Delayed administration of the GLP-1 receptor agonist liraglutide improves metabolic and functional recovery after cerebral ischemia in rats

Dong, Wei; Miao, Yunping; Chen, Aiying; Cheng, Min; Ye, Xiaodi; Song, Fahuan; Zheng, Guoqiang

doi:10.1016/j.neulet.2017.01.045

Cited by 24 publications

(30 citation statements)

References 27 publications

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“…However, in one study, exenatide was not beneficial when administered more than 3 h after ischemic stroke, suggesting that there is a limited time frame for this treatment [ 35 ]. In contrast, liraglutide improved the functional outcome even when administered 1 day after stroke [ 32 ]. In studies that compared different times of administration after stroke, GLP-1 receptor agonists appeared to be more beneficial when administered immediately after the ischemic insult [ 33 , 35 ].…”

Section: Glp-1 Receptor Agonists and Acute Ischemic Strokementioning

confidence: 99%

Incretin-Based Antihyperglycemic Agents for the Management of Acute Ischemic Stroke in Patients with Diabetes Mellitus: A Review

et al. 2019

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Diabetes mellitus (DM) is a major risk factor for ischemic stroke. Moreover, patients with DM suffer more severe strokes and have worse functional outcome following an acute stroke than patients without DM. In this context, data from animal studies and emerging evidence from clinical studies suggest that incretin-based antihyperglycemic agents might exert beneficial effects in patients with DM who suffer ischemic stroke. It appears that these agents exert neuroprotective actions that might both reduce infarct size and promote recovery. The present review summarizes the evidence on the potential role of incretin-based antihyperglycemic agents in the management of acute ischemic stroke.

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Section: Glp-1 Receptor Agonists and Acute Ischemic Strokementioning

confidence: 99%

Incretin-Based Antihyperglycemic Agents for the Management of Acute Ischemic Stroke in Patients with Diabetes Mellitus: A Review

et al. 2019

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“…Mice that lack the GLP‐1 receptor are deficient in learning and in neuroprotection, and defects in endogenous GLP‐1 signalling have been implicated in the progressive loss of neurons that characterizes neurodegenerative disorders . In laboratory models of brain injury and ischaemia, potentiation of GLP‐1 receptor signalling reduces cerebral infarct size and neuronal inflammation, promotes progenitor cell proliferation, and improves cognition . In experimental models of Alzheimer's disease, inhibition of GLP‐1 degradation minimizes amyloid‐beta deposition, tau protein phosphorylation and neuroinflammatory markers; reduces the neurotoxicity of beta‐amyloid deposits; and ameliorates the impairment of synaptic plasticity and memory formation .…”

Section: Interplay Of Glucagon‐like Peptide‐1 Signalling and Neprilysmentioning

confidence: 99%

Augmentation of glucagon‐like peptide‐1 receptor signalling by neprilysin inhibition: potential implications for patients with heart failure

Packer

2018

European J of Heart Fail

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Augmentation of glucagon-like peptide-1 (GLP-1) receptor signalling is an established approach to the treatment of type 2 diabetes. However, endogenous GLP-1 and long-acting GLP-1 receptor analogues are degraded not only by dipeptidyl peptidase-4, but also by neprilysin. This observation raises the possibilities that endogenous GLP-1 contributes to the clinical effects of neprilysin inhibition and that patients concurrently treated with sacubitril/valsartan and incretin-based drugs may experience important drug-drug interactions. Specifically, potentiation of GLP-1 receptor signalling may underlie the antihyperglycaemic actions of sacubitril/valsartan. Neprilysin inhibitors may also be able to augment the effects of long-acting GLP-1 analogues to increase heart rate and myocardial cyclic AMP, and thus, potentiate these deleterious actions; if so, concomitant treatment with GLP-1 receptor agonists may limit the efficacy of neprilysin inhibitors in patients with both heart failure and diabetes. For patients not concurrently treated with GLP-1 analogues, the action of neprilysin to enhance the effects of GLP-1 may be particularly relevant in the brain, where augmentation of GLP-1 and other endogenous peptides may act to inhibit amyloid-induced neuroinflammation and cytotoxicity and improve memory formation and executive functioning. Experimentally, neprilysin inhibitors may also potentiate the effects of endogenous GLP-1 and GLP-1 receptor agonists on blood vessels and the kidney. The role of neprilysin in the metabolism of endogenous GLP-1 and long-acting GLP-1 analogues points to a range of potential pathophysiological effects that may be clinically relevant to patients with heart failure, with or without diabetes.

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“…It also improved mitochondrial function by activating AKT and ERK pathways and inhibiting phosphorylation of c-Jun-NH2-terminal kinase (JNK) and p38 in neurons in both OGD in vitro and middle cerebral artery occlusion (MCAO) in vivo studies [ 116 ]. Another study showed that delayed administration of liraglutide, starting one day after MCAO, still improves metabolic and functional recovery of neurons, astrocytes, and endothelia after cerebral ischemia in rats [ 117 ].…”

Section: The Glucagon-like Peptide-1 Receptor (Glp-1r) In Neurologmentioning

confidence: 99%

The Emerging Role of GLP-1 Receptors in DNA Repair: Implications in Neurological Disorders

Yang

Chen

2017

IJMS

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Glucagon-like peptide-1 (GLP-1) is originally found as a metabolic hormone (incretin) that is able to regulate blood-glucose levels via promoting synthesis and secretion of insulin. GLP-1 and many analogues are approved for treatment of type II diabetes. Accumulating results imply that GLP-1 performs multiple functions in various tissues and organs beyond regulation of blood-glucose. The neuroprotective function of GLP-1 has been extensively explored during the past two decades. Three of our previous studies have shown that apurinic/apyrimidinic endonuclease 1 (APE1) is the only protein of the base excision repair (BER) pathway able to be regulated by oxidative stress or exogenous stimulations in rat primary cortical neurons. In this article, we review the role of APE1 in neurodegenerative diseases and its relationship to neuroprotective mechanisms of the activated GLP-1 receptor (GLP-1R) in neurodegenerative disorders. The purpose of this article is to provide new insight, from the aspect of DNA damage and repair, for studying potential treatments in neurodegenerative diseases.

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Delayed administration of the GLP-1 receptor agonist liraglutide improves metabolic and functional recovery after cerebral ischemia in rats

Cited by 24 publications

References 27 publications

Incretin-Based Antihyperglycemic Agents for the Management of Acute Ischemic Stroke in Patients with Diabetes Mellitus: A Review

Incretin-Based Antihyperglycemic Agents for the Management of Acute Ischemic Stroke in Patients with Diabetes Mellitus: A Review

Augmentation of glucagon‐like peptide‐1 receptor signalling by neprilysin inhibition: potential implications for patients with heart failure

The Emerging Role of GLP-1 Receptors in DNA Repair: Implications in Neurological Disorders

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