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  1. Article ; Online: Blood microbiota dysbiosis is associated with the onset of cardiovascular events in a large general population: the D.E.S.I.R. study.

    Amar, Jacques / Lange, Céline / Payros, Gaëlle / Garret, Celine / Chabo, Chantal / Lantieri, Olivier / Courtney, Michael / Marre, Michel / Charles, Marie Aline / Balkau, Beverley / Burcelin, Rémy

    PloS one

    2013  Volume 8, Issue 1, Page(s) e54461

    Abstract: ... and incident cardiovascular disease.: Methods and results: D.E.S.I.R. is a longitudinal study ... positively correlated with Pbac (r = 0.59; P<0.0001). In those destined to have cardiovascular complications ...

    Abstract Aim: We recently described a human blood microbiome and a connection between this microbiome and the onset of diabetes. The aim of the current study was to assess the association between blood microbiota and incident cardiovascular disease.
    Methods and results: D.E.S.I.R. is a longitudinal study with the primary aim of describing the natural history of the metabolic syndrome and its complications. Participants were evaluated at inclusion and at 3-, 6-, and 9-yearly follow-up visits. The 16S ribosomal DNA bacterial gene sequence, that is common to the vast majority of bacteria (Eubac) and a sequence that mostly represents Proteobacteria (Pbac), were measured in blood collected at baseline from 3936 participants. 73 incident cases of acute cardiovascular events, including 30 myocardial infarctions were recorded. Eubac was positively correlated with Pbac (r = 0.59; P<0.0001). In those destined to have cardiovascular complications, Eubac was lower (0.14±0.26 vs 0.12±0.29 ng/µl; P = 0.02) whereas a non significant increase in Pbac was observed. In multivariate Cox analysis, Eubac was inversely correlated with the onset of cardiovascular complications, (hazards ratio 0.50 95% CI 0.35-0.70) whereas Pbac (1.56, 95%CI 1.12-2.15) was directly correlated.
    Conclusion: Pbac and Eubac were shown to be independent markers of the risk of cardiovascular disease. This finding is evidence for the new concept of the role played by blood microbiota dysbiosis on atherothrombotic disease. This concept may help to elucidate the relation between bacteria and cardiovascular disease.
    MeSH term(s) Adult ; Age of Onset ; Aged ; Bacteria/genetics ; Bacteria/isolation & purification ; Biomarkers/blood ; Cardiovascular Diseases/complications ; Cardiovascular Diseases/diagnosis ; Cardiovascular Diseases/epidemiology ; Cardiovascular Diseases/microbiology ; Female ; France/epidemiology ; Humans ; Incidence ; Longitudinal Studies ; Male ; Metabolic Syndrome/complications ; Metabolic Syndrome/diagnosis ; Metabolic Syndrome/epidemiology ; Metabolic Syndrome/microbiology ; Metagenome/genetics ; Middle Aged ; Proportional Hazards Models ; Proteobacteria/genetics ; Proteobacteria/isolation & purification ; RNA, Ribosomal, 16S/blood ; RNA, Ribosomal, 16S/genetics ; RNA, Ribosomal, 16S/isolation & purification ; Risk
    Chemical Substances Biomarkers ; RNA, Ribosomal, 16S
    Language English
    Publishing date 2013-01-25
    Publishing country United States
    Document type Journal Article ; Research Support, Non-U.S. Gov't
    ISSN 1932-6203
    ISSN (online) 1932-6203
    DOI 10.1371/journal.pone.0054461
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  2. Article ; Online: Microbiote intestinal et dialogue immunitaire au cours de la maladie métabolique.

    Burcelin, Rémy

    Biologie aujourd'hui

    2017  Volume 211, Issue 1, Page(s) 1–18

    Abstract: The aim of the review is to discuss about the role played by the defence crosstalk between the gut microbiota and the intestinal immune system, in the development of metabolic disease focusing on obesity and diabetes. Starting from physiological and ... ...

    Title translation Gut microbiota and immune crosstalk in metabolic disease.
    Abstract The aim of the review is to discuss about the role played by the defence crosstalk between the gut microbiota and the intestinal immune system, in the development of metabolic disease focusing on obesity and diabetes. Starting from physiological and pathological stand points and based on the latest published data, this review is addressing how the concept of the hologenome theory of evolution can drive the fate of metabolic disease. The notion of "metabolic infection" to explain the "metabolic inflammation" is discussed. This imply comments about the process of bacterial translocation and impaired intestinal immune defense against commensals. Eventually this review sets the soil for personalized medicine. The monthly increase in the number of publications on the gut microbiota to intestinal immune defense and the control of metabolism demonstrate the importance of this field of investigation. The notion of commensal as "self or non-self" has to be reevaluated in the light of the current data. Furthermore, data demonstrate the major role played by short chain fatty acids, secondary bile acids, LPS, peptidoglycans, indole derivatives, and other bacteria-related molecules on the shaping of cells involved in the intestinal protection against commensals is now becoming a central player in the incidence of metabolic diseases. The literature demonstrates that the onset of metabolic diseases and some specific co-morbidities can be explained by a gut microbiota to intestinal immune system crosstalk. Therefore, one should now consider this avenue of investigation as a putative source of biomarkers and therapeutic targets to personalize the treatment of metabolic disease and its co-morbidities. Gut microbiota is considered as a major regulator of metabolic disease. This reconciles the notion of metabolic inflammation and the epidemic development of the disease. In addition to evidence showing that a specific gut microbiota characterizes patients with obesity, type 2 diabetes, and hepatic steatosis, the mechanisms causal to the disease could be related to the translocation of microbiota from the gut to the tissues, which induces inflammation. The mechanisms regulating such a process are based on the crosstalk between the gut microbiota and the host immune system. The hologenome theory of evolution supports this concept and implies that therapeutic strategies aiming to control glycemia should take into account both the gut microbiota and the host immune system. This review discusses the latest evidence regarding the bidirectional impact of the gut microbiota on host immune system crosstalk for the control of metabolic disease, hyperglycemia, and obesity. To avoid redundancies with the literature, we will focus our attention on the intestinal immune system, identifying evidence for the generation of novel therapeutic strategies, which could be based on the control of the translocation of gut bacteria to tissues. Such novel strategies should hamper the role played by gut microbiota dysbiosis on the development of metabolic inflammation. Recent evidence in rodents allows us to conclude that an impaired intestinal immune system characterizes and could be causal in the development of metabolic disease. The fine understanding of the molecular mechanisms should allow for the development of a first line of treatment for metabolic disease and its co-morbidities.
    Language French
    Publishing date 2017
    Publishing country France
    Document type English Abstract ; Journal Article
    ISSN 2105-0686
    ISSN (online) 2105-0686
    DOI 10.1051/jbio/2017008
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  3. Article ; Online: When gut fermentation controls satiety: A PYY story.

    Burcelin, Rémy

    Molecular metabolism

    2016  Volume 6, Issue 1, Page(s) 10–11

    MeSH term(s) Fermentation ; Glucagon-Like Peptide 1 ; Obesity ; Peptide YY ; Satiation ; Satiety Response
    Chemical Substances Peptide YY (106388-42-5) ; Glucagon-Like Peptide 1 (89750-14-1)
    Language English
    Publishing date 2016-11-21
    Publishing country Germany
    Document type Journal Article ; Comment
    ISSN 2212-8778
    ISSN (online) 2212-8778
    DOI 10.1016/j.molmet.2016.11.005
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  4. Article: Gut microbiota and immune crosstalk in metabolic disease.

    Burcelin, Rémy

    Molecular metabolism

    2016  Volume 5, Issue 9, Page(s) 771–781

    Abstract: Background: Gut microbiota is considered as a major regulator of metabolic disease. This reconciles the notion of metabolic inflammation and the epidemic development of the disease. In addition to evidence showing that a specific gut microbiota ... ...

    Abstract Background: Gut microbiota is considered as a major regulator of metabolic disease. This reconciles the notion of metabolic inflammation and the epidemic development of the disease. In addition to evidence showing that a specific gut microbiota characterizes patients with obesity, type 2 diabetes, and hepatic steatosis, the mechanisms causal to the disease could be related to the translocation of microbiota from the gut to the tissues, inducing inflammation. The mechanisms regulating such a process are based on the crosstalk between the gut microbiota and the host immune system. The hologenome theory of evolution supports this concept and implies that therapeutic strategies aiming to control glycemia should take into account both the gut microbiota and the host immune system.
    Scope of review: This review discusses the latest evidence regarding the bidirectional impact of the gut microbiota on host immune system crosstalk for the control of metabolic disease, hyperglycemia, and obesity. To avoid redundancies with the literature, we will focus our attention on the intestinal immune system, identifying evidence for the generation of novel therapeutic strategies, which could be based on the control of the translocation of gut bacteria to tissues. Such novel strategies should hamper the role played by gut microbiota dysbiosis on the development of metabolic inflammation.
    Major conclusions: Recent evidence in rodents allows us to conclude that an impaired intestinal immune system characterizes and could be causal in the development of metabolic disease. The fine understanding of the molecular mechanisms should allow for the development of a first line of treatment for metabolic disease and its co-morbidities. This article is part of a special issue on microbiota.
    Language English
    Publishing date 2016-09
    Publishing country Germany
    Document type Journal Article ; Review
    ISSN 2212-8778
    ISSN 2212-8778
    DOI 10.1016/j.molmet.2016.05.016
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  5. Article ; Online: The antidiabetic gutsy role of metformin uncovered?

    Burcelin, Rémy

    Gut

    2014  Volume 63, Issue 5, Page(s) 706–707

    MeSH term(s) Animals ; Blood Glucose/drug effects ; Homeostasis/drug effects ; Hypoglycemic Agents/pharmacology ; Intestines/drug effects ; Metformin/pharmacology ; Microbiota/drug effects ; Verrucomicrobia/growth & development
    Chemical Substances Blood Glucose ; Hypoglycemic Agents ; Metformin (9100L32L2N)
    Language English
    Publishing date 2014-05
    Publishing country England
    Document type Comment ; Journal Article
    ZDB-ID 80128-8
    ISSN 1468-3288 ; 0017-5749
    ISSN (online) 1468-3288
    ISSN 0017-5749
    DOI 10.1136/gutjnl-2013-305370
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  6. Article ; Online: The gut microbiota to the brain axis in the metabolic control.

    Grasset, Estelle / Burcelin, Remy

    Reviews in endocrine & metabolic disorders

    2019  Volume 20, Issue 4, Page(s) 427–438

    Abstract: The regulation of glycemia is under a tight neuronal detection of glucose levels performed by the gut-brain axis and an efficient efferent neuronal message sent to the peripheral organs, as the pancreas to induce insulin and inhibit glucagon secretions. ... ...

    Abstract The regulation of glycemia is under a tight neuronal detection of glucose levels performed by the gut-brain axis and an efficient efferent neuronal message sent to the peripheral organs, as the pancreas to induce insulin and inhibit glucagon secretions. The neuronal detection of glucose levels is performed by the autonomic nervous system including the enteric nervous system and the vagus nerve innervating the gastro-intestinal tractus, from the mouth to the anus. A dysregulation of this detection leads to the one of the most important current health issue around the world i.e. diabetes mellitus. Furthemore, the consequences of diabetes mellitus on neuronal homeostasis and activities participate to the aggravation of the disease establishing a viscious circle. Prokaryotic cells as bacteria, reside in our gut. The strong relationship between prokaryotic cells and our eukaryotic cells has been established long ago, and prokaryotic and eukaryotic cells in our body have evolved synbiotically. For the last decades, studies demonstrated the critical role of the gut microbiota on the metabolic control and how its shift can induce diseases such as diabetes. Despite an important increase of knowledge, few is known about 1) how the gut microbiota influences the neuronal detection of glucose and 2) how the diabetes mellitus-induced gut microbiota shift observed participates to the alterations of autonomic nervous system and the gut-brain axis activity.
    MeSH term(s) Animals ; Brain/metabolism ; Diabetic Neuropathies/metabolism ; Diabetic Neuropathies/microbiology ; Gastrointestinal Microbiome/physiology ; Glucose/metabolism ; Humans ; Peripheral Nervous System/metabolism
    Chemical Substances Glucose (IY9XDZ35W2)
    Language English
    Publishing date 2019-11-11
    Publishing country Germany
    Document type Journal Article ; Research Support, Non-U.S. Gov't ; Review
    ZDB-ID 2185718-0
    ISSN 1573-2606 ; 1389-9155
    ISSN (online) 1573-2606
    ISSN 1389-9155
    DOI 10.1007/s11154-019-09511-1
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  7. Article: L'intestin métabolique: dualité fonctionnelle des incré- tines et de la flore intestinale.

    Burcelin, Rémy

    Bulletin de l'Academie nationale de medecine

    2013  Volume 197, Issue 1, Page(s) 79–92

    Abstract: Our research focuses on the molecular mechanisms controlling glycemia in healthy and diabetic individuals. Diabetes is now considered as a worldwide epidemic by WHO, and is predicted to affect several hundred million people in the near future. Current ... ...

    Title translation New insights into adipose cell biology.
    Abstract Our research focuses on the molecular mechanisms controlling glycemia in healthy and diabetic individuals. Diabetes is now considered as a worldwide epidemic by WHO, and is predicted to affect several hundred million people in the near future. Current therapies have failed to prevent or control hyperglycemia, as well as the deleterious cardiovascular consequences of the disease have increased. New paradigms are thus needed to develop novel therapeutic strategies. Over the last 15 years, we have been studying the intestine as a major regulator of the integrated cross-talk between the brain, liver, pancreas, muscles and blood vessels required for glycemic control. As a first example, we identified that during a meal the glucose transporter GLUT2 and the intestinal hormone glucagon-like peptide-1 (GLP-1) are involved in glucose detection by the entero-portal system. This was done using highly innovative experimental techniques in the awake free moving mouse. We then found that the enteric-vagal nervous system transmits this nutritional information towards the brain stem and hypothalamus, where leptin, neuropeptide Y and GLP-1 relay the enteric signal to control the endocrine pancreas (insulin-glucagon secretion), the liver (glycogen metabolism), the vascular system (vasodilation, arterial flow), and muscle metabolism. This "anticipatory metabolic reflex " is altered during diabetes and might thus represent a new pharmacological target. Subsequently, while investigating the molecular mechanisms responsible for regulating this new physiological pathway, we discovered that a fat-rich diabetogenic diet alters the intestinal microbiota and permeability. This leads to an increase in the concentration of plasma lipopolysaccharides (LPS), which causes metabolic endotoxemia responsible for the induction of low-grade inflammation that characterizes type 2 diabetes, insulin resistance, adipose tissue development and hepatic lipid storage. We then showed that bacteria can be translocated from the intestine towards tissues and the bloodstream. Bacterial DNA present in blood was found to be predictive of diabetes, 6-9 years before disease onset (patent), presenting new molecular targets in the microbiota-host relationship. This should enable the scientific community to discover new functional relationships between the genome and metagenome and thus to develop original preventive and therapeutic strategies for metabolic diseases. Four biotechnology companies have already been created on the basis of our findings.
    MeSH term(s) Adipocytes/physiology ; Adipose Tissue/physiology ; Animals ; Diabetes Mellitus, Type 2/etiology ; Humans ; Incretins/physiology ; Intestines/metabolism ; Intestines/microbiology ; Mice ; Microbiota/physiology
    Chemical Substances Incretins
    Language French
    Publishing date 2013-01
    Publishing country Netherlands
    Document type English Abstract ; Journal Article ; Review
    ZDB-ID 213227-8
    ISSN 0001-4079
    ISSN 0001-4079
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  8. Article ; Online: Regulation of metabolism: a cross talk between gut microbiota and its human host.

    Burcelin, Rémy

    Physiology (Bethesda, Md.)

    2012  Volume 27, Issue 5, Page(s) 300–307

    Abstract: The recent epidemic of obesity and diabetes and the diversity at the individual level could be explained by the intestinal microbiota-to-host relationship. More than four million gene products from the microbiome could interact with the immune system to ... ...

    Abstract The recent epidemic of obesity and diabetes and the diversity at the individual level could be explained by the intestinal microbiota-to-host relationship. More than four million gene products from the microbiome could interact with the immune system to induce a tissue metabolic infection, which is the molecular origin of the low-grade inflammation that characterizes the onset of obesity and diabetes.
    MeSH term(s) Diabetes Mellitus/physiopathology ; Gastrointestinal Tract/microbiology ; Gastrointestinal Tract/physiology ; Humans ; Immune System/physiology ; Metabolic Diseases/physiopathology ; Metabolism/physiology ; Metagenome/physiology ; Obesity/physiopathology
    Language English
    Publishing date 2012-10
    Publishing country United States
    Document type Journal Article ; Review
    ZDB-ID 2158667-6
    ISSN 1548-9221 ; 1548-9213
    ISSN (online) 1548-9221
    ISSN 1548-9213
    DOI 10.1152/physiol.00023.2012
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    Zs.A 2164: Show issues Location:
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  9. Article ; Online: The gut-brain axis: a major glucoregulatory player.

    Burcelin, R

    Diabetes & metabolism

    2010  Volume 36 Suppl 3, Page(s) S54–8

    Abstract: Glucose homeostasis corresponds to the overall physiological, cellular, and molecular mechanisms which tightly maintain the glycaemia between ∼4.5 and ∼6 mM. The resulting blood glucose concentration is the consequence of a balance between the mechanisms ...

    Abstract Glucose homeostasis corresponds to the overall physiological, cellular, and molecular mechanisms which tightly maintain the glycaemia between ∼4.5 and ∼6 mM. The resulting blood glucose concentration is the consequence of a balance between the mechanisms that ensure the entry and the output of glucose in the blood. A dynamic balance needs hence to be perfectly achieved in order to maintain a physiological glycaemic concentration. Specialized cells from the intestine continuously detect changes in glucose concentration and send signals to peripheral tissues and the brain through the vagus nerve. The molecular mechanisms involved in glucose detection have not been perfectly defined but could resemble those from the insulin-secreting beta cells. The brain then integrates the enteric and circulating endocrine signals to generate a new signal towards peripheral tissues such as the pancreas, liver, muscles, and blood vessels. This metabolic reflex is called anticipatory since it allows the peripheral tissues to prepare for the adequate handling of nutrients. Diabetes is associated with an impaired anticipatory reflex, which hampers the proper detection of nutrients and leads to hyperglycaemic episodes. Recently, GLP-1-based therapies have demonstrated the improvement of glucose detection and their efficacy on glycaemic control. Although not yet fully demonstrated, GLP-1-based therapies regulate glucose sensors, which leads to the glycaemic improvement. Certainly other molecular targets could be identified to further generate new therapeutic strategies.
    MeSH term(s) Animals ; Autonomic Nervous System/metabolism ; Brain/physiology ; Diabetes Mellitus/metabolism ; Glucose/metabolism ; Humans ; Incretins/metabolism ; Intestines/physiology ; Signal Transduction
    Chemical Substances Incretins ; Glucose (IY9XDZ35W2)
    Language English
    Publishing date 2010-10
    Publishing country France
    Document type Journal Article ; Review
    ZDB-ID 1315751-6
    ISSN 1878-1780 ; 1262-3636 ; 0338-1684
    ISSN (online) 1878-1780
    ISSN 1262-3636 ; 0338-1684
    DOI 10.1016/S1262-3636(10)70468-7
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  10. Article ; Online: Harnessing glucagon-like peptide-1 receptor agonists for the pharmacological treatment of overweight and obesity.

    Burcelin, R / Gourdy, P

    Obesity reviews : an official journal of the International Association for the Study of Obesity

    2017  Volume 18, Issue 1, Page(s) 86–98

    Abstract: Over the past 30 years, there has been a dramatic rise in global obesity prevalence, resulting in significant economic and social consequences. Attempts to develop pharmacological agents to treat obesity have met with many obstacles including the lack of ...

    Abstract Over the past 30 years, there has been a dramatic rise in global obesity prevalence, resulting in significant economic and social consequences. Attempts to develop pharmacological agents to treat obesity have met with many obstacles including the lack of long-term effectiveness and the potential for adverse effects. Historically, there have been limited treatment options for overweight and obesity; however, since 2012, a number of new drugs have become available. A number of peptides produced in the gut act as key mediators of the gut-brain axis, which is involved in appetite regulation. This review discusses the role of the gut-brain axis in appetite regulation with special focus on glucagon-like peptide-1. Liraglutide 3.0 mg, a glucagon-like peptide-1 receptor agonist that targets this pathway, is now approved for the treatment of obesity and overweight (body mass index ≥27 kg/m
    MeSH term(s) Appetite Regulation/drug effects ; Comorbidity ; Diabetes Mellitus, Type 2/drug therapy ; Glucagon-Like Peptide 1/metabolism ; Glucagon-Like Peptide-1 Receptor/agonists ; Glucagon-Like Peptide-1 Receptor/metabolism ; Humans ; Hypoglycemic Agents/therapeutic use ; Liraglutide/therapeutic use ; Obesity/drug therapy ; Overweight/drug therapy ; Randomized Controlled Trials as Topic ; Weight Loss
    Chemical Substances Glucagon-Like Peptide-1 Receptor ; Hypoglycemic Agents ; Liraglutide (839I73S42A) ; Glucagon-Like Peptide 1 (89750-14-1)
    Language English
    Publishing date 2017-01
    Publishing country England
    Document type Journal Article ; Review
    ZDB-ID 2147980-X
    ISSN 1467-789X ; 1467-7881
    ISSN (online) 1467-789X
    ISSN 1467-7881
    DOI 10.1111/obr.12465
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