Guide Sensory and Metabolic Control of Energy Balance: 52 (Results and Problems in Cell Differentiation)

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Circulating PYY levels are low in obese subjects [ 17 , 23 ], and they are higher in patients with anorexia nervosa when compared with control subjects [ 24 ]. Studies of circulating levels of PYY in obese and lean people have yielded inconsistent results [ 25 , 26 ]; however, a blunted postprandial rise in PYY in obese subjects suggests a possible association with impaired postprandial satiety during obesity [ 21 ].

This effect is likely to be mediated through the Y2 receptor since the anorectic effect of peripheral PYY 3—36 administration is blocked in Y2 receptor-null mice, and intraarcuate injection of a Y2 receptor selective agonist also supresses food intake [ 16 ].

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Although conflicting results have been reported [ 27 ], the vagal-brainstem may also signal the actions of PYY on food intake. Two independent laboratories have observed that vagotomy abolishes anorexia c-fos activation following peripheral PYY 3—36 administration [ 28 , 29 ]. In contrast to the anorectic effects observed by peripheral and intraarcuate PYY 3—36 administration, direct administration of PYY 3—36 into the third ventricle of the brain [ 30 ] or paraventricular nucleus PVN [ 31 ] increases in food intake.

This paradoxical action may be explained by considering that such effects might be endogenously mediated by the orexigenic CNS-distributed peptide, NPY, through an action on Y1 receptor and Y5 receptors [ 32 ]. PYY may also act in the brain areas other than the hypothalamus and brainstem. In a clinical study using functional MRI by Batterham et al.

Neuropeptide Y2 receptors have cardiovascular effects in addition to their metabolic effects. Y2 agonism is implicated in the pathogenesis of hypertension in hypertensive rats [ 36 ]. Nordheim and Hofbauer [ 37 ] reported that Y2 receptor stimulation by PYY 3—36 demonstrated cardiovascular effects of endogenous NPY in rats on different dietary regimens. In food-restricted rats, PYY 3—36 increased mean arterial pressure and heart rate, whereas PYY 3—36 did not influence mean arterial pressure and heart rate in high-fat diet rats. However, human studies thus far have not demonstrated any hypertensive changes as a result of PYY administration.

PP is secreted from PP cells in the pancreatic islets of Langerhans in response to a meal. Anorectic effects of PP are thought to be mediated by directly through the Y4 receptor in the brainstem and hypothalamus. In addition, it may act also via the vagus nerve, as the anorectic effects of PP are abolished by vagotomy in rodents [ 38 ]. Like PYY, paradoxical effects on food intake are observed following PP injection, depending on its route of administration.

In contrast to the anorectic effects observed with peripheral PP administration, central PP administration stimulates food intake [ 41 ]. Although the exact mechanism of this phenomenon is unclear, these differential effects may be mediated by activation of distinct populations of receptors. PP also has other physiological effects, such as delaying gastric emptying, attenuating pancreatic exocrine secretion, and inhibiting gallbladder contraction [ 42 ].

Plasma PP levels show diurnal variations: The release of postprandial PP is biphasic. Circulating PP concentrations increase after a meal in proportion to the caloric intake, and increased levels remain for up to 6 hours postprandially [ 43 ]. Circulating PP levels seem to be inversely proportional to adiposity; higher levels are reported in subjects with anorexia nervosa [ 44 ]. Some, but not all [ 45 , 46 ], studies have demonstrated significant reductions in circulating levels of PP in obese subjects [ 47 , 48 ].

Furthermore, obese patients with Prader-Willi syndrome PWS have been reported to have reduced PP release both basally and postprandially [ 49 ]. In mice, acute and chronic peripheral PP administration results in reduced food intake. Furthermore, transgenic mice overexpressing PP have reduced food intake when compared with wild-type controls [ 50 ]. Agonists to the Y4 receptor designed to mimic the actions of PP have been developed and are under further investigation as potential novel therapies for obesity. The proglucagon gene is expressed in the pancreas, in the L-cells of the small intestine and in the NTS of the brainstem [ 53 , 54 ].

The latter truncated form is the major circulating form in humans, although both active isoforms of GLP-1 have equivalent potency [ 56 ]. Signals arising from the hepatoportal GLP-1R promote glucose clearance, which are independent of changes in insulin secretion [ 62 , 63 ]. GLP-1R is widely distributed particularly in the brain, gastrointestinal tract, and pancreas [ 64 , 65 ]. In the brain, binding sites for GLP-1Rs have been found in the hypothalamus, striatum, brainstem, substantia nigra, and subventricular zone among other structures [ 64 , 66 ].

GLP-1Rs are present on both glia and neuronal cell types [ 66 ]. In addition, GLP-1Rs are expressed in the nodose ganglion [ 67 ]. Furthermore bilateral subdiaphragmatic total truncal vagotomy or brainstem-hypothalamic pathway transetioning abolishes the suppressing actions of GLP-1 on food intake [ 28 ]; this suggests that the vagus contributes to the actions of GLP-1 on food intake.

Circulating GLP-1 levels rise postprandially and fall in the fasted state. Recent evidence also suggests that GLP-1 levels rise in anticipation of a meal [ 68 ]. GLP-1 not only reduces food intake, but also suppresses glucagon secretion and delays gastric emptying [ 69 ]. Intravenous administration of GLP-1 is associated with a dose-dependent reduction of food intake in both normal weight and obese subjects [ 70 ], although obese subjects may be less responsive [ 64 ].

GLP-1 possesses a potent incretin effect in addition to its anorectic action; it stimulates insulin secretion in a glucose-dependent manner following ingestion of carbohydrate. However, its use as obesity treatment was limited for many years by its short plasma half-life of minutes [ 71 ], which is partly attributed to enzymatic degradation by DPP-IV and renal clearance that rapidly inactivate and remove GLP-1 from plasma circulation [ 72 , 73 ].

Continuous subcutaneous infusion of GLP-1 to patients with type 2 diabetes for 6 weeks reduces appetite, and body weight, and improves glycaemic control [ 74 ]. Exenatide improves glycaemic control and decreases body weight in patients with type 2 diabetes. GLP-1 possesses trophic effects on pancreatic beta cells in animal models [ 77 ]. GLP-1 and exendin-4 have been recently shown to promote cellular growth and reduce apoptosis in nervous tissues [ 78 ], but trophic effects on pancreatic beta cells have not been demonstrated clinically in human subjects.

GLP-1 agonists are, therefore, a good example of how research in this area has been translated into clinical practice. A three-year duration of treatment with exenatide has been reported to improve beta cell function; however, when adjusting for weight loss associated with exenatide therapy, this effect remains speculative [ 79 ]. DPP-IV inhibitors, such as sitagliptin and vildagliptin, which are licensed for the treatment of type 2 diabetes, do not result in decrease in body weight.

GLPbased therapies are promising novel treatments for type 2 diabetes, however, long-term outcome data are not yet available. The reported side effects of GLP-1 agonists are nausea and vomiting. Animal safety studies with liraglutide have identified C-cell carcinoma of the thyroid. Acute pancreatitis has been reported in humans treated with liraglutide or exenatide [ 81 ]. Further outcome data will, therefore, be important in confirming the long-term safety of GLPbased therapies.

OXM is a amino acid peptide originally isolated from porcine jejunoileal cells and is found to show glucagon-like activity in the liver [ 82 ]. OXM is another product of the proglucagon gene and is cosecreted with GLP-1 and PYY by the L-cells of the distal gastrointestinal tract, in response to ingested food and in proportion to caloric intake [ 83 ]. OXM has anorectic effects and shows incretin activity with a much lower potency when compared with GLP-1 [ 84 ].

OXM also inhibits gastric acid secretion and delays in gastric emptying [ 85 ]. Administration of OXM is associated with decreased food intake and increases energy expenditure in both rodents and humans [ 86 — 88 ]. These data suggest that a further receptor through which OXM mediates its anorectic effect has yet to be identified.

The role of glucagon in glucose homeostasis is well established; glucagon is produced by alpha cells of the pancreatic islets and increases glucose concentration in response to hypoglycaemia. However, glucagon administration also decreases food intake, possibly by modulating vagal tone and gastric emptying [ 97 , 98 ]. However, the administration of the dual agonists stimulating both glucagon and GLP-1 receptors achieved improvement of diet-induced obesity and glucose intolerance [ , ].

It is, therefore, plausible that dual agonism of glucagon and GLP-1 receptors may offer novel targets for antiobesity treatment. Ghrelin was identified originally as an endogenous ligand for the growth hormone secretagogue receptor GHS-R in rat stomach [ ]. Ghrelin comprises a chain of 28 amino acids with esterification of the hydroxyl group of the third serine residue by octanoic acid, and it is the only known orexigenic gut hormone. Ghrelin also acts as a neurotransmitter, being expressed within the ARC and periventricular area of the hypothalamus [ , ].

Serum ghrelin levels are increased by fasting and decreased by refeeding or oral glucose administration, but they are not decreased by water ingestion [ ]. In rats, ghrelin levels show a diurnal pattern, with the bimodal peaks occurring before dark and light periods [ ]. Levels of circulating ghrelin rise preprandially and fall rapidly in the postprandial period [ ]. Both central and peripheral administration of ghrelin increase food intake and body weight along with a reduction in fat utilisation in rodents [ , ].

Negative correlations between circulating ghrelin levels and body mass index are found in human. Fasting plasma levels of ghrelin are reported to be high in patients with anorexia nervosa [ ] and subjects with diet-induced weight loss [ ]. In contrast, obese subjects show a less marked drop in plasma ghrelin after meal ingestion [ ]. In patients with heart failure, increased levels of plasma ghrelin are reported in cachectic patients when compared with noncachectic patients [ ]. Furthermore, in patients with PWS, elevated circulating ghrelin levels are found, when compared with individuals with nonsyndromic forms of obesity [ ].

The brainstem and vagus nerve may also contribute to the effects of ghrelin on food intake.

Sensory and Metabolic Control of Energy Balance

GHS-R is found to be expressed in the vagus nerve. Furthermore, blockade of gastric vagal afferents in rats abolishes ghrelin-induced feeding and prevents the ghrelin-induced rise in c-fos expression within the ARC [ ]. In addition to its potent orexigenic property, ghrelin also increases gastric motility, upstimulates the hypothalamo-pituitary-adrenal axis, and possesses cardiovascular effects such as vasodilatation and enhanced cardiac contractility [ ]. Ghrelin may promote food intake in part by enhancing the hedonic responses to food cues, which is demonstrated by the recent study by Malik et al.

In their study, functional MRI was performed during exposure to food pictures, and the study results demonstrated increased activation in the amygdala, orbitofrontal cortex, anterior insula, and striatum, during intravenous infusion of ghrelin. Obestatin is a amino acid peptide hormone which is derived from posttranslational cleavage of preproghrelin, and released from the stomach [ ]. In contrast to ghrelin which has orexigenic properties, obestatin may have anorectic effects by decreasing food intake, delaying gastric emptying, and reducing body weight in rodents [ ].

However, the potential anorectic of obestatin remains controversial, since other investigators have failed to demonstrate effects on food intake in lean or obese rodents [ ]. CCK was the first gut hormone found to be implicated in appetite control [ ]. CCK is secreted postprandially by the I cell of the small intestine into circulation [ ], with a short plasma half-life of a few minutes. Plasma CCK levels rise within 15 minutes after meal ingestion [ ]. Infusion of C-terminal octapeptide of CCK decreased food intake in 12 lean men [ ].

However, intermittent prandial CCK infusion reduces meal size in rats but causes a compensatory increase in meal frequency [ ]. A 2-week continuous intraperitoneal infusion of CCK failed to suppress food intake at any time point [ ]. Other physiological functions of CCK include stimulating the release of enzymes from the pancreas and gall bladder, promoting intestinal motility, and delaying gastric emptying. CCK 1 and 2 receptors are widely distributed in brain including the brainstem and hypothalamus [ ]. Some studies suggest that leptin and CCK may interact synergistically to induce short-term inhibition of food intake and long-term reduction of body weight [ ].

Leptin-deficient mice are insensitive to the meal-terminating effect of CCK administration. Furthermore, leptin signalling pathways to brain are dampened in the absence of interaction with CCK release after a meal or in the setting of CCK-A receptor blockade [ ]. Amylin is coreleased with insulin in response to meal ingestion, and it may function as an anorectic hormone. Circulating levels of amylin are found to be higher in obese than lean subjects [ , ].

Administration of amylin is associated with reduced food intake and body weight [ ].

The anorectic effects of amylin may be mediated by modulating activity of the serotonin, histamine, and dopaminergic system in the brain as well as inhibition of NPY release [ ]. Molecular Interactions of Actin Cristobal G. Heat Shock and Development Lawrence E. Mouse Brain Development Andre M. Genetic Mosaics and Cell Differentiation W. Cortical Development Christine F. Back cover copy The prevalence of obesity has dramatically increased in western and westernized societies, making the disease the second leading cause of unnecessary deaths in the US.

Obesity results from imbalanced metabolic regulation leading to excessive lipid storage. As important novel entities in metabolic regulation, taste receptors and their cells are critical elements that adapt the gustatory system to metabolic signals and vice versa. The role of taste receptor genes in gastrointestinal tissues, as well as their dynamic regulation in gustatory and non-gustatory tissues in response to metabolic cues, has become the focus of an entirely new and rapidly developing research field with impacts on fuel sensing, metabolic control, and ingestive behavior.

This book reflects the recent scientific progress in the field of fuel sensing in the mouth, GI tract, and brain and examines the olfactory bulb as a potential metabolic sensor and the brain-gut endocrine axis. It also touches on relevant novel molecular and cellular mechanisms regulating lipid storage and metabolism and covers the identification and functional characterization of obesity genes. The human bitter taste receptor hTAS2R50 is activated by the two natural bitter terpenoids Andrographolide and Amarogentin. Intracellular degradation of somatostatin following somatostatin-receptor 3-mediated endocytosis in rat insulinoma cells.

Functions of human bitter taste receptors depend on N-glycosylation. Deletion of glucose transporter GLUT8 in mice increases locomotor activity. A role of the epithelial sodium channel in human salt taste transduction?.

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Gustatory expression pattern of the human TAS2R bitter receptor gene family reveals a heterogenous population of bitter responsive taste receptor cells. Broad tuning of the human bitter taste receptor hTAS2R46 to various sesquiterpene lactones, clerodane and labdane diterpenoids, strychnine, and denatonium.

Early developmental expression of leptin receptor gene and [ I]leptin binding in the rat forebrain. Leptin sensitivity in the developing rat hypothalamus. Endocrinology , Role of neuromedin-U in the central control of feeding behavior: Somatostatin, a negative-regulator of central leptin action in the rat hypothalamus.

The binding site for neohesperidin dihydrochalcone at the human sweet taste receptor. Molecular biology of human bitter taste receptors. The molecular basis of individual differences in phenylthiocarbamide and propylthiouracil bitterness perception. Identification of specific ligands for orphan olfactory receptors. G protein-dependent agonism and antagonism of odorants. Valine and lysine in the fifth transmembrane domain of rTas1r3 mediate insensitivity towards lactisole of the rat sweet taste receptor. The human taste receptor hTAS2R14 responds to a variety of different bitter compounds.

Molecular cloning and characterisation of DESC4, a new transmembrane serine protease. Bitter taste receptors for saccharin and acesulfame K. Leptin-target neurons of rat hypothalamus express somatostatin receptors. Presence of a plasma membrane targeting sequence in the amino-terminal region of the rat somatostatin receptor 3. A two-dimensional map and database of soluble nuclear proteins from HepG2 cells as reference for identification of nutrient-regulated transcription factors.

The central pyrogenic action of interleukin-6 is related to nuclear translocation of STAT3 in the anteroventral preoptic area of the rat brain. Leptin-induced nuclear translocation of STAT3 immunoreactivity in hypothalamic nuclei involved in body weight regulation. Agonist-mediated endocytosis of rat somatostatin receptor subtype 3 Involves beta-arrestin and clathrin coated vesicles.

Method for the immunological detection of silver-stained proteins on nitrocellulose membranes. Biotechniques 30, , , Nature , The POU domain transcription foactor Tst-1 activates somatostatin receptor 1 gene expression in pancreatic beta-cells.

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Dual regulation of somatostatin receptor subtype 1 gene expression by Pit-1 in anterior pituitary GH3 cells. Translocation of the interleukin-1 receptor-associated kinase-1 IRAK-1 into the nucleus. FEBS Letters , Induction of membrane chloride currents in Xenopus laevis oocytes by the sulfonyl amide sweeteners acesulfame K and saccharin. Central angiotensin receptor blockade impairs thermolytic and dipsogenic responses to heat exposure in rats.

Glycosylation affects agonist binding and signal transduction of the rat somatostatin receptor subtype 3. Paris 94, Bitterless guaifenesin prodrugs - design, synthesis, characterization, in vitro kinetics and bitterness studies. Molecular features underlying selectivity in chicken bitter taste receptors. Intestinal bitter taste receptor activation alters hormone secretion and imparts metabolic benefits.

The crystal structure of Gurmarin, a sweet taste-suppressing protein: Identification of the amino acid residues essential for inhibition. Senses 43, Human sweet receptor T1R3 is functional in human gastric parietal tumor cells HGT-1 and modulates cyclamate and acesulfame K-induced mnechanisms of gastric acid secretion.

Probing the evolutionary history of human bitter taste receptor pseudogenes by restoring their function. A sweet taste receptor-dependent mechanism of glucosensing in hypothalamic tanycytes. Glia 65, Open Access From cell to beak: Ligand binding modes from low resolution GPCR models and mutagenesis: Amino acid sensing in hypothalamic tanycytes via umami taste receptors.

Caffeine induces gastric acid secretion via bitter taste signaling in gastric parietal cells. Structural motifs, ligand interactions and agonist-to-antagonist ratios. Rubemamine and rubescenamine, two naturally occurring N-cinnamoyl phenethylamines with umami taste modulating properties. TAS2R bitter taste receptors regulate thyroid function.

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Identification of cholinergic chemosensory cells in mouse tracheal and laryngeal glandular ducts. A binary genetic approach to characterize TRPM5 cells in mice. The role of 5-HT3 receptors in signaling from taste buds to nerves. Variability in human bitter taste sensitivity to chemically diverse compounds can be accounted for by differential TAS2R activation. Cholinergic chemosensory cells of the thymic medulla express the bitter receptor Tas2r Bitter taste receptor agonists elicit G-protein-dependent negative inotropy in the murine heart.

Expression, regulation and putative nutrient-sensing function of taste GPCRs in the heart. Gustatory sensory cells express a receptor responsive to protein breakdown products GPR Taste responses in mice lacking taste receptor subunit T1R1. Different phenolic compounds activate distinct human bitter taste receptors.

Human psychometric and taste receptor responses to steviol glycosides. Sensomics analysis of taste compounds in balsamic vinegar and discovery of 5-acetoxymethylfuraldehyde as a novel sweet taste modulator. Expression of Tas1 taste receptors in mammalian spermatozoa: Functional characterization of an allatotropin receptor expressed in the corpora allata of mosquitoes. Peptides 34,