Vagal and splanchnic afferents are not necessary for the anorexia produced by peripheral IL-1beta, LPS, and MDP (original) (raw)
Related papers
American Journal of Physiology-Regulatory, Integrative and Comparative Physiology, 1998
We investigated the extrinsic gut neural mediation of the suppression of food intake in male Sprague-Dawley rats induced by peripheral intraperitoneal administration of 2 μg/kg interleukin-1β (IL-1β), 100 μg/kg bacterial lipopolysaccharide (LPS), and 2 mg/kg muramyl dipeptide (MDP). Food intake during the first 3 and 6 h of the dark cycle was measured in rats with subdiaphragmatic vagal deafferentation ( n = 9), celiac superior mesenteric ganglionectomy ( n = 9), combined vagotomy and ganglionectomy ( n = 9), and sham deafferentation ( n = 9). IL-1β, LPS, and MDP suppressed food intake at 3 and 6 h in all surgical groups. The results demonstrate that neither vagal nor nonvagal afferent nerves from the upper gut are necessary for the feeding-suppressive effects of intraperitoneal IL-1β, LPS, or MDP in the rat and suggest that peripheral administration of immunomodulators produces anorexia via a humoral pathway.
Interleukin-1beta sensitizes the response of the gastric vagal afferent to cholecystokinin in rat
Neuroscience Letters
Interleukin-1b (IL-1b) and cholecystokinin (CCK) are important mediators in the development of anorexic response during disease. The role of IL-1b and CCK in the peripheral mechanisms of anorexia was studied by recording the mass afferent activity of the gastric vagal nerve in anesthetized rats. The i.v. administration of CCK (1 nmol) increased the activity of the vagal nerve, and this response was raised by 55-72% 2 h after i.v. injection of IL-1b. It is proposed that IL-1b-induced anorexia is mediated via the sensitization of type A CCK receptors in the periphery.
Interleukin-1b sensitizes the response of the gastric vagal afferent to cholecystokinin in rat
Interleukin-1b (IL-1b) and cholecystokinin (CCK) are important mediators in the development of anorexic response during disease. The role of IL-1b and CCK in the peripheral mechanisms of anorexia was studied by recording the mass afferent activity of the gastric vagal nerve in anesthetized rats. The i.v. administration of CCK (1 nmol) increased the activity of the vagal nerve, and this response was raised by 55–72% 2 h after i.v. injection of IL-1b. It is proposed that IL-1b-induced anorexia is mediated via the sensitization of type A CCK receptors in the periphery.
Interleukin-1β sensitizes the response of the gastric vagal afferent to cholecystokinin in rat
Neuroscience Letters, 1997
Interleukin-1b (IL-1b) and cholecystokinin (CCK) are important mediators in the development of anorexic response during disease. The role of IL-1b and CCK in the peripheral mechanisms of anorexia was studied by recording the mass afferent activity of the gastric vagal nerve in anesthetized rats. The i.v. administration of CCK (1 nmol) increased the activity of the vagal nerve, and this response was raised by 55-72% 2 h after i.v. injection of IL-1b. It is proposed that IL-1b-induced anorexia is mediated via the sensitization of type A CCK receptors in the periphery.
Rimonabant induced anorexia in rodents is not mediated by vagal or sympathetic gut afferents
Neuroscience Letters, 2009
The selective CB1 receptor antagonist rimonabant is a novel weight control agent. Although CB1 receptors and binding sites are present in both the rodent central and peripheral nervous systems, including the afferent vagus nerve, the role of gut afferents in mediating anorexia following CB1R blockade is still debated. In the present study we examined rimonabant-induced anorexia in male C57BL/6J mice with subdiaphragmatic vagotomy (VGX) as well as in male Sprague-Dawley rats subjected to either subdiaphragmatic vagal deafferentation (SDA) alone or in combination with a complete celiac-superior mesenteric ganglionectomy (CGX). Irrespective of the operational procedure, rimonabant (10 mg/kg) effectively reduced standard chow as well as palatable diet (ensure) intake. In conclusion, the data clearly demonstrate that neither vagal gut afferents, nor gut afferents traveling via the sympathetic nervous system, are required for rimonabant to inhibit food intake leading to the hypothesis that centrally located CB1 receptors are the prime mediators of rimonabant-induced anorexia.
Obesity surgery, 2014
It is conceivable that overstimulation of chemo- and mechano-sensors in the Roux and common limbs by uncontrolled influx of undigested nutrients after Roux-en-Y gastric bypass surgery (RYGB) could lead to exaggerated satiety signaling via vagal afferents and contribute to body weight loss. Because previous clinical and preclinical studies using vagotomy came to different conclusions, the aim was to examine the effects of selective and histologically verified celiac branch vagotomy on reduced food intake and body weight loss induced by RYGB. Male Sprague-Dawley rats underwent either RYGB + celiac branch vagotomy (RYGB/VgX, n=15), RYGB + sham celiac branch vagotomy (RYGB/Sham VgX; n=6), Sham RYGB + celiac branch vagotomy (Sham/VgX; n=6), or sham RYGB + sham celiac branch vagotomy (Sham/Sham; n=6), and body weight, body composition, and food choice were monitored for 3 months after intervention. In rats with RYGB, histologically confirmed celiac branch vagotomy significantly moderated ...
The vagus nerve, food intake and obesity
Regulatory Peptides, 2008
Food interacts with sensors all along the alimentary canal to provide the brain with information regarding its composition, energy content, and beneficial effect. Vagal afferents innervating the gastrointestinal tract, pancreas, and liver provide a rapid and discrete account of digestible food in the alimentary canal, as well as circulating and stored fuels, while vagal efferents together with the sympathetic nervous system and hormonal mechanisms codetermine the rate of nutrient absorption, partitioning, storage, and mobilization. Although vagal sensory mechanisms play a crucial role in the neural mechanism of satiation, there is little evidence suggesting a significant role in long-term energy homeostasis. However, increasing recognition of vagal involvement in the putative mechanisms making bariatric surgeries the most effective treatment for obesity should greatly stimulate future research to uncover the many details regarding the specific transduction mechanisms in the periphery and the inter-and intra-neuronal signaling cascades disseminating vagal information across the neuraxis.
Central Neurocircuits Regulating Food Intake in Response to Gut Inputs—Preclinical Evidence
Nutrients
The regulation of energy balance requires the complex integration of homeostatic and hedonic pathways, but sensory inputs from the gastrointestinal (GI) tract are increasingly recognized as playing critical roles. The stomach and small intestine relay sensory information to the central nervous system (CNS) via the sensory afferent vagus nerve. This vast volume of complex sensory information is received by neurons of the nucleus of the tractus solitarius (NTS) and is integrated with responses to circulating factors as well as descending inputs from the brainstem, midbrain, and forebrain nuclei involved in autonomic regulation. The integrated signal is relayed to the adjacent dorsal motor nucleus of the vagus (DMV), which supplies the motor output response via the efferent vagus nerve to regulate and modulate gastric motility, tone, secretion, and emptying, as well as intestinal motility and transit; the precise coordination of these responses is essential for the control of meal size...
Peptides, 2011
We previously showed that medullary thyrotropin-releasing hormone (TRH) or the stable TRH agonist, RX-77368 administered intracisternally induces vagal-dependent activation of gastric myenteric neurons and prevents post surgery-induced delayed gastric emptying in rats. We investigated whether abdominal surgery alters intracisternal (ic) RX-77368 (50 ng)-induced gastric myenteric neuron activation. Under 10 min enflurane anesthesia, rats underwent an ic injection of saline or RX-77368 followed by a laparotomy and a 1-min cecal palpation, or no surgery and were euthanized 90 min later. Longitudinal muscle/myenteric plexus whole-mount preparations of gastric corpus and antrum were processed for immunohistochemical detection of Fos alone or double labeled with protein gene-product 9.5 (PGP 9.5) and vesicular acetylcholine transporter (VAChT). In the non surgery groups, ic RX-77368 induced a 17 fold increase in Fos-expression in both gastric antrum and corpus myenteric neurons compared to saline injected rats. PGP 9.5 ascertained the neuronal identity of myenteric cells expressing Fos. In the abdominal surgery groups, ic RX-77368 induced a significant increase in Fos-expression in both the corpus and antrum myenteric ganglia compared with ic saline injected rats which has no Fos in the gastric myenteric ganglia. However, the response was reduced by 73-78% compared with that induced by ic RX 77368 without surgery. Abundant VAChT positive nerve fibers were present around Fos positive neurons. These results indicate a bidirectional interaction between central vagal stimulation of gastric myenteric neurons and abdominal surgery. The modulation of gastric vagusmyenteric neuron activity could play an important role in the recovery phase of postoperative gastric ileus.