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Start Over Author "Carpentier, André" Publication Type Academic Journals
444 results on '"Carpentier, André"'

12. High-fructose feeding suppresses cold-stimulated brown adipose tissue glucose uptake independently of changes in thermogenesis and the gut microbiome

Author

Richard, Gabriel, Blondin, Denis P., Syed, Saad A., Rossi, Laura, Fontes, Michelle E., Fortin, Mélanie, Phoenix, Serge, Frisch, Frédérique, Dubreuil, Stéphanie, Guérin, Brigitte, Turcotte, Éric E., Lepage, Martin, Surette, Michael G., Schertzer, Jonathan D., Steinberg, Gregory R., Morrison, Katherine M., and Carpentier, André C.

Published
2022
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15. Lower brown adipose tissue activity is associated with non-alcoholic fatty liver disease but not changes in the gut microbiota

Author

Ahmed, Basma A., Ong, Frank J., Barra, Nicole G., Blondin, Denis P., Gunn, Elizabeth, Oreskovich, Stephan M., Szamosi, Jake C., Syed, Saad A., Hutchings, Emily K., Konyer, Norman B., Singh, Nina P., Yabut, Julian M., Desjardins, Eric M., Anhê, Fernando F., Foley, Kevin P., Holloway, Alison C., Noseworthy, Michael D., Haman, Francois, Carpentier, Andre C., Surette, Michael G., Schertzer, Jonathan D., Punthakee, Zubin, Steinberg, Gregory R., and Morrison, Katherine M.

Published
2021
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17. IGFBP-2 partly mediates the early metabolic improvements caused by bariatric surgery

Author

Faramia, Justine, Hao, Zheng, Mumphrey, Michael B., Townsend, R. Leigh, Miard, Stéphanie, Carreau, Anne-Marie, Nadeau, Mélanie, Frisch, Frédérique, Baraboi, Elena-Dana, Grenier-Larouche, Thomas, Noll, Christophe, Li, Meng, Biertho, Laurent, Marceau, Simon, Hould, Frédéric-Simon, Lebel, Stéfane, Morrison, Christopher D., Münzberg, Heike, Richard, Denis, Carpentier, André C., Tchernof, André, Berthoud, Hans-Rudolf, and Picard, Frédéric

Published
2021
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20. The effects of the β1‐adrenergic receptor antagonist bisoprolol administration on mirabegron‐stimulated human brown adipose tissue thermogenesis.

Author

Dumont, Lauralyne, Caron, Alexandre, Richard, Gabriel, Croteau, Etienne, Fortin, Mélanie, Frisch, Frédérique, Phoenix, Serge, Dubreuil, Stéphanie, Guérin, Brigitte, Turcotte, Éric E., Carpentier, André C., and Blondin, Denis P.

Subjects
BROWN adipose tissue, BISOPROLOL, BODY temperature regulation, ORAL drug administration, SYSTOLIC blood pressure
Abstract

Aim: Pharmacological stimulation of human brown adipose tissue (BAT) has been hindered by ineffective activation or undesirable off‐target effects. Oral administration of the maximal allowable dose of mirabegron (200 mg), a β3‐adrenergic receptor (β3‐AR) agonist, has been effective in stimulating BAT thermogenesis and whole‐body energy expenditure. However, this has been accompanied by undesirable cardiovascular effects. Therefore, we hypothesized that combining mirabegron with a β1‐AR antagonist could suppress these unwanted effects and increase the stimulation of the β3‐AR and β2‐AR in BAT. Methods: We performed a randomized crossover trial (NCT04823442) in 8 lean men. Mirabegron (200 mg) was administered orally with or without the β1‐AR antagonist bisoprolol (10 mg). Dynamic [11C]‐acetate and 2‐deoxy‐2‐[18F]fluoro‐d‐glucose PET/CT scans were performed sequentially after oral administration of mirabegron ± bisoprolol. Results: Compared to room temperature, mirabegron alone increased BAT oxidative metabolism (0.84 ± 0.46 vs. 1.79 ± 0.91 min−1, p = 0.0433), but not when combined with bisoprolol. The metabolic rate of glucose in BAT, measured using [18F]FDG PET, was significantly higher with mirabegron than mirabegron with bisoprolol (24 ± 10 vs. 16 ± 8 nmol/g/min, p = 0.0284). Bisoprolol inhibited the mirabegron‐induced increase in systolic blood pressure and heart rate. Conclusion: The administration of bisoprolol decreases the adverse cardiovascular effects of mirabegron. However, the provided dose also blunted the mirabegron‐stimulated increase in BAT lipolysis, thermogenesis, and glucose uptake. The attenuation in BAT blood flow induced by the large dose of bisoprolol may have limited BAT thermogenesis. [ABSTRACT FROM AUTHOR]

Published
2024
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21. Brown adipose tissue metabolism in women is dependent on ovarian status.

Author

Blondin, Denis P., Haman, François, Swibas, Tracy M., Hogan-Lamarre, Sophie, Dumont, Lauralyne, Guertin, Jolan, Richard, Gabriel, Weissenburger, Quentin, Hildreth, Kerry L., Schauer, Irene, Panter, Shelby, Wyland, Liza, Carpentier, André C., Miao, Yubin, Shi, Jiayuan, Juarez-Colunga, Elizabeth, Kohrt, Wendy M., and Melanson, Edward L.

Subjects
BROWN adipose tissue, TISSUE metabolism, POSITRON emission tomography, BATS, GONADOTROPIN releasing hormone, BODY mass index, PRECOCIOUS puberty
Abstract

In rodents, loss of estradiol (E2) reduces brown adipose tissue (BAT) metabolic activity. Whether E2 impacts BAT activity in women is not known. BAT oxidative metabolism was measured in premenopausal (n = 27; 35 ± 9 yr; body mass index = 26.0 ± 5.3 kg/m2) and postmenopausal (n = 25; 51 ± 8 yr; body mass index = 28.0 ± 5.0 kg/m2) women at room temperature and during acute cold exposure using [11C]acetate with positron emission tomography coupled with computed tomograph. BAT glucose uptake was also measured during acute cold exposure using 2-deoxy-2-[18F]fluoro- d -glucose. To isolate the effects of ovarian hormones from biological aging, measurements were repeated in a subset of premenopausal women (n = 8; 40 ± 4 yr; BMI = 28.0 ± 7.2 kg/m2) after 6 mo of gonadotropin-releasing hormone agonist therapy to suppress ovarian hormones. At room temperature, there was no difference in BAT oxidative metabolism between premenopausal (0.56 ± 0.31 min−1) and postmenopausal women (0.63 ± 0.28 min−1). During cold exposure, BAT oxidative metabolism (1.28 ± 0.85 vs. 0.91 ± 0.63 min−1, P = 0.03) and net BAT glucose uptake (84.4 ± 82.5 vs. 29.7 ± 31.4 nmol·g−1·min−1, P < 0.01) were higher in premenopausal than postmenopausal women. In premenopausal women who underwent gonadotropin-releasing hormone agonist, cold-stimulated BAT oxidative metabolism was reduced to a similar level (from 1.36 ± 0.66 min−1 to 0.91 ± 0.41 min−1) to that observed in postmenopausal women (0.91 ± 0.63 min−1). These results provide the first evidence in humans that reproductive hormones are associated with BAT oxidative metabolism and suggest that BAT may be a target to attenuate age-related reduction in energy expenditure and maintain metabolic health in postmenopausal women. NEW & NOTEWORTHY: In rodents, loss of estrogen reduces brown adipose tissue (BAT) activity. Whether this is true in humans is not known. We found that BAT oxidative metabolism and glucose uptake were lower in postmenopausal compared to premenopausal women. In premenopausal women who underwent ovarian suppression to reduce circulating estrogen, BAT oxidative metabolism was reduced to postmenopausal levels. Thus the loss of ovarian function in women leads to a reduction in BAT metabolic activity independent of age. [ABSTRACT FROM AUTHOR]

Published
2024
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22. Human Brown Adipocyte Thermogenesis Is Driven by β2-AR Stimulation

Author

Blondin, Denis P., Nielsen, Soren, Kuipers, Eline N., Severinsen, Mai C., Jensen, Verena H., Miard, Stéphanie, Jespersen, Naja Z., Kooijman, Sander, Boon, Mariëtte R., Fortin, Mélanie, Phoenix, Serge, Frisch, Frédérique, Guérin, Brigitte, Turcotte, Éric E., Haman, François, Richard, Denis, Picard, Frédéric, Rensen, Patrick C.N., Scheele, Camilla, and Carpentier, André C.

Published
2020
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24. Specific loss of adipocyte CD248 improves metabolic health via reduced white adipose tissue hypoxia, fibrosis and inflammation

Author

Petrus, Paul, Fernandez, Tara L., Kwon, Michelle M., Huang, Jenny L., Lei, Victor, Safikhan, Nooshin Seyed, Karunakaran, Subashini, O'Shannessy, Daniel J., Zheng, Xiaowei, Catrina, Sergiu-Bogdan, Albone, Earl, Laine, Jukka, Virtanen, Kirsi, Clee, Susanne M., Kieffer, Timothy J., Noll, Christophe, Carpentier, André C., Johnson, James D., Rydén, Mikael, and Conway, Edward M.

Published
2019
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33. Cardiorenal ketone metabolism: a positron emission tomography study in healthy humans.

Author

Cuenoud, Bernard, Croteau, Etienne, St-Pierre, Valérie, Richard, Gabriel, Fortier, Mélanie, Vandenberghe, Camille, Carpentier, André C., and Cunnane, Stephen C.

Subjects
POSITRON emission tomography, KETONES, ORGANS (Anatomy), KIDNEY cortex, KIDNEY pelvis
Abstract

Ketones are alternative energy substrates for the heart and kidney but no studies have investigated their metabolism simultaneously in both organs in humans. The present double tracer positron emission tomography (PET) study evaluated the organ distribution and basal kinetic rates of the radiolabeled ketone, 11C-acetoacetate (11C-AcAc), in the heart and kidney compared to 11C-acetate (11C-Ac), which is a well-validated metabolic radiotracer. Both tracers were highly metabolized by the left ventricle and the renal cortex. In the heart, kinetic rates were similar for both tracers. But in the renal cortex, uptake of 11C-Ac was higher compared to 11C-AcAc, while the reverse was observed for the clearance. Interestingly, infusion of 11C-AcAc led to a significantly delayed release of radioactivity in the renal medulla and pelvis, a phenomenon not observed with 11C-Ac. This suggests an equilibrium of 11C-AcAc with the other ketone, 11C-D-beta-hydroxybutyrate, and a different clearance profile. Overall, this suggests that in the kidney, the absorption and metabolism of 11C-AcAc is different compared to 11C-Ac. This dual tracer PET protocol provides the opportunity to explore the relative importance of ketone metabolism in cardiac and renal diseases, and to improve our mechanistic understanding of new metabolic interventions targeting these two organs. [ABSTRACT FROM AUTHOR]

Published
2023
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38. Human brown adipose tissue is not enough to combat cardiometabolic diseases.

Author

Carpentier, André C. and Blondin, Denis P.

Subjects
*BROWN adipose tissue, *HEART metabolism disorders, *HYPERGLYCEMIA, *CHYLOMICRONS
Abstract

The article offers information on brown adipose tissue (BAT) and its role in energy expenditure through uncoupling protein 1 (UCP1). Topics include the renewed interest in BAT in adult humans, primarily assessed through 18F-fluoro-deoxyglucose (18FDG) PET imaging, and its potential relevance to obesity, type 2 diabetes (T2D), and cardiometabolic diseases. The article posits that, unlike rodents, human BAT may not be sufficient to combat cardiometabolic diseases.

Published
2023
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40. Brown Adipose Tissue—A Translational Perspective.

Author

Carpentier, André C, Blondin, Denis P, Haman, François, and Richard, Denis

Subjects
BROWN adipose tissue, HEART metabolism disorders, OXIDATIVE phosphorylation
Abstract

Brown adipose tissue (BAT) displays the unique capacity to generate heat through uncoupled oxidative phosphorylation that makes it a very attractive therapeutic target for cardiometabolic diseases. Here, we review BAT cellular metabolism, its regulation by the central nervous and endocrine systems and circulating metabolites, the plausible roles of this tissue in human thermoregulation, energy balance, and cardiometabolic disorders, and the current knowledge on its pharmacological stimulation in humans. The current definition and measurement of BAT in human studies relies almost exclusively on BAT glucose uptake from positron emission tomography with 18F-fluorodeoxiglucose, which can be dissociated from BAT thermogenic activity, as for example in insulin-resistant states. The most important energy substrate for BAT thermogenesis is its intracellular fatty acid content mobilized from sympathetic stimulation of intracellular triglyceride lipolysis. This lipolytic BAT response is intertwined with that of white adipose (WAT) and other metabolic tissues, and cannot be independently stimulated with the drugs tested thus far. BAT is an interesting and biologically plausible target that has yet to be fully and selectively activated to increase the body's thermogenic response and shift energy balance. The field of human BAT research is in need of methods able to directly, specifically, and reliably measure BAT thermogenic capacity while also tracking the related thermogenic responses in WAT and other tissues. Until this is achieved, uncertainty will remain about the role played by this fascinating tissue in human cardiometabolic diseases. [ABSTRACT FROM AUTHOR]

Published
2023
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