Extrahypothalamic Expression of the Glucagon-Like Peptide-2 Receptor Is Coupled to Reduction of Glutamate-Induced Cell Death in Cultured Hippocampal Cells

Lovshin, Julie A.; Huang, Qingling; Seaberg, Raewyn M.; Brubaker, Patricia L.; Drucker, Daniel J.

doi:10.1210/en.2004-0100

Cited by 71 publications

(56 citation statements)

References 56 publications

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“…infusion of GLP2 in rats (Tang-Christensen et al 2000), the anorectic effects of [Gly 2 ]GLP2 were blocked by pretreatment with the GLP1R antagonist exendin (9-39), suggesting that the effects of GLP2 on feeding require the functional activity of GLP1R signaling. It is unlikely that [Gly 2 ]GLP2 directly interacts with GLP1R because previously it was reported that the peptide has no effect in cells transfected with GLP1R (Lovshin et al 2001) and increases cAMP accumulation in neuronal cultures derived from GLP1R null mice (Lovshin et al 2004). Indeed, the finding that exendin (9-39) eliminates the GLP2-mediated inhibitory effects on food intake might imply that the GLP1R antagonist acts also as a GLP2R antagonist, as in the past it was proposed (Wheeler et al 1995, Munroe et al 1999, Tang-Christensen et al 2000.…”

Section: Discussionmentioning

confidence: 99%

“…Indeed, the finding that exendin (9-39) eliminates the GLP2-mediated inhibitory effects on food intake might imply that the GLP1R antagonist acts also as a GLP2R antagonist, as in the past it was proposed (Wheeler et al 1995, Munroe et al 1999, Tang-Christensen et al 2000. However, more recent studies clearly demonstrate that exendin (9-39) does not act as a functional GLP2R antagonist (Lovshin et al 2001(Lovshin et al , 2004. In mice intracerebroventricular GLP2 inhibits dark-phase feeding more potently after GLP1R blockade or complete disruption of GLP1R in GLP1R knockout mice (Lovshin et al 2001).…”

Section: Discussionmentioning

confidence: 99%

“…whether the GLP2 inhibitory effect directly involves some of the brain centers regulating food intake or if it is indirect through peripheral sites. Indeed, participation of both central and peripheral sites in the GLP2-induced anorectic effect might be considered because a number of studies have shown that peripheral administration of neuropeptides labels the blood-brain barrier-free area postrema and diffuses into the adjacent regions (Whitcomb et al 1990), and GLP2Rs have been described in the nucleus of the solitary tract (Lovshin et al 2004). In addition, functional GLP2R has been localized to the cell bodies of vagal afferents in the nodose ganglion, at least in the rat (Nelson et al 2007), then i.p.…”

Section: Lovshinmentioning

confidence: 99%

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Food intake in lean and obese mice after peripheral administration of glucagon-like peptide 2

Baldassano¹,

Bellanca²,

Serio³

et al. 2012

Journal of Endocrinology

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We investigated the potential anorectic action of peripherally administered glucagon-like peptide 2 (GLP2) in lean and diet-induced obese (DIO) mice. Mice, fasted for 16 h, were injected i.p. with native GLP2 or [Gly 2 ]GLP2, stable analog of GLP2, before or after GLP2 (3-33), a GLP2 receptor (GLP2R) antagonist, or exendin (9-39), a GLP1R antagonist. Food intake was measured at intervals 1, 2, 4, 8, and 24 h postinjection. In addition, we tested in lean mice the influence of [Gly 2 ]GLP2 on gastric emptying and the effects of GLP1 alone or in combination with [Gly 2 ]GLP2 on food intake. [Gly 2 ]GLP2 dose dependently and significantly inhibited food intake in lean and DIO mice. The reduction of food intake occurred in the first hour postinjection and it was sustained until 4 h postinjection in lean mice while it was sustained until 2 h postinjection in DIO mice. GLP2 significantly inhibited food intake in both lean and DIO mice but only in the first hour postinjection. ]GLP2 decreased the gastric emptying rate. Results suggest that GLP2 can reduce food intake in mice in the short term, likely acting at a peripheral level. DIO mice are less sensitive to the anorectic effect of the peptide.

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Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

Section: Lovshinmentioning

confidence: 99%

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Food intake in lean and obese mice after peripheral administration of glucagon-like peptide 2

Baldassano¹,

Bellanca²,

Serio³

et al. 2012

Journal of Endocrinology

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“…GLP2R is also expressed in the central nervous system (CNS), specifically in key regions of the brain for energy balance, including the hypothalamus, hippocampus and brainstem (Tang-Christensen et al 2000, Lovshin et al 2004, Guan et al 2012. As a neurotransmitter, GLP2 may mediate preproglucagonergic (PPG) neuron-induced synaptic transmission linking the hypothalamus and the brainstem and may act as a satiation signal in the control of feeding behaviour (Tang-Christensen et al 2000).…”

Section: Overview On Glp2mentioning

confidence: 99%

GLP2: an underestimated signal for improving glycaemic control and insulin sensitivity

Amato¹,

Baldassano²,

Mulè³

2016

Journal of Endocrinology

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Glucagon-like peptide 2 (GLP2) is a proglucagon-derived peptide produced by intestinal enteroendocrine L-cells and by a discrete population of neurons in the brainstem, which projects mainly to the hypothalamus. The main biological actions of GLP2 are related to the regulation of energy absorption and maintenance of mucosal morphology, function and integrity of the intestine; however, recent experimental data suggest that GLP2 exerts beneficial effects on glucose metabolism, especially in conditions related to increased uptake of energy, such as obesity, at least in the animal model. Indeed, mice lacking GLP2 receptor selectively in hypothalamic neurons that express proopiomelanocortin show impaired postprandial glucose tolerance and hepatic insulin resistance (by increased gluconeogenesis). Moreover, GLP2 acts as a beneficial factor for glucose metabolism in mice with high-fat diet-induced obesity. Thus, the aim of this review is to update and summarize current knowledge about the role of GLP2 in the control of glucose homeostasis and to discuss how this molecule could exert protective effects against the onset of related obesity type 2 diabetes.

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“…2000; Lovshin et al . 2004). Thus, GLP‐2 is considered as an anorexigenic neurotransmitter in mammals.…”

Section: Introductionmentioning

confidence: 99%

Glucagon‐related peptides and the regulation of food intake in chickens

Honda

2016

Animal Science Journal

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The regulatory mechanisms underlying food intake in chickens have been a focus of research in recent decades to improve production efficiency when raising chickens. Lines of evidence have revealed that a number of brain‐gut peptides function as a neurotransmitter or peripheral satiety hormone in the regulation of food intake both in mammals and chickens. Glucagon, a 29 amino acid peptide hormone, has long been known to play important roles in maintaining glucose homeostasis in mammals and birds. However, the glucagon gene encodes various peptides that are produced by tissue‐specific proglucagon processing: glucagon is produced in the pancreas, whereas oxyntomodulin (OXM), glucagon‐like peptide (GLP)‐1 and GLP‐2 are produced in the intestine and brain. Better understanding of the roles of these peptides in the regulation of energy homeostasis has led to various physiological roles being proposed in mammals. For example, GLP‐1 functions as an anorexigenic neurotransmitter in the brain and as a postprandial satiety hormone in the peripheral circulation. There is evidence that OXM and GLP‐2 also induce anorexia in mammals. Therefore, it is possible that the brain‐gut peptides OXM, GLP‐1 and GLP‐2 play physiological roles in the regulation of food intake in chickens. More recently, a novel GLP and its specific receptor were identified in the chicken brain. This review summarizes current knowledge about the role of glucagon‐related peptides in the regulation of food intake in chickens.

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Extrahypothalamic Expression of the Glucagon-Like Peptide-2 Receptor Is Coupled to Reduction of Glutamate-Induced Cell Death in Cultured Hippocampal Cells

Cited by 71 publications

References 56 publications

Food intake in lean and obese mice after peripheral administration of glucagon-like peptide 2

Food intake in lean and obese mice after peripheral administration of glucagon-like peptide 2

GLP2: an underestimated signal for improving glycaemic control and insulin sensitivity

Glucagon‐related peptides and the regulation of food intake in chickens

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