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Article ; Online: mTORC1 in energy expenditure: consequences for obesity.

Allard, Camille / Miralpeix, Cristina / López-Gambero, Antonio J / Cota, Daniela

2024 Volume 20, Issue 4, Page(s) 239–251

Abstract: In eukaryotic cells, the mammalian target of rapamycin complex 1 (sometimes referred to as the mechanistic target of rapamycin complex 1; mTORC1) orchestrates cellular metabolism in response to environmental energy availability. As a result, at the ... ...

Abstract	In eukaryotic cells, the mammalian target of rapamycin complex 1 (sometimes referred to as the mechanistic target of rapamycin complex 1; mTORC1) orchestrates cellular metabolism in response to environmental energy availability. As a result, at the organismal level, mTORC1 signalling regulates the intake, storage and use of energy by acting as a hub for the actions of nutrients and hormones, such as leptin and insulin, in different cell types. It is therefore unsurprising that deregulated mTORC1 signalling is associated with obesity. Strategies that increase energy expenditure offer therapeutic promise for the treatment of obesity. Here we review current evidence illustrating the critical role of mTORC1 signalling in the regulation of energy expenditure and adaptive thermogenesis through its various effects in neuronal circuits, adipose tissue and skeletal muscle. Understanding how mTORC1 signalling in one organ and cell type affects responses in other organs and cell types could be key to developing better, safer treatments targeting this pathway in obesity.
MeSH term(s)	Humans ; Mechanistic Target of Rapamycin Complex 1/metabolism ; Obesity/metabolism ; Signal Transduction/physiology ; Insulin/metabolism ; Energy Metabolism/physiology
Chemical Substances	Mechanistic Target of Rapamycin Complex 1 (EC 2.7.11.1) ; Insulin
Language	English
Publishing date	2024-01-15
Publishing country	England
Document type	Journal Article ; Review
ZDB-ID	2489381-X
ISSN	1759-5037 ; 1759-5029
ISSN (online)	1759-5037
ISSN	1759-5029
DOI	10.1038/s41574-023-00934-0
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Article ; Online: Poly-Agonist Pharmacotherapies for Metabolic Diseases: Hopes and New Challenges.

Allard, Camille / Cota, Daniela / Quarta, Carmelo

Drugs

2023 Volume 84, Issue 2, Page(s) 127–148

Abstract: The use of glucagon-like peptide-1 (GLP-1) receptor-based multi-agonists in the treatment of type 2 diabetes and obesity holds great promise for improving glycaemic control and weight management. Unimolecular dual and triple agonists targeting multiple ... ...

Abstract	The use of glucagon-like peptide-1 (GLP-1) receptor-based multi-agonists in the treatment of type 2 diabetes and obesity holds great promise for improving glycaemic control and weight management. Unimolecular dual and triple agonists targeting multiple gut hormone-related pathways are currently in clinical trials, with recent evidence supporting their efficacy. However, significant knowledge gaps remain regarding the biological mechanisms and potential adverse effects associated with these multi-target agents. The mechanisms underlying the therapeutic efficacy of GLP-1 receptor-based multi-agonists remain somewhat mysterious, and hidden threats may be associated with the use of gut hormone-based polyagonists. In this review, we provide a critical analysis of the benefits and risks associated with the use of these new drugs in the management of obesity and diabetes, while also exploring new potential applications of GLP-1-based pharmacology beyond the field of metabolic disease.
MeSH term(s)	Humans ; Diabetes Mellitus, Type 2/drug therapy ; Diabetes Mellitus, Type 2/metabolism ; Glucagon-Like Peptide 1/therapeutic use ; Obesity/drug therapy ; Obesity/metabolism ; Metabolic Diseases/drug therapy ; Glucagon-Like Peptide-1 Receptor ; Hypoglycemic Agents/pharmacology ; Hypoglycemic Agents/therapeutic use
Chemical Substances	Glucagon-Like Peptide 1 (89750-14-1) ; Glucagon-Like Peptide-1 Receptor ; Hypoglycemic Agents
Language	English
Publishing date	2023-12-21
Publishing country	New Zealand
Document type	Journal Article ; Review
ZDB-ID	120316-2
ISSN	1179-1950 ; 0012-6667
ISSN (online)	1179-1950
ISSN	0012-6667
DOI	10.1007/s40265-023-01982-6
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Zs.A 762: Show issues

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Article ; Online: Food intake and body weight in rodent studies: the devil is in the details.

Allard, Camille / Zizzari, Philippe / Quarta, Carmelo / Cota, Daniela

Nature metabolism

2022 Volume 4, Issue 11, Page(s) 1424–1426

MeSH term(s)	Animals ; Rodentia ; Body Weight ; Eating
Language	English
Publishing date	2022-10-17
Publishing country	Germany
Document type	Journal Article
ISSN	2522-5812
ISSN (online)	2522-5812
DOI	10.1038/s42255-022-00658-x
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Article ; Online: Single cell tracing of Pomc neurons reveals recruitment of 'Ghost' subtypes with atypical identity in a mouse model of obesity.

Leon, Stéphane / Simon, Vincent / Lee, Thomas H / Steuernagel, Lukas / Clark, Samantha / Biglari, Nasim / Lesté-Lasserre, Thierry / Dupuy, Nathalie / Cannich, Astrid / Bellocchio, Luigi / Zizzari, Philippe / Allard, Camille / Gonzales, Delphine / Le Feuvre, Yves / Lhuillier, Emeline / Brochard, Alexandre / Nicolas, Jean Charles / Teillon, Jérémie / Nikolski, Macha /

Marsicano, Giovanni / Fioramonti, Xavier / Brüning, Jens C / Cota, Daniela / Quarta, Carmelo

Nature communications

2024 Volume 15, Issue 1, Page(s) 3443

Abstract: The hypothalamus contains a remarkable diversity of neurons that orchestrate behavioural and metabolic outputs in a highly plastic manner. Neuronal diversity is key to enabling hypothalamic functions and, according to the neuroscience dogma, it is ... ...

Abstract	The hypothalamus contains a remarkable diversity of neurons that orchestrate behavioural and metabolic outputs in a highly plastic manner. Neuronal diversity is key to enabling hypothalamic functions and, according to the neuroscience dogma, it is predetermined during embryonic life. Here, by combining lineage tracing of hypothalamic pro-opiomelanocortin (Pomc) neurons with single-cell profiling approaches in adult male mice, we uncovered subpopulations of 'Ghost' neurons endowed with atypical molecular and functional identity. Compared to 'classical' Pomc neurons, Ghost neurons exhibit negligible Pomc expression and are 'invisible' to available neuroanatomical approaches and promoter-based reporter mice for studying Pomc biology. Ghost neuron numbers augment in diet-induced obese mice, independent of neurogenesis or cell death, but weight loss can reverse this shift. Our work challenges the notion of fixed, developmentally programmed neuronal identities in the mature hypothalamus and highlight the ability of specialised neurons to reversibly adapt their functional identity to adult-onset obesogenic stimuli.
MeSH term(s)	Animals ; Pro-Opiomelanocortin/metabolism ; Pro-Opiomelanocortin/genetics ; Neurons/metabolism ; Obesity/metabolism ; Obesity/pathology ; Male ; Mice ; Hypothalamus/metabolism ; Hypothalamus/cytology ; Single-Cell Analysis ; Disease Models, Animal ; Diet, High-Fat ; Mice, Inbred C57BL ; Mice, Transgenic ; Neurogenesis ; Mice, Obese
Chemical Substances	Pro-Opiomelanocortin (66796-54-1)
Language	English
Publishing date	2024-04-24
Publishing country	England
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	2553671-0
ISSN	2041-1723 ; 2041-1723
ISSN (online)	2041-1723
ISSN	2041-1723
DOI	10.1038/s41467-024-47877-2
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Article ; Online: Challenges of combining work and unpaid care, and solutions: A scoping review.

Spann, Alice / Vicente, Joana / Allard, Camille / Hawley, Mark / Spreeuwenberg, Marieke / de Witte, Luc

Health & social care in the community

2019 Volume 28, Issue 3, Page(s) 699–715

Abstract: The number of people who combine work and unpaid care is increasing rapidly as more people need care, public and private care systems are progressively under pressure and more people are required to work for longer. Without adequate support, these ... ...

Abstract	The number of people who combine work and unpaid care is increasing rapidly as more people need care, public and private care systems are progressively under pressure and more people are required to work for longer. Without adequate support, these working carers may experience detrimental effects on their well-being. To adequately support working carers, it is important to first understand the challenges they face. A scoping review was carried out, using Arksey and O'Malley's framework, to map the challenges of combining work and care and solutions described in the literature to address these challenges. The search included academic and grey literature between 2008 and 2018 and was conducted in April 2018, using electronic academic databases and reference list checks. Ninety-two publications were mapped, and the content analysed thematically. A conceptual framework was derived from the analysis which identified primary challenges (C1), directly resulting from combining work and care, primary solutions (S1) aiming to address these, secondary challenges (C2) resulting from solutions and secondary solutions (S2) aiming to address secondary challenges. Primary challenges were: (a) high and/or competing demands; (b) psychosocial/-emotional stressors; (c) distance; (d) carer's health; (e) returning to work; and (f) financial pressure. This framework serves to help those aiming to support working carers to better understand the challenges they face and those developing solutions for the challenges of combining work and care to consider potential consequences or barriers. Gaps in the literature have been identified and discussed.
MeSH term(s)	Caregiver Burden/economics ; Home Care Agencies ; Humans ; Internationality ; Social Support ; Workload/economics
Language	English
Publishing date	2019-12-17
Publishing country	England
Document type	Journal Article ; Research Support, Non-U.S. Gov't ; Review
ZDB-ID	1155902-0
ISSN	1365-2524 ; 0966-0410
ISSN (online)	1365-2524
ISSN	0966-0410
DOI	10.1111/hsc.12912
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Zs.A 3728: Show issues

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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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Zs.A 5488: Show issues

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Article ; Online: Efficacy of glucagon-like peptide-1 and estrogen dual agonist in pancreatic islets protection and pre-clinical models of insulin-deficient diabetes.

Fuselier, Taylor / Mota de Sa, Paula / Qadir, M M Fahd / Xu, Beibei / Allard, Camille / Meyers, Mathew M / Tiano, Joseph P / Yang, Bin S / Gelfanov, Vasily / Lindsey, Sarah H / Dimarchi, Richard D / Mauvais-Jarvis, Franck

Cell reports. Medicine

2022 Volume 3, Issue 4, Page(s) 100598

Abstract: We study the efficacy of a glucagon-like peptide-1 (GLP-1) and estrogen dual agonist (GLP1-E2) in pancreatic islet protection. GLP1-E2 provides superior protection from insulin-deficient diabetes induced by multiple low-dose streptozotocin (MLD-STZ- ... ...

Abstract	We study the efficacy of a glucagon-like peptide-1 (GLP-1) and estrogen dual agonist (GLP1-E2) in pancreatic islet protection. GLP1-E2 provides superior protection from insulin-deficient diabetes induced by multiple low-dose streptozotocin (MLD-STZ-diabetes) and by the Akita mutation in mice than a GLP-1 monoagonist. GLP1-E2 does not protect from MLD-STZ-diabetes in estrogen receptor-α (ERα)-deficient mice and fails to prevent diabetes in Akita mice following GLP-1 receptor (GLP-1R) antagonism, demonstrating the requirement of GLP-1R and ERα for GLP1-E2 antidiabetic actions. In the MIN6 β cell model, GLP1-E2 activates estrogen action following clathrin-dependent, GLP-1R-mediated internalization and lysosomal acidification. In cultured human islet, proteomic bioinformatic analysis reveals that GLP1-E2 amplifies the antiapoptotic pathways activated by monoagonists. However, in cultured mouse islets, GLP1-E2 provides antiapoptotic protection similar to monoagonists. Thus, GLP1-E2 promotes GLP-1 and E2 antiapoptotic signals in cultured islets, but
MeSH term(s)	Animals ; Diabetes Mellitus/metabolism ; Estrogen Receptor alpha/metabolism ; Estrogens/metabolism ; Glucagon-Like Peptide 1/pharmacology ; Insulin/metabolism ; Insulin, Regular, Human/metabolism ; Islets of Langerhans/metabolism ; Mice ; Proteomics ; Streptozocin/toxicity
Chemical Substances	Estrogen Receptor alpha ; Estrogens ; Insulin ; Insulin, Regular, Human ; Streptozocin (5W494URQ81) ; Glucagon-Like Peptide 1 (89750-14-1)
Language	English
Publishing date	2022-04-07
Publishing country	United States
Document type	Journal Article ; Research Support, U.S. Gov't, Non-P.H.S. ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
ISSN	2666-3791
ISSN (online)	2666-3791
DOI	10.1016/j.xcrm.2022.100598
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Article ; Online: The role of androgens in metabolism, obesity, and diabetes in males and females.

Navarro, Guadalupe / Allard, Camille / Xu, Weiwei / Mauvais-Jarvis, Franck

Obesity (Silver Spring, Md.)

2015 Volume 23, Issue 4, Page(s) 713–719

Abstract: Objective: In men, androgen deprivation contributes to the development of metabolic syndrome and type 2 diabetes (T2D). In women, androgen excess predisposes to insulin resistance and T2D. There is a bidirectional modulation of glucose homeostasis by ... ...

Abstract	Objective: In men, androgen deprivation contributes to the development of metabolic syndrome and type 2 diabetes (T2D). In women, androgen excess predisposes to insulin resistance and T2D. There is a bidirectional modulation of glucose homeostasis by androgens in males and females that is analyzed in this review. Methods: We reviewed the literature in both rodents and humans on the role of androgens and the androgen receptor (AR) in the control of glucose and energy metabolism in health, obesity, and T2D. Results: Sex-specific activation of AR in the hypothalamus, skeletal muscle, liver, adipose tissue, and pancreatic islet β-cells accounts for maintenance or disruption in energy metabolism and glucose homeostasis. Conclusions: We argue that AR is a target to prevent androgen-related metabolic disorders.
MeSH term(s)	Adipose Tissue/metabolism ; Androgens/metabolism ; Animals ; Diabetes Mellitus, Type 2/metabolism ; Female ; Humans ; Insulin Resistance/physiology ; Male ; Metabolic Diseases/metabolism ; Metabolic Syndrome/metabolism ; Muscle, Skeletal/metabolism ; Obesity/metabolism ; Receptors, Androgen/metabolism ; Sex Factors
Chemical Substances	Androgens ; Receptors, Androgen
Language	English
Publishing date	2015-04
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't ; Review
ZDB-ID	2230457-5
ISSN	1930-739X ; 1071-7323 ; 1930-7381
ISSN (online)	1930-739X
ISSN	1071-7323 ; 1930-7381
DOI	10.1002/oby.21033
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Zs.A 4061: Show issues			Location: Je nach Verfügbarkeit (siehe Angabe bei Bestand) bis Jg. 1994: Bestellungen von Artikeln über das Online-Bestellformular Jg. 1995 - 2021: Lesesall (2.OG) ab Jg. 2022: Lesesaal (EG)
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Article ; Online: CB1 and GLP-1 Receptors Cross Talk Provides New Therapies for Obesity.

Zizzari, Philippe / He, Rongjun / Falk, Sarah / Bellocchio, Luigi / Allard, Camille / Clark, Samantha / Lesté-Lasserre, Thierry / Marsicano, Giovanni / Clemmensen, Christoffer / Perez-Tilve, Diego / Finan, Brian / Cota, Daniela / Quarta, Carmelo

Diabetes

2020 Volume 70, Issue 2, Page(s) 415–422

Abstract: Glucagon-like peptide 1 receptor (GLP-1R) agonists effectively improve glycemia and body weight in patients with type 2 diabetes and obesity but have limited weight-lowering efficacy and minimal insulin sensitizing action. In preclinical models, ... ...

Abstract	Glucagon-like peptide 1 receptor (GLP-1R) agonists effectively improve glycemia and body weight in patients with type 2 diabetes and obesity but have limited weight-lowering efficacy and minimal insulin sensitizing action. In preclinical models, peripherally restricted cannabinoid receptor type 1 (CB1R) inhibitors, which are devoid of the neuropsychiatric adverse effects observed with brain-penetrant CB1R blockers, ameliorate obesity and its multiple metabolic complications. Using mouse models with genetic loss of CB1R or GLP-1R, we demonstrate that these two metabolic receptors modulate food intake and body weight via reciprocal functional interactions. In diet-induced obese mice, the coadministration of a peripheral CB1R inhibitor with long-acting GLP-1R agonists achieves greater reduction in body weight and fat mass than monotherapies by promoting negative energy balance. This cotreatment also results in larger improvements in systemic and hepatic insulin action, systemic dyslipidemia, and reduction of hepatic steatosis. Thus, peripheral CB1R blockade may allow safely potentiating the antiobesity and antidiabetic effects of currently available GLP-1R agonists.
MeSH term(s)	Animals ; Blood Glucose/metabolism ; Body Composition/physiology ; Body Weight/physiology ; Diet, High-Fat ; Eating/physiology ; Energy Metabolism ; Glucagon-Like Peptide-1 Receptor/genetics ; Glucagon-Like Peptide-1 Receptor/metabolism ; Insulin/blood ; Leptin/blood ; Male ; Mice ; Mice, Knockout ; Obesity/genetics ; Obesity/metabolism ; Receptor, Cannabinoid, CB1/genetics ; Receptor, Cannabinoid, CB1/metabolism
Chemical Substances	Blood Glucose ; Glucagon-Like Peptide-1 Receptor ; Insulin ; Leptin ; Receptor, Cannabinoid, CB1
Language	English
Publishing date	2020-11-03
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	80085-5
ISSN	1939-327X ; 0012-1797
ISSN (online)	1939-327X
ISSN	0012-1797
DOI	10.2337/db20-0162
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Article ; Online: Activation of hepatic estrogen receptor-α increases energy expenditure by stimulating the production of fibroblast growth factor 21 in female mice.

Allard, Camille / Bonnet, Fabrice / Xu, Beibei / Coons, Laurel / Albarado, Diana / Hill, Cristal / Fagherazzi, Guy / Korach, Kenneth S / Levin, Ellis R / Lefante, John / Morrison, Christopher / Mauvais-Jarvis, Franck

Molecular metabolism

2019 Volume 22, Page(s) 62–70

Abstract: Objective: The endogenous estrogen 17β-estradiol (E2) promotes metabolic homeostasis in premenopausal women. In a mouse model of post-menopausal metabolic syndrome, we reported that estrogens increased energy expenditure, thus preventing estrogen ... ...

Abstract	Objective: The endogenous estrogen 17β-estradiol (E2) promotes metabolic homeostasis in premenopausal women. In a mouse model of post-menopausal metabolic syndrome, we reported that estrogens increased energy expenditure, thus preventing estrogen deficiency-induced adiposity. Estrogens' prevention of fat accumulation was associated with increased serum concentrations of fibroblast growth factor 21 (FGF21), suggesting that FGF21 participates in estrogens' promotion of energy expenditure. Methods: We studied the effect of E2 on FGF21 production and the role of FGF21 in E2 stimulation of energy expenditure and prevention of adiposity, using female estrogen receptor (ER)- and FGF21-deficient mice fed a normal chow and a cohort of ovariectomized women from the French E3N prospective cohort study. Results: E2 acting on the hepatocyte ERα increases hepatic expression and production of FGF21 in female mice. In vivo activation of ERα increases the transcription of Fgf21 via an estrogen response element outside the promoter of Fgf21. Treatment with E2 increases oxygen consumption and energy expenditure and prevents whole body fat accumulation in ovariectomized female WT mice. The effect of E2 on energy expenditure is not observed in FGF21-deficient mice. While E2 treatment still prevents fat accumulation in FGF21-deficient mice, this effect is decreased compared to WT mice. In an observational cohort of ovariectomized women, E2 treatment was associated with lower serum FGF21 concentrations, which may reflect a healthier metabolic profile. Conclusions: In female mice, E2 action on the hepatocyte ERα increases Fgf21 transcription and FGF21 production, thus promoting energy expenditure and partially decreasing fat accumulation.
MeSH term(s)	Animals ; Energy Metabolism ; Estrogen Receptor alpha/metabolism ; Female ; Fibroblast Growth Factors/biosynthesis ; Fibroblast Growth Factors/deficiency ; Mice ; Mice, Inbred C57BL ; Mice, Knockout
Chemical Substances	Estrogen Receptor alpha ; fibroblast growth factor 21 ; Fibroblast Growth Factors (62031-54-3)
Language	English
Publishing date	2019-02-14
Publishing country	Germany
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't ; Research Support, U.S. Gov't, Non-P.H.S.
ISSN	2212-8778
ISSN (online)	2212-8778
DOI	10.1016/j.molmet.2019.02.002
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