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At least 37 records · Page 2Linked to original sources
PubMed2006

Importance of the gut-brain axis in the control of glucose homeostasis.

Adult mammals finely match glucose production to glucose utilization, thus allowing glycaemia to be maintained in a physiological range of 0.8-1.2mg/dl whatever the energetic status of the mammal (i.e. fed or fasted, rested or exercised). To accomplish this, peripheral signals originating from the gut 'inform' the central nervous system, which in turn is able to monitor the status of both peripheral glucose stores and ongoing fuel availability. Indeed, both secretion and action of hormones regulating endogenous glucose production and utilization are regulated by the autonomic nervous system. These gut signals are either hormonal (e.g. glucagon-like peptide-1, ghrelin and cholecystokinine) or neuronal (e.g. afferent vagus nerve fibres). Recent data, combined with the development of incretin analogues for treatment of diabetes, highlight the importance of the gut-brain axis, especially glucagon-like peptide-1 and ghrelin, in the control of glucose homeostasis.

Animals↗
PubMed1992

Gastric antisecretory and antiulcer actions of interleukin-1. Evidence for the presence of an "immune-brain-gut" axis.

Increasing evidence suggests that interleukin-1 (IL-1), a cytokine mainly produced by activated monocytes/macrophages, has various biological actions in addition to its immunological activities. In the present study, we examined the effect of IL-1 on gastric secretion and gastric ulcer formation in rats. Gastric secretion was assessed in conscious pylorus-ligated rats weighing approximately 200 g. The peripheral injection of IL-1 resulted in a dose-related inhibition of gastric acid output. The central injection of IL-1 similarly reduced gastric acid secretion at 100 times smaller doses than peripherally injected IL-1, suggesting that this gastric antisecretory action of IL-1 is mediated by the central nervous system. In addition, it was found that this inhibitory effect of IL-1, either peripherally or centrally administered, was still evident at 8 h after injection, indicating the long-lasting property of this IL-1 action. On the basis of these antisecretory actions of IL-1, we determined whether or not pretreatment with IL-1 would prevent experimentally induced gastric ulcer formation. As expected, the central administration of IL-1 dose-dependently suppressed the development of gastric mucosal lesions induced by water-immersion restraint stress, a well-established ulcerogenic procedure. These results clearly demonstrated that IL-1 has potent antisecretory and antiulcer effects that are mediated by the central nervous system. Moreover, these findings suggest that there may exist an "immune-brain-gut" axis, which is involved in the regulation of gastric secretion and mucosal homeostasis, especially under certain pathophysiological conditions that activate the immune system to release various cytokines including IL-1.

Animals↗
PubMed2001

Receptors and transmission in the brain-gut axis: potential for novel therapies. IV. GABA(B) receptors in the brain-gastroesophageal axis.

GABA(B) receptors are inhibitory G protein-coupled receptors that are commonly associated with presynaptic inhibition of transmitter release in the central nervous system. In the brain-gastroesophageal axis, a role has recently been demonstrated for GABA(B) receptors on extrinsic afferent endings within the stomach and esophagus, where they reduce mechanosensitivity. This action is compounded by inhibition of communication centrally from these afferents in the brain stem and within central circuits. There is a final peripheral action on the motor pathway where GABA(B) receptors reduce output of acetylcholine from vagal preganglionic motoneurons. These potent, multiple actions of GABA(B) receptors may have therapeutic benefit by reducing the triggering of transient lower esophageal relaxations, which are the major cause of gastroesophageal reflux. An important clinical application is therefore emerging for this recent discovery.

Afferent Pathways↗
PubMed2000

Bombesin and the brain-gut axis.

Bombesin is the first peptide shown to act in the brain to influence gastric function and the most potent peptide to inhibit acid secretion when injected into the cerebrospinal fluid (CSF) in rats and dogs. Bombesin responsive sites include specific hypothalamic nuclei (paraventricular nucleus, preoptic area and anterior hypothalamus), the dorsal vagal complex as well as spinal sites at T9-T10. The antisecretory effect of central bombesin encompasses a variety of endocrine/paracrine (gastrin, histamine) or neuronal stimulants. Bombesin into the CSF induces an integrated gastric response (increase in bicarbonate, and mucus, inhibition of acid, pepsin, vagally mediated contractions) enhancing the resistance of the mucosa to injury through autonomic pathways. The physiological significance of central action of bombesin on gastric function is still to be unraveled.

Animals↗
PubMed1980

Evidence for a cholecystokinin gut-brain axis with modulation by bombesin.

The relationship between cerebrospinal fluid and plasma cholecystokinin (CCK) levels was investigated by simultaneous withdrawal of CSF and blood from anesthetized mongrel dogs and measurement of CCK immunoreactivity by radioimmunoassay. A significant correlation occurred between CSF and plasma levels of CCK. During a CCK IV infusion, a statistically significant inverse correlation was noted between CSF and plasma values, while no significant relationship was noted during a bombesin (BBS) IV infusion. When infusion data were analyzed together with the appropriate baseline data, polynomial analysis revealed significant biphasic relationships for both CCK and BBS infusion studies. Intraventricular infusion of CCK did not alter plasma levels. These data suggest that existence of a mechanism relating CSF to plasma CCK levels (a gut to brain axis) with possible modulation or suppression by BBS.

Animals↗
PubMedDate not supplied

[Brain-gut axis: implications on the genesis of peptic ulcer].

Clinical and laboratory evidence indicate that the brain exerts mayor control on the gastro-intestinal tract. Specific brain loci and circuits send efferent viscerotropic projections to the gut have been summarized. A variety of aminergic and peptidergic neurotransmitters have been shown specially and their function on gastric acid secretion and implications for ulcer disease. These findings suggest that ulcer disease may represents a brain-driven event, which may be the result of a neurochemical imbalance within the brain.

Brain↗
PubMed1987

The peptidergic brain-gut axis: influence on gastric ulcer formation.

The existence of a relationship between the brain and the formation of gastric ulcers has been suspected since the last century. The advancement of stereotaxic procedures and the use of electrical lesion or stimulation have allowed localization within the limbic system, hypothalamus and brain stem, of discrete nuclei that influence the formation of gastric ulceration in experimental animals. Recently, further progress in the understanding of how the brain may influence gastric pathogenesis has been made by the demonstration that specific peptides act in the central nervous system to induce or prevent the formation of gastric ulcers and to markedly alter gastric secretory and motor function. Peptides established to have a centrally mediated protective effect are bombesin, calcitonin, corticotropin-releasing factor, neurotensin and opioid peptides. Growing evidence suggests a possible role for endogenous thyroptropin-releasing hormone in mediating cold-restraint stress induced gastric lesions. Circadian variations of the content and release of these peptides have been demonstrated in specific brain structures. To what extent such rhythms of peptide secretion are potentially linked to the circadian changes in the susceptibility to ulcer formation is worth investigating.

Animals↗
PubMed2004

Brain-gut axis and its role in the control of food intake.

Gastrointestinal tract (GIT) and nervous system, both central (CNS) and enteric (ENS), are involved in two-way extrinsic communication by parasympathetic and sympathetic nerves, each comprising efferents fibers such as cholinergic and noradrenergic, respectively, and afferent sensory fibers required for gut-brain signaling. Afferent nerves are equipped with numerous sensors at their terminals in the gut related to visceral mechano- chemo- and noci-receptors, whose excitations may trigger a variety of visceral reflexes regulating GIT functions, including the appetitive behaviour. Food intake depends upon various influences from the CNS as well as from the body energy stores (adipocytes) that express and release the product of Ob gene, leptin, in proportion to fat stored and acting in long-term regulation of food intake. Leptin acts through receptors (Ob-R) present in afferent visceral nerves and hypothalamic arcuate nucleus (ARC), whose neurons are capable of expressing and releasing neuropeptide Y (NPY) and agouti related protein (AgRP) that activate the ingestive behaviour through paraventricular nucleus (PVN) (iVfeeding centerli). In addition, to this long-term regulation, a short-term regulation, on meal-to-meal basis, is secured by several gut hormones, such as cholecystokinin (CCK), peptides YY (PYY) and oxyntomodulin (OXM), released from the endocrine intestinal cells and acting via G-protein coupled receptors (GPCR) either on afferent nerves or directly on ARC neurons, which in turn inhibit expression and release of food-intake stimulating NPY and AgRP, thereby inducing satiety through inhibition of PVN. In contrast, during fasting, the GIT, especially oxyntic mucosa, expresses and releases appetite stimulating (orexigenic) factors such as ghrelin and orexins (OX) -A and OX-B, and cannabinoid CB1 agonist. Ghrelin activates growth-hormone secretagogue receptor (GHS-R) in hypothalamic ARC and stimulates growth hormone (GH) release and in vagal afferents to promote the expression and release of hypothalamic NPY and AgRP stimulating PVN and driving ingestive behaviour. The balance and interaction between anorexigenic (CCK, PYY, OXM) and orexigenic (ghrelin and OX) factors originating from GIT appears to play an important role in short-term regulation of food intake and growth hormone (GH) release. An impairment of this balance may result in disorders of feeding behaviour and weight gain (obesity) or weight loss (cachexia).

Animals↗
PubMed2003

[Appetite regulation by ghrelin - a novel neuro-endocrine gastric peptide hormone in the gut-brain-axis].

Ghrelin a novel peptide consisting of 28 amino acids was first identified in the stomach in 1999. It is mainly produced in endocrine cells of the human gastric mucosa, but it was also found in several other tissues e. g. in the pituitary, the hypothalamus and the pancreas. The functional receptor belongs to the family of the 7-transmembrane G-protein receptors and is predominantly detected in the pituitary and at lower levels in hypothalamic nuclei, the stomach, heart, lungs, kidneys, gut, the adipose and many other tissues. According to the widespread distribution of the peptide and its receptor, ghrelin has multiple biological effects: it stimulates the release of growth hormone in the pituitary and induces a rise in the serum concentration of ACTH, cortisol, catecholamines and prolactin. Ghrelin causes an increase of food intake and body weight by stimulating the production of neuropeptide Y (NPY) and agouti-related protein (AGP) in the nucleus arcuatus. It further leads to elevated concentrations of plasma glucose. A physiological antagonism between ghrelin and GLP-1 in the hypothalamic regulation of appetite is being discussed. The basic serum level of ghrelin depends on the state of nutrition and is negatively correlated with the body-mass-index. It shows a certain pattern of variation before and after food intake with a preprandial increase and a postprandial decrease. Ghrelin modulates gastric acid secretion and the gastrointestinal motility via vagal cholinergic pathways. The discovery of ghrelin definitely contributes to the understanding of the growth-hormone secretion and of the regulation of appetite and food intake.

Adrenocorticotropic Hormone↗