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  1. Article ; Online: The role of endoplasmic reticulum-mitochondria contact sites in the control of glucose homeostasis: an update.

    Rieusset, Jennifer

    Cell death & disease

    2018  Volume 9, Issue 3, Page(s) 388

    Abstract: The contact sites that the endoplasmic reticulum (ER) forms with mitochondria, called mitochondria-associated membranes (MAMs), are a hot topic in biological research, and both their molecular determinants and their numerous roles in several signaling ... ...

    Abstract The contact sites that the endoplasmic reticulum (ER) forms with mitochondria, called mitochondria-associated membranes (MAMs), are a hot topic in biological research, and both their molecular determinants and their numerous roles in several signaling pathways are is continuously evolving. MAMs allow the exchange between both organelles of lipids, calcium (Ca
    MeSH term(s) Animals ; Calcium/metabolism ; Endoplasmic Reticulum/genetics ; Endoplasmic Reticulum/metabolism ; Glucose/metabolism ; Homeostasis ; Humans ; Mitochondria/genetics ; Mitochondria/metabolism
    Chemical Substances Glucose (IY9XDZ35W2) ; Calcium (SY7Q814VUP)
    Language English
    Publishing date 2018-03-09
    Publishing country England
    Document type Journal Article ; Review
    ZDB-ID 2541626-1
    ISSN 2041-4889 ; 2041-4889
    ISSN (online) 2041-4889
    ISSN 2041-4889
    DOI 10.1038/s41419-018-0416-1
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  2. Article: Role of Endoplasmic Reticulum-Mitochondria Communication in Type 2 Diabetes.

    Rieusset, Jennifer

    Advances in experimental medicine and biology

    2017  Volume 997, Page(s) 171–186

    Abstract: Although mitochondrial dysfunction, endoplasmic reticulum (ER) stress, and disrupted lipid and calcium ( ... ...

    Abstract Although mitochondrial dysfunction, endoplasmic reticulum (ER) stress, and disrupted lipid and calcium (Ca
    Language English
    Publishing date 2017
    Publishing country United States
    Document type Journal Article
    ISSN 2214-8019 ; 0065-2598
    ISSN (online) 2214-8019
    ISSN 0065-2598
    DOI 10.1007/978-981-10-4567-7_13
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  3. Article ; Online: Mitochondria-associated membranes (MAMs): An emerging platform connecting energy and immune sensing to metabolic flexibility.

    Rieusset, Jennifer

    Biochemical and biophysical research communications

    2017  Volume 500, Issue 1, Page(s) 35–44

    Abstract: Living organisms have the capacity to sense both nutrients and immune signals in order to adapt their metabolism to the needs, and both metabolic inflexibility and exacerbated immune responses are associated with metabolic diseases. Over the past decade, ...

    Abstract Living organisms have the capacity to sense both nutrients and immune signals in order to adapt their metabolism to the needs, and both metabolic inflexibility and exacerbated immune responses are associated with metabolic diseases. Over the past decade, mitochondria emerged as key nutrient and immune sensors regulating numerous signalling pathways, and mitochondria dysfunction has been extensively implicated in metabolic diseases. Interestingly, mitochondria interact physically and functionally with the endoplasmic reticulum (ER, in contact sites named mitochondria-associated membranes (MAMs), in order to exchange metabolites and calcium and regulate cellular homeostasis. Emerging evidences suggest that MAMs provide a platform for hormone and nutrient signalling pathways and for innate immune responses, then regulating mitochondrial bioenergetics and apoptosis. Here, I thus propose the concept that MAMs could be attractive nutrient and immune sensors that regulate mitochondria physiology in order to adapt metabolism and cell fate, and that organelle miscommunication could be involved in the metabolic inflexibility and the pro-inflammatory status associated with metabolic diseases.
    MeSH term(s) Animals ; Apoptosis/genetics ; Calcium/immunology ; Calcium/metabolism ; Calcium Signaling/immunology ; Endoplasmic Reticulum/immunology ; Endoplasmic Reticulum/metabolism ; Energy Metabolism/immunology ; Homeostasis ; Humans ; Immunity, Innate ; Insulin Resistance/immunology ; Metabolic Diseases/immunology ; Metabolic Diseases/metabolism ; Metabolic Diseases/pathology ; Mitochondria/immunology ; Mitochondria/metabolism ; Mitochondrial Dynamics/immunology ; Mitochondrial Membranes/immunology ; Mitochondrial Membranes/metabolism
    Chemical Substances Calcium (SY7Q814VUP)
    Language English
    Publishing date 2017-06-21
    Publishing country United States
    Document type Journal Article ; Research Support, Non-U.S. Gov't ; Review
    ZDB-ID 205723-2
    ISSN 1090-2104 ; 0006-291X ; 0006-291X
    ISSN (online) 1090-2104 ; 0006-291X
    ISSN 0006-291X
    DOI 10.1016/j.bbrc.2017.06.097
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    In stock of ZB MED Cologne/Königswinter

    Zs.A 116: Show issues Location:
    Je nach Verfügbarkeit (siehe Angabe bei Bestand)
    bis Jg. 1994: Bestellungen von Artikeln über das Online-Bestellformular
    Jg. 1995 - 2021: Lesesall (1.OG)
    ab Jg. 2022: Lesesaal (EG)

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  4. Article: Endoplasmic reticulum-mitochondria calcium signaling in hepatic metabolic diseases.

    Rieusset, Jennifer

    Biochimica et biophysica acta. Molecular cell research

    2017  Volume 1864, Issue 6, Page(s) 865–876

    Abstract: The liver plays a central role in glucose homeostasis, and both metabolic inflexibility and insulin resistance predispose to the development of hepatic metabolic diseases. Mitochondria and endoplasmic reticulum (ER), which play a key role in the control ... ...

    Abstract The liver plays a central role in glucose homeostasis, and both metabolic inflexibility and insulin resistance predispose to the development of hepatic metabolic diseases. Mitochondria and endoplasmic reticulum (ER), which play a key role in the control of hepatic metabolism, also interact at contact points defined as mitochondria-associated membranes (MAM), in order to exchange metabolites and calcium (Ca
    MeSH term(s) Animals ; Calcium Signaling ; Endoplasmic Reticulum/metabolism ; Glucose/metabolism ; Homeostasis ; Humans ; Liver Diseases/metabolism ; Metabolic Diseases/metabolism ; Mitochondria/metabolism
    Chemical Substances Glucose (IY9XDZ35W2)
    Language English
    Publishing date 2017-01-04
    Publishing country Netherlands
    Document type Journal Article ; Research Support, Non-U.S. Gov't ; Review
    ZDB-ID 60-7
    ISSN 1879-2596 ; 1879-260X ; 1872-8006 ; 1879-2642 ; 1879-2618 ; 1879-2650 ; 0167-4889 ; 0006-3002 ; 0005-2728 ; 0005-2736 ; 0304-4165 ; 0167-4838 ; 1388-1981 ; 0167-4781 ; 0304-419X ; 1570-9639 ; 0925-4439 ; 1874-9399
    ISSN (online) 1879-2596 ; 1879-260X ; 1872-8006 ; 1879-2642 ; 1879-2618 ; 1879-2650
    ISSN 0167-4889 ; 0006-3002 ; 0005-2728 ; 0005-2736 ; 0304-4165 ; 0167-4838 ; 1388-1981 ; 0167-4781 ; 0304-419X ; 1570-9639 ; 0925-4439 ; 1874-9399
    DOI 10.1016/j.bbamcr.2017.01.001
    Database MEDical Literature Analysis and Retrieval System OnLINE

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    Uc I Zs.247: Show issues Location:
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  5. Article ; Online: Calcium signalling in hepatic metabolism: Health and diseases.

    Humbert, Alexandre / Lefebvre, Rémy / Nawrot, Margaux / Caussy, Cyrielle / Rieusset, Jennifer

    Cell calcium

    2023  Volume 114, Page(s) 102780

    Abstract: The flexibility between the wide array of hepatic functions relies on calcium ( ... ...

    Abstract The flexibility between the wide array of hepatic functions relies on calcium (Ca
    MeSH term(s) Humans ; Liver/metabolism ; Calcium/metabolism ; Diabetes Mellitus, Type 2/metabolism ; Hepatocytes/metabolism ; Calcium Signaling/physiology
    Chemical Substances Calcium (SY7Q814VUP)
    Language English
    Publishing date 2023-07-15
    Publishing country Netherlands
    Document type Journal Article
    ZDB-ID 757687-0
    ISSN 1532-1991 ; 0143-4160
    ISSN (online) 1532-1991
    ISSN 0143-4160
    DOI 10.1016/j.ceca.2023.102780
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    In stock of ZB MED Cologne/Königswinter

    Zs.A 1596: Show issues Location:
    Je nach Verfügbarkeit (siehe Angabe bei Bestand)
    bis Jg. 1994: Bestellungen von Artikeln über das Online-Bestellformular
    Jg. 1995 - 2021: Lesesall (1.OG)
    ab Jg. 2022: Lesesaal (EG)

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  6. Article: Mitochondria-associated membranes (MAMs): An emerging platform connecting energy and immune sensing to metabolic flexibility

    Rieusset, Jennifer

    Biochemical and biophysical research communications. 2017,

    2017  

    Abstract: Living organisms have the capacity to sense both nutrients and immune signals in order to adapt their metabolism to the needs, and both metabolic inflexibility and exacerbated immune responses are associated with metabolic diseases. Over the past decade, ...

    Abstract Living organisms have the capacity to sense both nutrients and immune signals in order to adapt their metabolism to the needs, and both metabolic inflexibility and exacerbated immune responses are associated with metabolic diseases. Over the past decade, mitochondria emerged as key nutrient and immune sensors regulating numerous signalling pathways, and mitochondria dysfunction has been extensively implicated in metabolic diseases. Interestingly, mitochondria interact physically and functionally with the endoplasmic reticulum (ER, in contact sites named mitochondria-associated membranes (MAMs), in order to exchange metabolites and calcium and regulate cellular homeostasis. Emerging evidences suggest that MAMs provide a platform for hormone and nutrient signalling pathways and for innate immune responses, then regulating mitochondrial bioenergetics and apoptosis. Here, I thus propose the concept that MAMs could be attractive nutrient and immune sensors that regulate mitochondria physiology in order to adapt metabolism and cell fate, and that organelle miscommunication could be involved in the metabolic inflexibility and the pro-inflammatory status associated with metabolic diseases.
    Keywords apoptosis ; calcium ; endoplasmic reticulum ; energy ; energy metabolism ; homeostasis ; immune response ; innate immunity ; metabolic diseases ; metabolites ; mitochondria ; nutrients ; signal transduction
    Language English
    Size p. .
    Publishing place Elsevier Inc.
    Document type Article
    Note Pre-press version
    ZDB-ID 205723-2
    ISSN 0006-291X ; 0006-291X
    ISSN (online) 0006-291X
    ISSN 0006-291X
    DOI 10.1016/j.bbrc.2017.06.097
    Database NAL-Catalogue (AGRICOLA)

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    In stock of ZB MED Bonn / Germany

    Z 71/706: Show issues
    Z 3.8: Show issues

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  7. Article ; Online: Mitochondria-SR interaction and mitochondrial fusion/fission in the regulation of skeletal muscle metabolism.

    Castro-Sepulveda, Mauricio / Fernández-Verdejo, Rodrigo / Zbinden-Foncea, Hermann / Rieusset, Jennifer

    Metabolism: clinical and experimental

    2023  Volume 144, Page(s) 155578

    Abstract: Mitochondria-endoplasmic/sarcoplasmic reticulum (ER/SR) interaction and mitochondrial fusion/fission are critical processes that influence substrate oxidation. This narrative review summarizes the evidence on the effects of substrate availability on ... ...

    Abstract Mitochondria-endoplasmic/sarcoplasmic reticulum (ER/SR) interaction and mitochondrial fusion/fission are critical processes that influence substrate oxidation. This narrative review summarizes the evidence on the effects of substrate availability on mitochondrial-SR interaction and mitochondria fusion/fission dynamics to modulate substrate oxidation in human skeletal muscle. Evidence shows that an increase in mitochondria-SR interaction and mitochondrial fusion are associated with elevated fatty acid oxidation. In contrast, a decrease in mitochondria-SR interaction and an increase in mitochondrial fission are associated with an elevated glycolytic activity. Based on the evidence reviewed, we postulate two hypotheses for the link between mitochondrial dynamics and insulin resistance in human skeletal muscle. First, glucose and fatty acid availability modifies mitochondria-SR interaction and mitochondrial fusion/fission to help the cell to adapt substrate oxidation appropriately. Individuals with an impaired response to these substrate challenges will accumulate lipid species and develop insulin resistance in skeletal muscle. Second, a chronically elevated substrate availability (e.g. overfeeding) increases mitochondrial production of reactive oxygen species and induced mitochondrial fission. This decreases fatty acid oxidation, thus leading to the accumulation of lipid species and insulin resistance in skeletal muscle. Altogether, we propose mitochondrial dynamics as a potential target for disturbances associated with low fatty acid oxidation.
    MeSH term(s) Humans ; Mitochondrial Dynamics ; Insulin Resistance ; Mitochondria/metabolism ; Muscle, Skeletal/metabolism ; Fatty Acids/metabolism ; Mitochondria, Muscle/metabolism
    Chemical Substances Fatty Acids
    Language English
    Publishing date 2023-05-08
    Publishing country United States
    Document type Journal Article ; Review ; Research Support, Non-U.S. Gov't
    ZDB-ID 80230-x
    ISSN 1532-8600 ; 0026-0495
    ISSN (online) 1532-8600
    ISSN 0026-0495
    DOI 10.1016/j.metabol.2023.155578
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    In stock of ZB MED Cologne/Königswinter

    Uc I Zs.316: Show issues Location:
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    bis Jg. 2021: Bestellungen von Artikeln über das Online-Bestellformular
    ab Jg. 2022: Lesesaal (EG)

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  8. Article ; Online: Mitochondria and endoplasmic reticulum: mitochondria-endoplasmic reticulum interplay in type 2 diabetes pathophysiology.

    Rieusset, Jennifer

    The international journal of biochemistry & cell biology

    2011  Volume 43, Issue 9, Page(s) 1257–1262

    Abstract: Mitochondria and endoplasmic reticulum (ER) are two important metabolic organelles for the maintenance of cellular homeostasis and their functional defects are suspected to participate to the aetiology of type 2 diabetes (T2D). Particularly, excessive ... ...

    Abstract Mitochondria and endoplasmic reticulum (ER) are two important metabolic organelles for the maintenance of cellular homeostasis and their functional defects are suspected to participate to the aetiology of type 2 diabetes (T2D). Particularly, excessive lipid intake and/or ectopic lipid accumulation in tissues (referred as lipotoxicity) are involved in alterations of both organelles and are closely linked to peripheral insulin resistance and defective insulin secretion. Since, mitochondria and ER are physically and functionally interconnected, their respective alterations during T2D could be interrelated. However, the mechanisms that coordinate the interplay between mitochondrial dysfunction and ER stress, and its relevance in the control of glucose homeostasis are unknown. Among these mechanisms, we will discuss on the potential role of altered mitochondria/ER crosstalk in organelle dysfunctions and in T2D pathophysiology.
    MeSH term(s) Animals ; Calcium/metabolism ; Diabetes Mellitus, Type 2/metabolism ; Diabetes Mellitus, Type 2/physiopathology ; Endoplasmic Reticulum/metabolism ; Endoplasmic Reticulum/pathology ; Homeostasis ; Humans ; Insulin/metabolism ; Insulin Secretion ; Lipid Metabolism ; Mitochondria/metabolism ; Mitochondria/pathology
    Chemical Substances Insulin ; Calcium (SY7Q814VUP)
    Language English
    Publishing date 2011-05-14
    Publishing country Netherlands
    Document type Journal Article ; Review
    ZDB-ID 1228429-4
    ISSN 1878-5875 ; 1357-2725
    ISSN (online) 1878-5875
    ISSN 1357-2725
    DOI 10.1016/j.biocel.2011.05.006
    Database MEDical Literature Analysis and Retrieval System OnLINE

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    In stock of ZB MED Cologne/Königswinter

    Zs.A 431: Show issues Location:
    Je nach Verfügbarkeit (siehe Angabe bei Bestand)
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  9. Article ; Online: Role of mitochondria in liver metabolic health and diseases.

    Morio, Béatrice / Panthu, Baptiste / Bassot, Arthur / Rieusset, Jennifer

    Cell calcium

    2020  Volume 94, Page(s) 102336

    Abstract: The liver is a major organ that coordinates the metabolic flexibility of the whole body, which is characterized by the ability to adapt dynamically in response to fluctuations in energy needs and supplies. In this context, hepatocyte mitochondria are key ...

    Abstract The liver is a major organ that coordinates the metabolic flexibility of the whole body, which is characterized by the ability to adapt dynamically in response to fluctuations in energy needs and supplies. In this context, hepatocyte mitochondria are key partners in fine-tuning metabolic flexibility. Here we review the metabolic and signalling pathways carried by mitochondria in the liver, the major pathways that regulate mitochondrial function and how they function in health and metabolic disorders associated to obesity, i.e. insulin resistance, non-alcoholic steatosis and steatohepatitis and hepatocellular carcinoma. Finally, strategies targeting mitochondria to counteract liver disorders are discussed.
    Language English
    Publishing date 2020-12-25
    Publishing country Netherlands
    Document type Journal Article ; Research Support, Non-U.S. Gov't
    ZDB-ID 757687-0
    ISSN 1532-1991 ; 0143-4160
    ISSN (online) 1532-1991
    ISSN 0143-4160
    DOI 10.1016/j.ceca.2020.102336
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    In stock of ZB MED Cologne/Königswinter

    Zs.A 1596: Show issues Location:
    Je nach Verfügbarkeit (siehe Angabe bei Bestand)
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  10. Article: Editorial: Metabolic Flexibility.

    Galgani, Jose E / Bergouignan, Audrey / Rieusset, Jennifer / Moro, Cedric / Nazare, Julie-Anne

    Frontiers in nutrition

    2022  Volume 9, Page(s) 946300

    Language English
    Publishing date 2022-06-02
    Publishing country Switzerland
    Document type Editorial
    ZDB-ID 2776676-7
    ISSN 2296-861X
    ISSN 2296-861X
    DOI 10.3389/fnut.2022.946300
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