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  1. Article ; Online: A New Role for Hypothalamic Glucose-Sensing Neurons in Hypoglycemia Unawareness.

    Fioramonti, Xavier

    Diabetes

    2023  Volume 72, Issue 8, Page(s) 1055–1056

    MeSH term(s) Mice ; Male ; Animals ; Modafinil ; Orexins ; Hypoglycemia ; Glucose ; Neurons/physiology
    Chemical Substances Modafinil (R3UK8X3U3D) ; Orexins ; Glucose (IY9XDZ35W2)
    Language English
    Publishing date 2023-07-14
    Publishing country United States
    Document type Editorial ; Research Support, Non-U.S. Gov't ; Comment
    ZDB-ID 80085-5
    ISSN 1939-327X ; 0012-1797
    ISSN (online) 1939-327X
    ISSN 0012-1797
    DOI 10.2337/dbi22-0038
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  2. Book ; Online: Brain Nutrient Sensing in the Control of Energy Balance: New Insights and Perspectives

    Cruciani-Guglielmacci, Céline / Fioramonti, Xavier

    2019  

    Keywords Science: general issues ; Physiology ; nutrient sensing ; energy balance ; hypothalamus ; olfactory bulb ; melanocortin system ; polyunsaturated fatty acids ; ceramides ; neural stem cells
    Size 1 electronic resource (114 pages)
    Publisher Frontiers Media SA
    Document type Book ; Online
    Note English ; Open Access
    HBZ-ID HT021230294
    ISBN 9782889458202 ; 2889458202
    Database ZB MED Catalogue: Medicine, Health, Nutrition, Environment, Agriculture

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  3. Article: Editorial: Brain Nutrient Sensing in the Control of Energy Balance: New Insights and Perspectives.

    Cruciani-Guglielmacci, Céline / Fioramonti, Xavier

    Frontiers in physiology

    2019  Volume 10, Page(s) 51

    Language English
    Publishing date 2019-02-05
    Publishing country Switzerland
    Document type Editorial
    ZDB-ID 2564217-0
    ISSN 1664-042X
    ISSN 1664-042X
    DOI 10.3389/fphys.2019.00051
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  4. Article ; Online: The impact of insulin on the serotonergic system and consequences on diabetes-associated mood disorders.

    Martin, Hugo / Bullich, Sébastien / Guiard, Bruno P / Fioramonti, Xavier

    Journal of neuroendocrinology

    2021  Volume 33, Issue 4, Page(s) e12928

    Abstract: The idea that insulin could influence emotional behaviours has long been suggested. However, the underlying mechanisms have yet to be solved and there is no direct and clear-cut evidence demonstrating that such action involves brain serotonergic neurones. ...

    Abstract The idea that insulin could influence emotional behaviours has long been suggested. However, the underlying mechanisms have yet to be solved and there is no direct and clear-cut evidence demonstrating that such action involves brain serotonergic neurones. Indeed, initial arguments in favour of the association between insulin, serotonin and mood arise from clinical or animal studies showing that impaired insulin action in type 1 or type 2 diabetes causes anxiety- and depressive symptoms along with blunted plasma and brain serotonin levels. The present review synthesises the main mechanistic hypotheses that might explain the comorbidity between diabetes and depression. It also provides a state of knowledge of the direct and indirect experimental evidence that insulin modulates brain serotonergic neurones. Finally, it highlights the literature suggesting that antidiabetic drugs present antidepressant-like effects and, conversely, that serotonergic antidepressants impact glucose homeostasis. Overall, this review provides mechanistic insights into how insulin signalling alters serotonergic neurotransmission and related behaviours bringing new targets for therapeutic options.
    Language English
    Publishing date 2021-01-28
    Publishing country United States
    Document type Journal Article ; Review
    ZDB-ID 1007517-3
    ISSN 1365-2826 ; 0953-8194
    ISSN (online) 1365-2826
    ISSN 0953-8194
    DOI 10.1111/jne.12928
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  5. Article ; Online: POMC Neurons Dysfunction in Diet-induced Metabolic Disease: Hallmark or Mechanism of Disease?

    Quarta, Carmelo / Fioramonti, Xavier / Cota, Daniela

    Neuroscience

    2019  Volume 447, Page(s) 3–14

    Abstract: One important lesson from the last decade of studies in the field of systemic energy metabolism is that obesity is first and foremost a brain disease. Hypothalamic neurons dysfunction observed in response to chronic metabolic stress is a key pathogenic ... ...

    Abstract One important lesson from the last decade of studies in the field of systemic energy metabolism is that obesity is first and foremost a brain disease. Hypothalamic neurons dysfunction observed in response to chronic metabolic stress is a key pathogenic node linking consumption of hypercaloric diets with body weight gain and associated metabolic sequelae. A key hypothalamic neuronal population expressing the neuropeptide Pro-opio-melanocortin (POMC) displays altered electrical activity and dysregulated neuropeptides production capacity after long-term feeding with hypercaloric diets. However, whether such neuronal dysfunction represents a consequence or a mechanism of disease, remains a subject of debate. Here, we will review and highlight emerging pathogenic mechanisms that explain why POMC neurons undergo dysfunctional activity in response to caloric overload, and critically address whether these mechanisms may be causally implicated in the physiopathology of obesity and of its associated co-morbidities.
    MeSH term(s) Diet ; Humans ; Hypothalamus/metabolism ; Metabolic Diseases/etiology ; Neurons/metabolism ; Pro-Opiomelanocortin/metabolism
    Chemical Substances Pro-Opiomelanocortin (66796-54-1)
    Language English
    Publishing date 2019-11-02
    Publishing country United States
    Document type Journal Article ; Research Support, Non-U.S. Gov't ; Review
    ZDB-ID 196739-3
    ISSN 1873-7544 ; 0306-4522
    ISSN (online) 1873-7544
    ISSN 0306-4522
    DOI 10.1016/j.neuroscience.2019.09.031
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  6. Article ; Online: The menace of obesity to depression and anxiety prevalence.

    Fulton, Stephanie / Décarie-Spain, Léa / Fioramonti, Xavier / Guiard, Bruno / Nakajima, Shingo

    Trends in endocrinology and metabolism: TEM

    2021  Volume 33, Issue 1, Page(s) 18–35

    Abstract: The incidence of depression and anxiety is amplified by obesity. Mounting evidence reveals that the psychiatric consequences of obesity stem from poor diet, inactivity, and visceral adipose accumulation. Resulting metabolic and vascular dysfunction, ... ...

    Abstract The incidence of depression and anxiety is amplified by obesity. Mounting evidence reveals that the psychiatric consequences of obesity stem from poor diet, inactivity, and visceral adipose accumulation. Resulting metabolic and vascular dysfunction, including inflammation, insulin and leptin resistance, and hypertension, have emerged as key risks to depression and anxiety development. Recent research advancements are exposing the important contribution of these different corollaries of obesity and their impact on neuroimmune status and the neural circuits controlling mood and emotional states. Along these lines, this review connects the clinical manifestations of depression and anxiety in obesity to our current understanding of the origins and biology of immunometabolic threats to central nervous system function and behavior.
    MeSH term(s) Anxiety ; Depression/epidemiology ; Depression/etiology ; Depression/metabolism ; Humans ; Inflammation/metabolism ; Obesity/complications ; Obesity/epidemiology ; Prevalence
    Language English
    Publishing date 2021-11-05
    Publishing country United States
    Document type Journal Article ; Research Support, Non-U.S. Gov't ; Review
    ZDB-ID 1042384-9
    ISSN 1879-3061 ; 1043-2760
    ISSN (online) 1879-3061
    ISSN 1043-2760
    DOI 10.1016/j.tem.2021.10.005
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  7. Article: Régimes hyperlipidiques et dépression

    Bullich, Sébastien / Martin, Hugo / Fioramonti, Xavier / Guiard, Bruno P.

    Société française de nutrition Cahiers de nutrition et de diététique. 2022 July 10,

    2022  

    Abstract: Major depression is a psychiatric pathology based on different neurobiological mechanisms. Among these mechanisms, there is a hypersensitivity of the hypothalamic-pituitary-adrenal axis and modifications of various processes such as inflammation and ... ...

    Abstract Major depression is a psychiatric pathology based on different neurobiological mechanisms. Among these mechanisms, there is a hypersensitivity of the hypothalamic-pituitary-adrenal axis and modifications of various processes such as inflammation and oxidative stress. Various arguments suggest that these mechanisms lead to a deficit in monoaminergic neurotransmission. In particular, major depression is thought to result from an attenuation of serotonin (5-HT) levels in the brain. There is increasing evidence that patients with type 1 and type 2 diabetes are more likely to develop mood disorders than patients without diabetes. These epidemiological data are supported by studies conducted in different animal models displaying deficit in insulin signaling (exposure to cytotoxic compounds to the insulin-producing beta cell or hyperlipidic diets) leads to depressive-like states. This article summarizes the evidence linking metabolic and psychiatric disorders. It then presents the different mechanistic hypotheses that may explain this comorbidity. Finally, it opens the way to new therapeutic avenues that would consist in using oral antidiabetic drugs alone or in combination with antidepressants for an optimal management of DM.
    Keywords animals ; brain ; comorbidity ; cytotoxicity ; emotions ; hypersensitivity ; inflammation ; insulin ; noninsulin-dependent diabetes mellitus ; oxidative stress ; serotonin ; synaptic transmission ; therapeutics
    Language English
    Dates of publication 2022-0710
    Publishing place Elsevier Masson SAS
    Document type Article
    Note Pre-press version
    ZDB-ID 840946-8
    ISSN 0007-9960
    ISSN 0007-9960
    DOI 10.1016/j.cnd.2022.07.001
    Database NAL-Catalogue (AGRICOLA)

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    Z 4882: Show issues

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  8. Article: State of the Science on Brain Insulin Resistance and Cognitive Decline Due to Alzheimer's Disease.

    Rhea, Elizabeth M / Leclerc, Manon / Yassine, Hussein N / Capuano, Ana W / Tong, Han / Petyuk, Vladislav A / Macauley, Shannon L / Fioramonti, Xavier / Carmichael, Owen / Calon, Frederic / Arvanitakis, Zoe

    Aging and disease

    2023  

    Abstract: Type 2 diabetes mellitus (T2DM) is common and increasing in prevalence worldwide, with devastating public health consequences. While peripheral insulin resistance is a key feature of most forms of T2DM and has been investigated for over a century, ... ...

    Abstract Type 2 diabetes mellitus (T2DM) is common and increasing in prevalence worldwide, with devastating public health consequences. While peripheral insulin resistance is a key feature of most forms of T2DM and has been investigated for over a century, research on brain insulin resistance (BIR) has more recently been developed, including in the context of T2DM and non-diabetes states. Recent data support the presence of BIR in the aging brain, even in non-diabetes states, and found that BIR may be a feature in Alzheimer's disease (AD) and contributes to cognitive impairment. Further, therapies used to treat T2DM are now being investigated in the context of AD treatment and prevention, including insulin. In this review, we offer a definition of BIR, and present evidence for BIR in AD; we discuss the expression, function, and activation of the insulin receptor (INSR) in the brain; how BIR could develop; tools to study BIR; how BIR correlates with current AD hallmarks; and regional/cellular involvement of BIR. We close with a discussion on resilience to both BIR and AD, how current tools can be improved to better understand BIR, and future avenues for research. Overall, this review and position paper highlights BIR as a plausible therapeutic target for the prevention of cognitive decline and dementia due to AD.
    Language English
    Publishing date 2023-08-17
    Publishing country United States
    Document type Journal Article ; Review
    ZDB-ID 2625789-0
    ISSN 2152-5250
    ISSN 2152-5250
    DOI 10.14336/AD.2023.0814
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  9. Article ; Online: Memory deficits in a juvenile rat model of type 1 diabetes are due to excess 11β-HSD1 activity, which is upregulated by high glucose concentrations rather than insulin deficiency.

    Brossaud, Julie / Bosch-Bouju, Clémentine / Marissal-Arvy, Nathalie / Campas-Lebecque, Marie-Neige / Helbling, Jean-Christophe / Webster, Scott P / Walker, Brian R / Fioramonti, Xavier / Ferreira, Guillaume / Barat, Pascal / Corcuff, Jean-Benoît / Moisan, Marie-Pierre

    Diabetologia

    2023  Volume 66, Issue 9, Page(s) 1735–1747

    Abstract: Aims/hypothesis: Children with diabetes may display cognitive alterations although vascular disorders have not yet appeared. Variations in glucose levels together with relative insulin deficiency in treated type 1 diabetes have been reported to impact ... ...

    Abstract Aims/hypothesis: Children with diabetes may display cognitive alterations although vascular disorders have not yet appeared. Variations in glucose levels together with relative insulin deficiency in treated type 1 diabetes have been reported to impact brain function indirectly through dysregulation of the hypothalamus-pituitary-adrenal axis. We have recently shown that enhancement of glucocorticoid levels in children with type 1 diabetes is dependent not only on glucocorticoid secretion but also on glucocorticoid tissue concentrations, which is linked to 11β-hydroxysteroid dehydrogenase type 1 (11β-HSD1) activity. Hypothalamus-pituitary-adrenal axis dysfunction and memory alteration were further dissected in a juvenile rat model of diabetes showing that excess 11β-HSD1 activity within the hippocampus is associated with hippocampal-dependent memory deficits. Here, to investigate the causal relationships between diabetes, 11β-HSD1 activity and hippocampus-dependent memory deficits, we evaluated the beneficial effect of 11β-HSD1 inhibition on hippocampal-related memory in juvenile diabetic rats. We also examined whether diabetes-associated enhancement of hippocampal 11β-HSD1 activity is due to an increase in brain glucose concentrations and/or a decrease in insulin signalling.
    Methods: Diabetes was induced in juvenile rats by daily i.p. injection of streptozotocin for 2 consecutive days. Inhibition of 11β-HSD1 was obtained by administrating the compound UE2316 twice daily by gavage for 3 weeks, after which hippocampal-dependent object location memory was assessed. Hippocampal 11β-HSD1 activity was estimated by the ratio of corticosterone/dehydrocorticosterone measured by LC/MS. Regulation of 11β-HSD1 activity in response to changes in glucose or insulin levels was determined ex vivo on acute brain hippocampal slices. The insulin regulation of 11β-HSD1 was further examined in vivo using virally mediated knockdown of insulin receptor expression specifically in the hippocampus.
    Results: Our data show that inhibiting 11β-HSD1 activity prevents hippocampal-related memory deficits in diabetic juvenile rats. A significant increase (53.0±9.9%) in hippocampal 11β-HSD1 activity was found in hippocampal slices incubated in high glucose conditions (13.9 mmol/l) vs normal glucose conditions (2.8 mmol/l) without insulin. However, 11β-HSD1 activity was not affected by variations in insulin concentration either in the hippocampal slices or after a decrease in hippocampal insulin receptor expression.
    Conclusions/interpretation: Together, these data demonstrate that an increase in 11β-HSD1 activity contributes to memory deficits observed in juvenile diabetic rats and that an excess of hippocampal 11β-HSD1 activity stems from high glucose levels rather than insulin deficiency. 11β-HSD1 might be a therapeutic target for treating cognitive impairments associated with diabetes.
    MeSH term(s) Rats ; Animals ; Insulin/metabolism ; Glucocorticoids ; 11-beta-Hydroxysteroid Dehydrogenase Type 1/metabolism ; Receptor, Insulin ; Diabetes Mellitus, Type 1 ; Diabetes Mellitus, Experimental ; Memory Disorders ; Glucose/pharmacology
    Chemical Substances Insulin ; Glucocorticoids ; 11-beta-Hydroxysteroid Dehydrogenase Type 1 (EC 1.1.1.146) ; Receptor, Insulin (EC 2.7.10.1) ; Glucose (IY9XDZ35W2)
    Language English
    Publishing date 2023-06-10
    Publishing country Germany
    Document type Journal Article ; Research Support, Non-U.S. Gov't
    ZDB-ID 1694-9
    ISSN 1432-0428 ; 0012-186X
    ISSN (online) 1432-0428
    ISSN 0012-186X
    DOI 10.1007/s00125-023-05942-3
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    Zs.A 279: Show issues Location:
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  10. Article ; Online: Hypothalamic Glucose Hypersensitivity-Induced Insulin Secretion in the Obese Zücker Rat Is Reversed by Central Ghrelin Treatment.

    Carneiro, Lionel / Fenech, Claire / Liénard, Fabienne / Grall, Sylvie / Abed, Besma / Haydar, Joulia / Allard, Camille / Desmoulins, Lucie / Paccoud, Romain / Brindisi, Marie-Claude / Mouillot, Thomas / Brondel, Laurent / Fioramonti, Xavier / Pénicaud, Luc / Jacquin-Piques, Agnès / Leloup, Corinne

    Antioxidants & redox signaling

    2023  

    Abstract: Aims: ...

    Abstract Aims:
    Language English
    Publishing date 2023-03-07
    Publishing country United States
    Document type Journal Article
    ZDB-ID 1483836-9
    ISSN 1557-7716 ; 1523-0864
    ISSN (online) 1557-7716
    ISSN 1523-0864
    DOI 10.1089/ars.2022.0031
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