (BCM) are not fully understood. Although the regulation of islet function by the autonomic nervous system (ANS) is well established, its potential roles in BCM homeostasis and compensatory growth have not been adequately explored. The parasympathetic vagal branch of the ANS serves to facilitate gastrointestinal function, metabolism, and pancreatic islet regulation of glucose homeostasis, including insulin secretion. Given the functional importance of the vagus nerve and its branches to the liver, gut, and pancreas in control of digestion, motility, feeding behavior, and glucose metabolism, it may also play a role in BCM regulation. We have begun to examine the potential roles of the parasympathetic nervous system in short-term BCM maintenance by performing a selective bilateral celiac branch-vagus nerve transection (CVX) in normal Sprague-Dawley rats. CVX resulted in no detectable effects on basic metabolic parameters or food intake through 1 wk postsurgery. Although there were no differences in BCM or apoptosis in this 1-wk time frame, ␤-cell proliferation was reduced 50% in the CVX rats, correlating with a marked reduction in activated protein kinase B/Akt. Unexpectedly, acinar proliferation was increased 50% in these rats. These data suggest that the ANS, via the vagus nerve, contributes to the regulation of BCM maintenance at the level of cell proliferation and may also mediate the drive for enhanced growth under physiological conditions when insulin requirements have increased. Furthermore, the disparate effects of CVX on ␤-cell and acinar cells suggest that the endocrine and exocrine pancreas respond to different neural signals in regard to mass homeostasis.␤-cell mass; celiac vagotomy THE PANCREATIC ␤-CELL HAS A TREMENDOUS CAPACITY to functionally compensate in response to physiological and pathophysiological changes in tissue insulin demands. A key feature of this adaptive response is the ability of the ␤-cell mass (BCM) to be dynamically regulated. For instance, BCM is normally maintained proportionally to body size. It increases during obesity and pregnancy (5,14,20) and regresses postpartum (42) to adjust to physiological insulin requirements. The steady-state BCM is determined by new cell recruitment by hyperplasia of existing cells and neogenesis from pancreatic epithelial progenitors, apoptotic death and clearance, and hypertrophy (5). The relative importance of each of these different processes is largely unknown and depends on the model under study; nonetheless, several recent reports suggest that proliferation from preexisting ␤-cells predominates in mice (10,11,29,30).The interplay of nutrients, growth factors, and hormones is known to impact ␤-cell growth; however, the influence of the nervous system on ␤-cell growth processes has been understudied. There are a handful of reports highlighting the importance of the vagus efferents in ␤-cell proliferation. A transient decrease in ␤-cell proliferation was observed in ob/ob mice, bu...

show abstract

Differential effects of selective vagotomy and tropisetron in aminoprivic feeding

Cited by 20 publications

References 30 publications

Autonomic involvement in the permanent metabolic programming of hyperinsulinemia in the high-carbohydrate rat model

Autonomic involvement in the permanent metabolic programming of hyperinsulinemia in the high-carbohydrate rat model

Serotonin-type 3 receptors mediate intestinal Polycose- and glucose-induced suppression of intake

Vagal control of pancreatic β-cell proliferation

Contact Info

Product

Resources

About