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  1. Article ; Online: Exploiting oxidized lipids and the lipid-binding GPCRs against cardiometabolic diseases.

    Guimarães, Raphael C / Gonçalves, Tiago T / Leiria, Luiz O

    British journal of pharmacology

    2020  Volume 178, Issue 3, Page(s) 531–549

    Abstract: Lipids govern vital cellular processes and drive physiological changes in response to different pathological or environmental cues. Lipid species can be roughly divided into structural and signalling lipids. The former is essential for membrane ... ...

    Abstract Lipids govern vital cellular processes and drive physiological changes in response to different pathological or environmental cues. Lipid species can be roughly divided into structural and signalling lipids. The former is essential for membrane composition, while the latter are usually oxidized lipids. These mediators provide beneficial effects against cardiometabolic diseases (CMDs), including fatty-liver diseases, atherosclerosis, thrombosis, obesity, and Type 2 diabetes. For instance, several oxylipins were recently found to improve glucose homeostasis, increase insulin secretion, and inhibit platelet aggregation, while specialized pro-resolving mediators (SPMs) are able to ameliorate CMD by shaping the immune system. These lipids act mainly by stimulating GPCRs. In this review, we provide an updated and comprehensive overview of the current state of the literature on signalling lipids in the context of CMD. We also highlight the network encompassing the lipid-modifying enzymes and the lipid-binding GPCRs, as well as their interactions in health and disease.
    MeSH term(s) Atherosclerosis ; Diabetes Mellitus, Type 2 ; Humans ; Lipids ; Obesity ; Protein Binding
    Chemical Substances Lipids
    Language English
    Publishing date 2020-12-23
    Publishing country England
    Document type Journal Article ; Research Support, Non-U.S. Gov't ; Review
    ZDB-ID 80081-8
    ISSN 1476-5381 ; 0007-1188
    ISSN (online) 1476-5381
    ISSN 0007-1188
    DOI 10.1111/bph.15321
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  2. Article ; Online: COVID-19-related hyperglycemia is associated with infection of hepatocytes and stimulation of gluconeogenesis.

    Barreto, Ester A / Cruz, Amanda S / Veras, Flavio P / Martins, Ronaldo / Bernardelli, Rafaella S / Paiva, Isadora M / Lima, Thais M / Singh, Youvika / Guimarães, Raphael C / Damasceno, Samara / Pereira, Nayara / Alves, João Manoel / Gonçalves, Tiago T / Forato, Julia / Muraro, Stéfanie P / Souza, Gabriela F / Batah, Sabrina Setembre / Proenca-Modena, José L / Mori, Marcelo A /
    Cunha, Fernando Q / Louzada-Junior, Paulo / Cunha, Thiago M / Nakaya, Helder I / Fabro, Alexandre / de Oliveira, Renê D R / Arruda, Eurico / Réa, Rosângela / Réa Neto, Álvaro / Fernandes da Silva, Miguel M / Leiria, Luiz Osório

    Proceedings of the National Academy of Sciences of the United States of America

    2023  Volume 120, Issue 21, Page(s) e2217119120

    Abstract: Occurrence of hyperglycemia upon infection is associated with worse clinical outcome in COVID-19 patients. However, it is still unknown whether SARS-CoV-2 directly triggers hyperglycemia. Herein, we interrogated whether and how SARS-CoV-2 causes ... ...

    Abstract Occurrence of hyperglycemia upon infection is associated with worse clinical outcome in COVID-19 patients. However, it is still unknown whether SARS-CoV-2 directly triggers hyperglycemia. Herein, we interrogated whether and how SARS-CoV-2 causes hyperglycemia by infecting hepatocytes and increasing glucose production. We performed a retrospective cohort study including patients that were admitted at a hospital with suspicion of COVID-19. Clinical and laboratory data were collected from the chart records and daily blood glucose values were analyzed to test the hypothesis on whether COVID-19 was independently associated with hyperglycemia. Blood glucose was collected from a subgroup of nondiabetic patients to assess pancreatic hormones.
    MeSH term(s) Humans ; COVID-19/complications ; SARS-CoV-2 ; Gluconeogenesis ; Blood Glucose ; Retrospective Studies ; Hepatocytes ; Hyperglycemia/complications ; Glucose
    Chemical Substances Blood Glucose ; Glucose (IY9XDZ35W2)
    Language English
    Publishing date 2023-05-15
    Publishing country United States
    Document type Journal Article ; Research Support, Non-U.S. Gov't
    ZDB-ID 209104-5
    ISSN 1091-6490 ; 0027-8424
    ISSN (online) 1091-6490
    ISSN 0027-8424
    DOI 10.1073/pnas.2217119120
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  3. Article ; Online: Adipocyte-specific mTORC2 deficiency impairs BAT and iWAT thermogenic capacity without affecting glucose uptake and energy expenditure in cold-acclimated mice.

    Castro, Érique / Vieira, Thayna S / Oliveira, Tiago E / Ortiz-Silva, Milene / Andrade, Maynara L / Tomazelli, Caroline A / Peixoto, Albert S / Sobrinho, Cleyton R / Moreno, Mayara F / Gilio, Gustavo R / Moreira, Rafael J / Guimarães, Raphael C / Perandini, Luiz A / Chimin, Patricia / Reckziegel, Patricia / Moretti, Eduardo H / Steiner, Alexandre A / Laplante, Mathieu / Festuccia, William T

    American journal of physiology. Endocrinology and metabolism

    2021  Volume 321, Issue 5, Page(s) E592–E605

    Abstract: Deletion of mechanistic target of rapamycin complex 2 (mTORC2) essential component rapamycin insensitive companion of mTOR (Rictor) by a Cre recombinase under control of the broad, nonadipocyte-specific aP2/FABP4 promoter impairs thermoregulation and ... ...

    Abstract Deletion of mechanistic target of rapamycin complex 2 (mTORC2) essential component rapamycin insensitive companion of mTOR (Rictor) by a Cre recombinase under control of the broad, nonadipocyte-specific aP2/FABP4 promoter impairs thermoregulation and brown adipose tissue (BAT) glucose uptake on acute cold exposure. We investigated herein whether adipocyte-specific mTORC2 deficiency affects BAT and inguinal white adipose tissue (iWAT) signaling, metabolism, and thermogenesis in cold-acclimated mice. For this, 8-wk-old male mice bearing Rictor deletion and therefore mTORC2 deficiency in adipocytes (adiponectin-Cre) and littermates controls were either kept at thermoneutrality (30 ± 1°C) or cold-acclimated (10 ± 1°C) for 14 days and evaluated for BAT and iWAT signaling, metabolism, and thermogenesis. Cold acclimation inhibited mTORC2 in BAT and iWAT, but its residual activity is still required for the cold-induced increases in BAT adipocyte number, total UCP-1 content and mRNA levels of proliferation markers Ki67 and cyclin 1 D, and de novo lipogenesis enzymes ATP-citrate lyase and acetyl-CoA carboxylase. In iWAT, mTORC2 residual activity is partially required for the cold-induced increases in multilocular adipocytes, mitochondrial mass, and uncoupling protein 1 (UCP-1) content. Conversely, BAT mTORC1 activity and BAT and iWAT glucose uptake were upregulated by cold independently of mTORC2. Noteworthy, the impairment in BAT and iWAT total UCP-1 content and thermogenic capacity induced by adipocyte mTORC2 deficiency had no major impact on whole body energy expenditure in cold-acclimated mice due to a compensatory activation of muscle shivering. In conclusion, adipocyte mTORC2 deficiency impairs, through different mechanisms, BAT and iWAT total UCP-1 content and thermogenic capacity in cold-acclimated mice, without affecting glucose uptake and whole body energy expenditure.
    MeSH term(s) Acclimatization/physiology ; Adipocytes/metabolism ; Adipose Tissue, Brown/physiology ; Adipose Tissue, White/physiology ; Animals ; Cold Temperature ; Energy Metabolism/physiology ; Gene Deletion ; Gene Expression Regulation/genetics ; Gene Expression Regulation/physiology ; Glucose/metabolism ; Male ; Mechanistic Target of Rapamycin Complex 2/deficiency ; Mechanistic Target of Rapamycin Complex 2/genetics ; Mice ; Mice, Inbred C57BL ; Thermogenesis/genetics ; Uncoupling Protein 1
    Chemical Substances Uncoupling Protein 1 ; Mechanistic Target of Rapamycin Complex 2 (EC 2.7.11.1) ; Glucose (IY9XDZ35W2)
    Language English
    Publishing date 2021-09-20
    Publishing country United States
    Document type Journal Article ; Research Support, Non-U.S. Gov't
    ZDB-ID 603841-4
    ISSN 1522-1555 ; 0193-1849
    ISSN (online) 1522-1555
    ISSN 0193-1849
    DOI 10.1152/ajpendo.00587.2020
    Database MEDical Literature Analysis and Retrieval System OnLINE

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