Glucagon-like peptide-2-induced memory improvement and anxiolytic effects in mice

Iwai, Takashi; Jin, Kazushi; Ohnuki, Tomoko; Sasaki-Hamada, Sachie; Nakamura, Masumi; Saitoh, Akiyoshi; Sugiyama, Azusa; Ikeda, Masaatsu; Tanabe, Mitsuo; Oka, Jun

doi:10.1016/j.npep.2014.11.001

Cited by 20 publications

(13 citation statements)

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“…The ICV administration (5 μl/ventricle) was performed according to the previously reported procedures 6,21 using a 50-μl Hamilton microsyringe with a 28-gauge needle under brief isoflurane anesthesia. Two doses of vehicle or STZ (3 mg/kg, ICV) were administered bilaterally on Days-1 and -3 according to the procedure of Sodhi and Singh 22 .…”

Section: Methodsmentioning

confidence: 99%

“…Centrally administered GLP-2 to rodents has been shown to suppress food intake 3,4 . Moreover, GLP-2 protected hippocampal neurons from glutamate excitotoxicity 4 , stimulated the proliferation of cultured rat cortical astrocytes 5 , and improved lipopolysaccharide (LPS)-induced memory impairments 6 . However, there has been no conclusive experimental evidence to explain the protective potential of GLP-2 in animal models of Alzheimer’s disease (AD).…”

Section: Introductionmentioning

confidence: 99%

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Glucagon-like peptide-2 rescues memory impairments and neuropathological changes in a mouse model of dementia induced by the intracerebroventricular administration of streptozotocin

Sasaki-Hamada

Ikeda

Oka

2019

Sci Rep

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Glucagon-like peptide 2 (GLP-2) is derived from the proglucagon gene expressed in the intestines, pancreas and brain. Our previous study showed that GLP-2 improved lipopolysaccharide-induced memory impairments. The current study was designed to further investigated the potential of GLP-2 in memory impairment induced by intracerebroventricular administration of streptozotocin (ICV-STZ) in mice, which have been used as an animal model of sporadic Alzheimer’s disease (AD). STZ was administered on alternate days (Day-1 and Day-3) in order to induce dementia in male ddY mice. ICV-STZ-treated mice were administered GLP-2 (0.6 μg/mouse, ICV) for 5 days from 14 days after the first ICV administration of STZ. In these mice, we examined spatial working memory, the biochemical parameters of oxidative stress, or neurogenesis. The GLP-2 treatment restored spatial working memory in ICV-STZ-treated mice. ICV-STZ-treated mice showed markedly increased thiobarbituric acid reactive species (TBARS) and decreased glutathione (GSH) levels, and GLP-2 significantly restored these ICV-STZ-induced changes. GLP-2 also significantly restored neurogenesis in the subgranular zone of the dentate gyrus in ICV-STZ-treated mice. We herein demonstrated that GLP-2 significantly restored ICV-STZ-induced memory impairments as well as biochemical and histopathological alterations, and accordingly, propose that the memory restorative ability of GLP-2 is due to its potential to reduce oxidative stress.

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Section: Methodsmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Glucagon-like peptide-2 rescues memory impairments and neuropathological changes in a mouse model of dementia induced by the intracerebroventricular administration of streptozotocin

Sasaki-Hamada

Ikeda

Oka

2019

Sci Rep

Self Cite

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“…Like GLP-1, GLP-2 also regulates the function of central nervous system ( 52 ). Activation of GLP-2 receptors can reduce stress-induced depression ( 53 , 54 ) and improve memory in animal experiments ( 55 ). It also plays a substantial role in bone metabolism via reducing bone reabsorption and improving bone mineral density ( 56 ).…”

Section: Overview Of Glp Functionmentioning

confidence: 99%

Role of Incretin Axis in Inflammatory Bowel Disease

et al. 2017

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The inflammatory bowel diseases (IBDs), including Crohn’s disease (CD) and ulcerative colitis (UC), are chronic inflammatory conditions of the gastrointestinal tract and involve a complicated reciprocity of environmental, genetic, and immunologic factors. Despite substantial advances in the foundational understanding of the immunological pathogenesis of IBD, the detailed mechanism of the pathological progression in IBD remains unknown. In addition to Th1/Th2 cells, whose role in IBD has been previously well defined, recent evidence indicates that Th17 cells and Tregs also play a crucial role in the development of IBD. Diets which contain excess sugars, salt, and fat may also be important actors in the pathogenesis of IBD, which may be the cause of high IBD incidence in western developed and industrialized countries. Up until now, the reason for the variance in prevalence of IBD between developed and developing countries has been unknown. This is partly due to the increasing popularity of western diets in developing countries, which makes the data harder to interpret. The enterocrinins glucagon-like peptides (GLPs), including GLP-1 and GLP-2, exhibit notable benefits on lipid metabolism, atherosclerosis formation, plasma glucose levels, and maintenance of gastric mucosa integrity. In addition to the regulation of nutrient metabolism, the emerging role of GLPs and their degrading enzyme dipeptidyl peptidase-4 (DPP-4) in gastrointestinal diseases has gained increasing attention. Therefore, here we review the function of the DPP-4/GLP axis in IBD.

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“…Although work in this area has been conducted primarily in rodents, intracerebroventricular administration of GLP-2 also reduces feed intake and circulating concentrations of glucose in 8-d-old chicks [84], indicating that similar pathways likely exist across avian and mammalian species. In addition, GLP-2 can reduce stress-induced depression [14] and hypertension in rodents [85] and improve memory in mice with experimentally induced brain inflammation [13] through the GLP-2R expressed in the central nervous system. Although these effects were based on central administration of GLP-2, it is believed that peripheral GLP-2 (both physiological and pharmacologic doses) may be able to cross the blood-brain barrier and have central effects [12].…”

Section: Physiological Effects Of Glp-2 On Extraintestinal Tissuesmentioning

confidence: 99%

“…Since that time, numerous subtypes of endocrine cells within the intestinal mucosa and their peptide products have been characterized [2]. These enteric peptides have become the subject of intensive scientific investigation regarding regulation of their release [3][4][5], mechanisms of action [6][7][8], and diverse physiological effects, including those outside the digestive system such as bone [9], liver [10], lung [11], and the central nervous system [12][13][14]. This primarily was due to the discovery that enteric peptides, such as glucagon-like peptide 1 (GLP-1), gastric inhibitory peptide, and peptide YY, play key roles in the regulation of appetite, energy metabolism [15][16][17], and gut function [18][19][20], making them targets for managing prevalent human diseases of obesity and diabetes.…”

Section: Introductionmentioning

confidence: 99%

Glucagon-like peptide 2 and its beneficial effects on gut function and health in production animals

Connor

Evock‐Clover

Wall³

et al. 2016

Domestic Animal Endocrinology

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Numerous endocrine cell subtypes exist within the intestinal mucosa and produce peptides contributing to the regulation of critical physiological processes including appetite, energy metabolism, gut function, and gut health. The mechanisms of action and the extent of the physiological effects of these enteric peptides are only beginning to be uncovered. One peptide in particular, glucagon-like peptide 2 (GLP-2) produced by enteroendocrine L cells, has been fairly well characterized in rodent and swine models in terms of its ability to improve nutrient absorption and healing of the gut after injury. In fact, a long-acting form of GLP-2 recently has been approved for the management and treatment of human conditions like inflammatory bowel disease and short bowel syndrome. However, novel functions of GLP-2 within the gut continue to be demonstrated, including its beneficial effects on intestinal barrier function and reducing intestinal inflammation. As knowledge continues to grow about GLP-2's effects on the gut and its mechanisms of release, the potential to use GLP-2 to improve gut function and health of food animals becomes increasingly more apparent. Thus, the purpose of this review is to summarize: (1) the current understanding of GLP-2's functions and mechanisms of action within the gut; (2) novel applications of GLP-2 (or stimulators of its release) to improve general health and production performance of food animals; and (3) recent findings, using dairy calves as a model, that suggest the therapeutic potential of GLP-2 to reduce the pathogenesis of intestinal protozoan infections.

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Glucagon-like peptide-2-induced memory improvement and anxiolytic effects in mice

Cited by 20 publications

References 44 publications

Glucagon-like peptide-2 rescues memory impairments and neuropathological changes in a mouse model of dementia induced by the intracerebroventricular administration of streptozotocin

Glucagon-like peptide-2 rescues memory impairments and neuropathological changes in a mouse model of dementia induced by the intracerebroventricular administration of streptozotocin

Role of Incretin Axis in Inflammatory Bowel Disease

Glucagon-like peptide 2 and its beneficial effects on gut function and health in production animals

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