Central chronic apelin infusion decreases energy expenditure and thermogenesis in mice

Drougard, Anne; Fournel, Audren; Marlin, Alysson; Meunier, Étienne; Abot, Anne; Bautzova, Tereza; Duparc, Thibaut; Louche, Katie; Batut, Aurélie; Lucas, Alexandre; Gonidec, Sophie Le; Lésage, Jean; Fioramonti, Xavier; Moro, Cédric; Valet, Philippe; Cani, Patrice D.; Knauf, Claude

doi:10.1038/srep31849

Cited by 19 publications

(10 citation statements)

References 60 publications

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“…Galanin is a peptide that has a beneficial impact on the maintenance of whole body glucose homeostasis. As opposed to numerous bioactive peptides such as apelin [24] , [26] , [27] , intravenous and intracerebroventricular injections of galanin improve insulin sensitivity in different models [11] , [28] . This total absence of deleterious effects on glycemia renders galanin as a player of interest for the treatment of T2D.…”

Section: Discussionmentioning

confidence: 99%

Galanin enhances systemic glucose metabolism through enteric Nitric Oxide Synthase-expressed neurons

Abot¹,

Lucas

Bautzova

et al. 2018

Molecular Metabolism

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ObjectiveDecreasing duodenal contraction is now considered as a major focus for the treatment of type 2 diabetes. Therefore, identifying bioactive molecules able to target the enteric nervous system, which controls the motility of intestinal smooth muscle cells, represents a new therapeutic avenue. For this reason, we chose to study the impact of oral galanin on this system in diabetic mice.MethodsEnteric neurotransmission, duodenal contraction, glucose absorption, modification of gut–brain axis, and glucose metabolism (glucose tolerance, insulinemia, glucose entry in tissue, hepatic glucose metabolism) were assessed.ResultsWe show that galanin, a neuropeptide expressed in the small intestine, decreases duodenal contraction by stimulating nitric oxide release from enteric neurons. This is associated with modification of hypothalamic nitric oxide release that favors glucose uptake in metabolic tissues such as skeletal muscle, liver, and adipose tissue. Oral chronic gavage with galanin in diabetic mice increases insulin sensitivity, which is associated with an improvement of several metabolic parameters such as glucose tolerance, fasting blood glucose, and insulin.ConclusionHere, we demonstrate that oral galanin administration improves glucose homeostasis via the enteric nervous system and could be considered a therapeutic potential for the treatment of T2D.

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Section: Discussionmentioning

confidence: 99%

Galanin enhances systemic glucose metabolism through enteric Nitric Oxide Synthase-expressed neurons

Abot¹,

Lucas

Bautzova

et al. 2018

Molecular Metabolism

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“…Thy1-YFP-Nampt −/− cKO mice also showed a progressive reduction in abdominal temperature. This could reflect multifactorial causes, including low locomotor activity, mitochondrial dysfunction, and reduced thermogenic potential ( Cannon and Nedergaard, 2011 ; Drougard et al, 2016 ; Weydt et al, 2006 ). Indeed, in an open-field test, the cKO mice were less active than the control mice.…”

Section: Discussionmentioning

confidence: 99%

Deletion of Nampt in Projection Neurons of Adult Mice Leads to Motor Dysfunction, Neurodegeneration, and Death

et al. 2017

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SUMMARYIntracellular nicotinamide phosphoribosyltransferase (iNAMPT) is the rate-limiting enzyme of the mammalian NAD+ biosynthesis salvage pathway. Using inducible and conditional knockout (cKO) mice, we show that Nampt gene deletion in adult projection neurons leads to a progressive loss of body weight, hypothermia, motor neuron (MN) degeneration, motor function deficits, paralysis, and death. Nampt deletion causes mitochondrial dysfunction, muscle fiber type conversion, and atrophy, as well as defective synaptic function at neuromuscular junctions (NMJs). When treated with nicotinamide mononucleotide (NMN), Nampt cKO mice exhibit reduced motor function deficits and prolonged lifespan. iNAMPT protein levels are significantly reduced in the spinal cord of amyotrophic lateral sclerosis (ALS) patients, indicating the involvement of NAMPT in ALS pathology. Our findings reveal that neuronal NAMPT plays an essential role in mitochondrial bioenergetics, motor function, and survival. Our study suggests that the NAMPT-mediated NAD+ biosynthesis pathway is a potential therapeutic target for degenerative MN diseases.

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“…Energy expenditure in response to apelin treatment has also been studied via thermogenesis ( Drougard et al, 2016 ). Brown adipose tissue (BAT) has a high density of mitochondria with high amounts of mitochondrial uncoupling protein 1 (UCP1), allowing the uncoupling of fatty acid oxidation from ATP production to generate heat ( Knauf et al, 2008 ; Lam et al, 2009 ).…”

Section: The Role Of Apelin In Lipid Metabolism and Thermogenesismentioning

confidence: 99%

The Role of Apelin/Apelin Receptor in Energy Metabolism and Water Homeostasis: A Comprehensive Narrative Review

Wang

Zhang

et al. 2021

Front. Physiol.

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The apelin receptor (APJ) is a member of the family A of G-protein-coupled receptors (GPCRs) and is involved in range of physiological and pathological functions, including fluid homeostasis, anxiety, and depression, as well as cardiovascular and metabolic disorders. APJ was classically described as a monomeric transmembrane receptor that forms a ternary complex together with its ligand and associated G proteins. More recently, increasing evidence indicates that APJ may interact with other GPCRs to form heterodimers, which may selectively modulate distinct intracellular signal transduction pathways. Besides, the apelin/APJ system plays important roles in the physiology and pathophysiology of several organs, including regulation of blood pressure, cardiac contractility, angiogenesis, metabolic balance, and cell proliferation, apoptosis, or inflammation. Additionally, the apelin/APJ system is widely expressed in the central nervous system, especially in neurons and oligodendrocytes. This article reviews the role of apelin/APJ in energy metabolism and water homeostasis. Compared with the traditional diuretics, apelin exerts a positive inotropic effect on the heart, while increases water excretion. Therefore, drugs targeting apelin/APJ system undoubtedly provide more therapeutic options for patients with congestive heart failure accompanied with hyponatremia. To provide more precise guidance for the development of clinical drugs, further in-depth studies are warranted on the metabolism and signaling pathways associated with apelin/APJ system.

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Central chronic apelin infusion decreases energy expenditure and thermogenesis in mice

Cited by 19 publications

References 60 publications

Galanin enhances systemic glucose metabolism through enteric Nitric Oxide Synthase-expressed neurons

Galanin enhances systemic glucose metabolism through enteric Nitric Oxide Synthase-expressed neurons

Deletion of Nampt in Projection Neurons of Adult Mice Leads to Motor Dysfunction, Neurodegeneration, and Death

The Role of Apelin/Apelin Receptor in Energy Metabolism and Water Homeostasis: A Comprehensive Narrative Review

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