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Article ; Online: Adipokines as Immune Cell Modulators in Multiple Sclerosis.

Rijnsburger, Merel / Djuric, Niek / Mulder, Inge A / de Vries, Helga E

International journal of molecular sciences

2021 Volume 22, Issue 19

Abstract: Multiple sclerosis (MS), a chronic inflammatory and demyelinating disease of the central nervous system (CNS), is a major clinical and societal problem, which has a tremendous impact on the life of patients and their proxies. Current immunomodulatory and ...

Abstract	Multiple sclerosis (MS), a chronic inflammatory and demyelinating disease of the central nervous system (CNS), is a major clinical and societal problem, which has a tremendous impact on the life of patients and their proxies. Current immunomodulatory and anti-inflammatory therapies prove to be relatively effective; however, they fail to concomitantly stop ongoing neurological deterioration and do not reverse acquired disability. The proportion to which genetic and environmental factors contribute to the etiology of MS is still incompletely understood; however, a recent association between MS etiology and obesity was shown, with obesity greatly increasing the risk of developing MS. An altered balance of adipokines, which are white adipose tissue (WAT) hormones, plays an important role in the low-grade chronic inflammation during obesity by their pervasive modification of local and systemic inflammation. Vice versa, inflammatory factors secreted by immune cells affect adipokine function. To explore the role of adipokines in MS pathology, we will here review the reciprocal effects of adipokines and immune cells and summarize alterations in adipokine levels in MS patient cohorts. Finally, we will discuss proof-of-concept studies demonstrating the therapeutic potential of adipokines to target both neuroinflammation and neurodegeneration processes in MS.
MeSH term(s)	Adipokines/metabolism ; Animals ; Humans ; Inflammation/immunology ; Multiple Sclerosis/immunology ; Multiple Sclerosis/metabolism ; Multiple Sclerosis/pathology
Chemical Substances	Adipokines
Language	English
Publishing date	2021-10-07
Publishing country	Switzerland
Document type	Journal Article ; Review
ZDB-ID	2019364-6
ISSN	1422-0067 ; 1422-0067 ; 1661-6596
ISSN (online)	1422-0067
ISSN	1422-0067 ; 1661-6596
DOI	10.3390/ijms221910845
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Article ; Online: Arachidonic acid-derived lipid mediators in multiple sclerosis pathogenesis: fueling or dampening disease progression?

Broos, Jelle Y / van der Burgt, Rianne T M / Konings, Julia / Rijnsburger, Merel / Werz, Oliver / de Vries, Helga E / Giera, Martin / Kooij, Gijs

Journal of neuroinflammation

2024 Volume 21, Issue 1, Page(s) 21

Abstract: Background: Multiple sclerosis (MS) is a chronic autoimmune disease of the central nervous system (CNS), characterized by neuroinflammation, demyelination, and neurodegeneration. Considering the increasing prevalence among young adults worldwide and the ...

Abstract	Background: Multiple sclerosis (MS) is a chronic autoimmune disease of the central nervous system (CNS), characterized by neuroinflammation, demyelination, and neurodegeneration. Considering the increasing prevalence among young adults worldwide and the disabling phenotype of the disease, a deeper understanding of the complexity of the disease pathogenesis is needed to ultimately improve diagnosis and personalize treatment opportunities. Recent findings suggest that bioactive lipid mediators (LM) derived from ω-3/-6 polyunsaturated fatty acids (PUFA), also termed eicosanoids, may contribute to MS pathogenesis. For example, disturbances in LM profiles and especially those derived from the ω-6 PUFA arachidonic acid (AA) have been reported in people with MS (PwMS), where they may contribute to the chronicity of neuroinflammatory processes. Moreover, we have previously shown that certain AA-derived LMs also associated with neurodegenerative processes in PwMS, suggesting that AA-derived LMs are involved in more pathological events than solely neuroinflammation. Yet, to date, a comprehensive overview of the contribution of these LMs to MS-associated pathological processes remains elusive. Main body: This review summarizes and critically evaluates the current body of literature on the eicosanoid biosynthetic pathway and its contribution to key pathological hallmarks of MS during different disease stages. Various parts of the eicosanoid pathway are highlighted, namely, the prostanoid, leukotriene, and hydroxyeicosatetraenoic acids (HETEs) biochemical routes that include specific enzymes of the cyclooxygenases (COXs) and lipoxygenases (LOX) families. In addition, cellular sources of LMs and their potential target cells based on receptor expression profiles will be discussed in the context of MS. Finally, we propose novel therapeutic approaches based on eicosanoid pathway and/or receptor modulation to ultimately target chronic neuroinflammation, demyelination and neurodegeneration in MS. Short conclusion: The eicosanoid pathway is intrinsically linked to specific aspects of MS pathogenesis. Therefore, we propose that novel intervention strategies, with the aim of accurately modulating the eicosanoid pathway towards the biosynthesis of beneficial LMs, can potentially contribute to more patient- and MS subtype-specific treatment opportunities to combat MS.
MeSH term(s)	Young Adult ; Humans ; Arachidonic Acid/metabolism ; Neuroinflammatory Diseases ; Multiple Sclerosis ; Eicosanoids/metabolism ; Fatty Acids, Omega-3 ; Disease Progression
Chemical Substances	Arachidonic Acid (27YG812J1I) ; Eicosanoids ; Fatty Acids, Omega-3
Language	English
Publishing date	2024-01-17
Publishing country	England
Document type	Journal Article ; Review
ZDB-ID	2156455-3
ISSN	1742-2094 ; 1742-2094
ISSN (online)	1742-2094
ISSN	1742-2094
DOI	10.1186/s12974-023-02981-w
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Article ; Online: Adipokines in multiple sclerosis patients are related to clinical and radiological measures.

Loonstra, Floor C / Falize, Kim F / de Ruiter, Lodewijk R J / Schoonheim, Menno M / Strijbis, Eva M M / Killestein, Joep / de Vries, Helga E / Uitdehaag, Bernard M J / Rijnsburger, Merel

Journal of neurology

2022 Volume 270, Issue 4, Page(s) 2018–2030

Abstract: Background: An imbalance of adipokines, hormones secreted by white adipose tissue, is suggested to play a role in the immunopathology of multiple sclerosis (MS). In people with MS (PwMS) of the same age, we aimed to determine whether the adipokines ... ...

Abstract	Background: An imbalance of adipokines, hormones secreted by white adipose tissue, is suggested to play a role in the immunopathology of multiple sclerosis (MS). In people with MS (PwMS) of the same age, we aimed to determine whether the adipokines adiponectin, leptin, and resistin are associated with MS disease severity. Furthermore, we aimed to investigate whether these adipokines mediate the association between body mass index (BMI) and MS disease severity. Methods: Adiponectin, resistin, and leptin were determined in serum using ELISA. 288 PwMS and 125 healthy controls (HC) were included from the Project Y cohort, a population-based cross-sectional study of people with MS born in the Netherlands in 1966, and age and sex-matched HC. Adipokine levels and BMI were related to demographic, clinical and disability measures, and MRI-based brain volumes. Results: Adiponectin levels were 1.2 fold higher in PwMS vs. HC, especially in secondary progressive MS. Furthermore, we found a sex-specific increase in adiponectin levels in primary progressive (PP) male patients compared to male controls. Leptin and resistin levels did not differ between PwMS and HC, however, leptin levels were associated with higher disability (EDSS) and resistin strongly related to brain volumes in progressive patients, especially in several grey matter regions in PPMS. Importantly, correction for BMI did not significantly change the results. Conclusion: In PwMS of the same age, we found associations between adipokines (adiponectin, leptin, and resistin) and a range of clinical and radiological metrics. These associations were independent of BMI, indicating distinct mechanisms.
MeSH term(s)	Female ; Humans ; Male ; Adipokines ; Leptin ; Resistin ; Adiponectin ; Multiple Sclerosis/diagnostic imaging ; Cross-Sectional Studies
Chemical Substances	Adipokines ; Leptin ; Resistin ; Adiponectin
Language	English
Publishing date	2022-12-23
Publishing country	Germany
Document type	Journal Article
ZDB-ID	187050-6
ISSN	1432-1459 ; 0340-5354 ; 0012-1037 ; 0939-1517 ; 1619-800X
ISSN (online)	1432-1459
ISSN	0340-5354 ; 0012-1037 ; 0939-1517 ; 1619-800X
DOI	10.1007/s00415-022-11519-8
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Article ; Online: Reduced Angiopoietin-Like 4 Expression in Multiple Sclerosis Lesions Facilitates Lipid Uptake by Phagocytes via Modulation of Lipoprotein-Lipase Activity.

Kamermans, Alwin / Rijnsburger, Merel / Chakraborty, Ananya / van der Pol, Susanne / de Vries, Helga E / van Horssen, Jack

Frontiers in immunology

2019 Volume 10, Page(s) 950

Abstract: Multiple sclerosis (MS) is a chronic inflammatory disorder of the central nervous system (CNS) characterized by the presence of focal demyelinated plaques. Sufficient clearance of myelin and cellular debris is one of the requirements for proper tissue ... ...

Abstract	Multiple sclerosis (MS) is a chronic inflammatory disorder of the central nervous system (CNS) characterized by the presence of focal demyelinated plaques. Sufficient clearance of myelin and cellular debris is one of the requirements for proper tissue repair and remyelination. The mechanisms underlying the clearance of such debris by phagocytes are not fully understood, but recent findings suggest a prominent role for lipoprotein-lipase (LPL) in this process. Here, we demonstrate that angiopoietin-like 4 (ANGPTL4), a potent inhibitor of LPL, is abundantly expressed in astrocytes in control white matter tissue and its expression is markedly reduced in active MS lesions. We provide evidence that ANGPTL4 inhibits the uptake of myelin-derived lipids by LPL-immunoreactive phagocytes. Taken together, our data suggest that the strong reduction in astrocytic ANGPTL4 expression in active demyelinating MS lesions enables phagocytes to adequately clear myelin debris, setting the stage for remyelination.
MeSH term(s)	Adult ; Aged ; Aged, 80 and over ; Angiopoietin-like 4 Protein/metabolism ; Brain/metabolism ; Cell Line, Tumor ; Female ; Humans ; Lipid Metabolism ; Lipoprotein Lipase/metabolism ; Macrophages/metabolism ; Male ; Middle Aged ; Multiple Sclerosis/metabolism ; Myelin Sheath/metabolism ; Phagocytes/metabolism
Chemical Substances	ANGPTL4 protein, human ; Angiopoietin-like 4 Protein ; Lipoprotein Lipase (EC 3.1.1.34)
Language	English
Publishing date	2019-05-03
Publishing country	Switzerland
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	2606827-8
ISSN	1664-3224 ; 1664-3224
ISSN (online)	1664-3224
ISSN	1664-3224
DOI	10.3389/fimmu.2019.00950
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Article ; Online: Dopamine in the nucleus accumbens shell controls systemic glucose metabolism via the lateral hypothalamus and hepatic vagal innervation in rodents.

Diepenbroek, Charlene / Rijnsburger, Merel / van Irsen, Astrid A S / Eggels, Leslie / Kisner, Alexandre / Foppen, Ewout / Unmehopa, Unga A / Berland, Chloé / Dólleman, Sophie / Hardonk, Marene / Cruciani-Guglielmacci, Céline / Faust, Rudolf P / Wenning, Rick / Maya-Monteiro, Clarissa M / Kalsbeek, Andries / Aponte, Yeka / Luquet, Serge / Serlie, Mireille J M / la Fleur, Susanne E

Metabolism: clinical and experimental

2023 Volume 150, Page(s) 155696

Abstract: Background: Growing evidence demonstrates the role of the striatal dopamine system in the regulation of glucose metabolism. Treatment with dopamine antagonists is associated with insulin resistance and hyperglycemia, while dopamine agonists are used in ... ...

Abstract	Background: Growing evidence demonstrates the role of the striatal dopamine system in the regulation of glucose metabolism. Treatment with dopamine antagonists is associated with insulin resistance and hyperglycemia, while dopamine agonists are used in treatment of type 2 diabetes. The mechanism underlying striatal dopamine effects in glucose metabolism, however is not fully understood. Here, we provide mechanistic insights into the role of nucleus accumbens shell (sNAc) dopaminergic signaling in systemic glucose metabolism. Methods: Endogenous glucose production (EGP), blood glucose and mRNA expression in the lateral hypothalamic area (LHA) in male Wistar rats were measured following infusion of vanoxerine (VNX, dopamine reuptake inhibitor) in the sNAc. Thereafter, we analyzed projections from sNAc Drd1-expressing neurons to LHA using D1-Cre male Long-Evans rats, Cre-dependent viral tracers and fluorescence immunohistochemistry. Brain slice electrophysiology in adult mice was used to study spontaneous excitatory postsynaptic currents of sNAc Drd1-expressing neurons following VNX application. Finally, we assessed whether GABAergic LHA activity and hepatic vagal innervation were required for the effect of sNAc-VNX on glucose metabolism by combining infusion of sNAc-VNX with LHA-bicuculline, performing vagal recordings and combining infusion of sNAc-VNX with hepatic vagal denervation. Results: VNX infusion in the sNAc strongly decreased endogenous glucose production, prevented glucose increases over time, reduced Slc17A6 and Hcrt mRNA in LHA, and increased vagal activity. Furthermore, sNAc Drd1-expressing neurons increased spontaneous firing following VNX application, and viral tracing of sNAc Drd1-expressing neurons revealed direct projections to LHA with on average 67 % of orexin cells directly targeted by sNAc Drd1-expressing neurons. Importantly, the sNAc-VNX-induced effect on glucose metabolism was dependent on GABAergic signaling in the LHA and on intact hepatic vagal innervation. Conclusions: We show that sNAc dopaminergic signaling modulates hepatic glucose metabolism through GABAergic inputs to glutamatergic LHA cells and hepatic vagal innervation. This demonstrates that striatal control of glucose metabolism involves a dopaminergic sNAc-LHA-liver axis and provides a potential explanation for the effects of dopamine agonists and antagonists on glucose metabolism.
MeSH term(s)	Rats ; Male ; Mice ; Animals ; Hypothalamic Area, Lateral/metabolism ; Nucleus Accumbens/metabolism ; Dopamine/metabolism ; Rodentia/metabolism ; Dopamine Agonists/metabolism ; Dopamine Agonists/pharmacology ; Diabetes Mellitus, Type 2/metabolism ; Rats, Wistar ; Rats, Long-Evans ; Glucose/metabolism ; Liver/metabolism ; RNA, Messenger/metabolism
Chemical Substances	Dopamine (VTD58H1Z2X) ; Dopamine Agonists ; Glucose (IY9XDZ35W2) ; RNA, Messenger
Language	English
Publishing date	2023-10-05
Publishing country	United States
Document type	Journal Article
ZDB-ID	80230-x
ISSN	1532-8600 ; 0026-0495
ISSN (online)	1532-8600
ISSN	0026-0495
DOI	10.1016/j.metabol.2023.155696
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Article ; Online: Altered secretory and neuroprotective function of the choroid plexus in progressive multiple sclerosis.

Rodríguez-Lorenzo, Sabela / Ferreira Francisco, David Miguel / Vos, Ricardo / van Het Hof, Bert / Rijnsburger, Merel / Schroten, Horst / Ishikawa, Hiroshi / Beaino, Wissam / Bruggmann, Rémy / Kooij, Gijs / de Vries, Helga E

Acta neuropathologica communications

2020 Volume 8, Issue 1, Page(s) 35

Abstract: The choroid plexus (CP) is a key regulator of the central nervous system (CNS) homeostasis through its secretory, immunological and barrier properties. Accumulating evidence suggests that the CP plays a pivotal role in the pathogenesis of multiple ... ...

Abstract	The choroid plexus (CP) is a key regulator of the central nervous system (CNS) homeostasis through its secretory, immunological and barrier properties. Accumulating evidence suggests that the CP plays a pivotal role in the pathogenesis of multiple sclerosis (MS), but the underlying mechanisms remain largely elusive. To get a comprehensive view on the role of the CP in MS, we studied transcriptomic alterations of the human CP in progressive MS and non-neurological disease controls using RNA sequencing. We identified 17 genes with significantly higher expression in progressive MS patients relative to that in controls. Among them is the newly described long non-coding RNA HIF1A-AS3. Next to that, we uncovered disease-affected pathways related to hypoxia, secretion and neuroprotection, while only subtle immunological and no barrier alterations were observed. In an ex vivo CP explant model, a subset of the upregulated genes responded in a similar way to hypoxic conditions. Our results suggest a deregulation of the Hypoxia-Inducible Factor (HIF)-1 pathway in progressive MS CP. Importantly, cerebrospinal fluid levels of the hypoxia-responsive secreted peptide PAI-1 were higher in MS patients with high disability relative to those with low disability. These findings provide for the first time a complete overview of the CP transcriptome in health and disease, and suggest that the CP environment becomes hypoxic in progressive MS patients, highlighting the altered secretory and neuroprotective properties of the CP under neuropathological conditions. Together, these findings provide novel insights to target the CP and promote the secretion of neuroprotective factors into the CNS of progressive MS patients.
MeSH term(s)	Adrenomedullin/cerebrospinal fluid ; Adrenomedullin/genetics ; Adult ; Aged ; Case-Control Studies ; Choroid Plexus/metabolism ; Female ; Gene Expression Profiling ; Gene Ontology ; Glycoproteins/cerebrospinal fluid ; Glycoproteins/genetics ; Humans ; Hypoxia/genetics ; Hypoxia-Inducible Factor 1 ; Hypoxia-Inducible Factor 1, alpha Subunit/genetics ; Intercellular Signaling Peptides and Proteins/cerebrospinal fluid ; Intercellular Signaling Peptides and Proteins/genetics ; Lateral Ventricles ; Male ; Metallothionein/genetics ; Middle Aged ; Multiple Sclerosis, Chronic Progressive/cerebrospinal fluid ; Multiple Sclerosis, Chronic Progressive/genetics ; Multiple Sclerosis, Relapsing-Remitting/cerebrospinal fluid ; Multiple Sclerosis, Relapsing-Remitting/genetics ; Neuroprotection/genetics ; Neurosecretion/genetics ; Plasminogen Activator Inhibitor 1/cerebrospinal fluid ; Plasminogen Activator Inhibitor 1/genetics ; RNA, Antisense/genetics ; RNA, Long Noncoding ; RNA-Seq
Chemical Substances	ADM protein, human ; Glycoproteins ; HIF1A protein, human ; Hypoxia-Inducible Factor 1 ; Hypoxia-Inducible Factor 1, alpha Subunit ; Intercellular Signaling Peptides and Proteins ; MT1A protein, human ; Plasminogen Activator Inhibitor 1 ; RNA, Antisense ; RNA, Long Noncoding ; STC2 protein, human ; Adrenomedullin (148498-78-6) ; Metallothionein (9038-94-2)
Language	English
Publishing date	2020-03-19
Publishing country	England
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	2715589-4
ISSN	2051-5960 ; 2051-5960
ISSN (online)	2051-5960
ISSN	2051-5960
DOI	10.1186/s40478-020-00903-y
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Article: Effects of Fat and Sugar, Either Consumed or Infused toward the Brain, on Hypothalamic ER Stress Markers.

Belegri, Evita / Rijnsburger, Merel / Eggels, Leslie / Unmehopa, Unga / Scheper, Wiep / Boelen, Anita / la Fleur, Susanne E

Frontiers in neuroscience

2017 Volume 11, Page(s) 270

Abstract: Protein-folding stress at the Endoplasmic Reticulum (ER) occurs in the hypothalamus during diet-induced obesity (DIO) and is linked to metabolic disease development. ER stress is buffered by the activation of the unfolded protein response (UPR), a ... ...

Abstract	Protein-folding stress at the Endoplasmic Reticulum (ER) occurs in the hypothalamus during diet-induced obesity (DIO) and is linked to metabolic disease development. ER stress is buffered by the activation of the unfolded protein response (UPR), a controlled network of pathways inducing a set of genes that recovers ER function. However, it is unclear whether hypothalamic ER stress during DIO results from obesity related changes or from direct nutrient effects in the brain. We here investigated mRNA expression of UPR markers in the hypothalamus of rats that were exposed to a free choice high-fat high-sugar (fcHFHS) diet for 1 week and then overnight fed
Language	English
Publishing date	2017-05-15
Publishing country	Switzerland
Document type	Journal Article
ZDB-ID	2411902-7
ISSN	1662-453X ; 1662-4548
ISSN (online)	1662-453X
ISSN	1662-4548
DOI	10.3389/fnins.2017.00270
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Article ; Online: Setmelanotide, a Novel, Selective Melanocortin Receptor-4 Agonist Exerts Anti-inflammatory Actions in Astrocytes and Promotes an Anti-inflammatory Macrophage Phenotype.

Kamermans, Alwin / Verhoeven, Tom / van Het Hof, Bert / Koning, Jasper J / Borghuis, Lauri / Witte, Maarten / van Horssen, Jack / de Vries, Helga E / Rijnsburger, Merel

Frontiers in immunology

2019 Volume 10, Page(s) 2312

Abstract: To date, available treatment strategies for multiple sclerosis (MS) are ineffective in preventing or reversing progressive neurologic deterioration, creating a high, and unmet medical need. One potential way to fight MS may be by limiting the detrimental ...

Abstract	To date, available treatment strategies for multiple sclerosis (MS) are ineffective in preventing or reversing progressive neurologic deterioration, creating a high, and unmet medical need. One potential way to fight MS may be by limiting the detrimental effects of reactive astrocytes, a key pathological hallmark for disease progression. One class of compounds that may exert beneficial effects via astrocytes are melanocortin receptor (MCR) agonists. Among the MCR, MC4R is most abundantly expressed in the CNS and several rodent studies have described that MC4R is-besides neurons-expressed by astrocytes. Activation of MC4R in astrocytes has shown to have potent anti-inflammatory as well as neuroprotective effects
MeSH term(s)	Adult ; Aged ; Anti-Inflammatory Agents/pharmacology ; Astrocytes/drug effects ; Cells, Cultured ; Cyclic AMP Response Element-Binding Protein/metabolism ; Female ; Humans ; Interleukin-11/biosynthesis ; Interleukin-6/biosynthesis ; Macrophages/drug effects ; Male ; Middle Aged ; Multiple Sclerosis/drug therapy ; Phenotype ; Phosphorylation ; Receptor, Melanocortin, Type 4/agonists ; Receptor, Melanocortin, Type 4/drug effects ; Receptor, Melanocortin, Type 4/genetics ; alpha-MSH/analogs & derivatives ; alpha-MSH/pharmacology
Chemical Substances	Anti-Inflammatory Agents ; Cyclic AMP Response Element-Binding Protein ; Interleukin-11 ; Interleukin-6 ; Receptor, Melanocortin, Type 4 ; setmelanotide ; alpha-MSH (581-05-5)
Language	English
Publishing date	2019-10-04
Publishing country	Switzerland
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	2606827-8
ISSN	1664-3224 ; 1664-3224
ISSN (online)	1664-3224
ISSN	1664-3224
DOI	10.3389/fimmu.2019.02312
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Article ; Online: The effect of diet interventions on hypothalamic nutrient sensing pathways in rodents.

Rijnsburger, Merel / Belegri, Evita / Eggels, Leslie / Unmehopa, Unga A / Boelen, Anita / Serlie, Mireille J / la Fleur, Susanne E

Physiology & behavior

2016 Volume 162, Page(s) 61–68

Abstract: The hypothalamus plays a fundamental role in regulating homeostatic processes including regulation of food intake. Food intake is driven in part by energy balance, which is sensed by specific brain structures through signaling molecules such as nutrients ...

Abstract	The hypothalamus plays a fundamental role in regulating homeostatic processes including regulation of food intake. Food intake is driven in part by energy balance, which is sensed by specific brain structures through signaling molecules such as nutrients and hormones. Both circulating glucose and fatty acids decrease food intake via a central mechanism involving the hypothalamus and brain stem. Besides playing a role in signaling energy status, glucose and fatty acids serve as fuel for neurons. This review focuses on the effects of glucose and fatty acids on hypothalamic pathways involved in regulation of energy metabolism as well as on the role of the family of peroxisome proliferator activated receptors (PPARs) which are implicated in regulation of central energy homeostasis. We further discuss the effects of different hypercaloric diets on these pathways.
MeSH term(s)	Animals ; Brain Stem/metabolism ; Diet/methods ; Eating ; Energy Metabolism/physiology ; Gene Expression Regulation/physiology ; Homeostasis ; Hypothalamus/metabolism ; Peroxisome Proliferator-Activated Receptors/genetics ; Peroxisome Proliferator-Activated Receptors/metabolism ; Rodentia ; Signal Transduction/physiology
Chemical Substances	Peroxisome Proliferator-Activated Receptors
Language	English
Publishing date	2016-08-01
Publishing country	United States
Document type	Journal Article ; Review
ZDB-ID	3907-x
ISSN	1873-507X ; 0031-9384
ISSN (online)	1873-507X
ISSN	0031-9384
DOI	10.1016/j.physbeh.2016.04.011
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Article: Alterations in blood glucose and plasma glucagon concentrations during deep brain stimulation in the shell region of the nucleus accumbens in rats.

Diepenbroek, Charlene / van der Plasse, Geoffrey / Eggels, Leslie / Rijnsburger, Merel / Feenstra, Matthijs G P / Kalsbeek, Andries / Denys, Damiaan / Fliers, Eric / Serlie, Mireille J / la Fleur, Susanne E

Frontiers in neuroscience

2013 Volume 7, Page(s) 226

Abstract: Deep brain stimulation (DBS) of the nucleus accumbens (NAc) is an effective therapy for obsessive compulsive disorder (OCD) and is currently under investigation as a treatment for eating disorders. DBS of this area is associated with altered food intake ... ...

Abstract	Deep brain stimulation (DBS) of the nucleus accumbens (NAc) is an effective therapy for obsessive compulsive disorder (OCD) and is currently under investigation as a treatment for eating disorders. DBS of this area is associated with altered food intake and pharmacological treatment of OCD is associated with the risk of developing type 2 diabetes. Therefore we examined if DBS of the NAc-shell (sNAc) influences glucose metabolism. Male Wistar rats were subjected to DBS, or sham stimulation, for a period of 1 h. To assess the effects of stimulation on blood glucose and glucoregulatory hormones, blood samples were drawn before, during and after stimulation. Subsequently, all animals were used for quantitative assessment of Fos immunoreactivity in the lateral hypothalamic area (LHA) using computerized image analysis. DBS of the sNAc rapidly increased plasma concentrations of glucagon and glucose while sham stimulation and DBS outside the sNAc were ineffective. In addition, the increase in glucose was dependent on DBS intensity. In contrast, the DBS-induced increase in plasma corticosterone concentrations was independent of intensity and region, indicating that the observed DBS-induced metabolic changes were not due to corticosterone release. Stimulation of the sNAc with 200 μA increased Fos immunoreactivity in the LHA compared to sham or 100 μA stimulated animals. These data show that DBS of the sNAc alters glucose metabolism in a region- and intensity- dependent manner in association with neuronal activation in the LHA. Moreover, these data illustrate the need to monitor changes in glucose metabolism during DBS-treatment of OCD patients.
Language	English
Publishing date	2013-12-10
Publishing country	Switzerland
Document type	Journal Article
ZDB-ID	2411902-7
ISSN	1662-453X ; 1662-4548
ISSN (online)	1662-453X
ISSN	1662-4548
DOI	10.3389/fnins.2013.00226
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