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Article ; Online: Caveolin-1 promotes mitochondrial health and limits mitochondrial ROS through ROCK/AMPK regulation of basal mitophagic flux.

Timmins, Logan R / Ortiz-Silva, Milene / Joshi, Bharat / Li, Y Lydia / Dickson, Fiona H / Wong, Timothy H / Vandevoorde, Kurt R / Nabi, Ivan R

FASEB journal : official publication of the Federation of American Societies for Experimental Biology

2023 Volume 38, Issue 1, Page(s) e23343

Abstract: Caveolin-1 (CAV1), the main structural component of caveolae, is phosphorylated at tyrosine-14 (pCAV1), regulates signal transduction, mechanotransduction, and mitochondrial function, and plays contrasting roles in cancer progression. We report that ... ...

Abstract	Caveolin-1 (CAV1), the main structural component of caveolae, is phosphorylated at tyrosine-14 (pCAV1), regulates signal transduction, mechanotransduction, and mitochondrial function, and plays contrasting roles in cancer progression. We report that CRISPR/Cas9 knockout (KO) of CAV1 increases mitochondrial oxidative phosphorylation, increases mitochondrial potential, and reduces ROS in MDA-MB-231 triple-negative breast cancer cells. Supporting a role for pCAV1, these effects are reversed upon expression of CAV1 phosphomimetic CAV1 Y14D but not non-phosphorylatable CAV1 Y14F. pCAV1 is a known effector of Rho-associated kinase (ROCK) signaling and ROCK1/2 signaling mediates CAV1 promotion of increased mitochondrial potential and decreased ROS production in MDA-MB-231 cells. CAV1/ROCK control of mitochondrial potential and ROS is caveolae-independent as similar results were observed in PC3 prostate cancer cells lacking caveolae. Increased mitochondrial health and reduced ROS in CAV1 KO MDA-MB-231 cells were reversed by knockdown of the autophagy protein ATG5, mitophagy regulator PINK1 or the mitochondrial fission protein Drp1 and therefore due to mitophagy. Use of the mitoKeima mitophagy probe confirmed that CAV1 signaling through ROCK inhibited basal mitophagic flux. Activation of AMPK, a major mitochondrial homeostasis protein inhibited by ROCK, is inhibited by CAV1-ROCK signaling and mediates the increased mitochondrial potential, decreased ROS, and decreased basal mitophagy flux observed in wild-type MDA-MB-231 cells. CAV1 regulation of mitochondrial health and ROS in cancer cells therefore occurs via ROCK-dependent inhibition of AMPK. This study therefore links pCAV1 signaling activity at the plasma membrane with its regulation of mitochondrial activity and cancer cell metabolism through control of mitophagy.
MeSH term(s)	Male ; Humans ; Caveolin 1/genetics ; Caveolin 1/metabolism ; AMP-Activated Protein Kinases/genetics ; AMP-Activated Protein Kinases/metabolism ; Reactive Oxygen Species/metabolism ; Mechanotransduction, Cellular ; Mitochondria/metabolism ; Prostatic Neoplasms/genetics ; Prostatic Neoplasms/metabolism ; Mitochondrial Proteins/metabolism ; rho-Associated Kinases/genetics ; rho-Associated Kinases/metabolism
Chemical Substances	Caveolin 1 ; AMP-Activated Protein Kinases (EC 2.7.11.31) ; Reactive Oxygen Species ; Mitochondrial Proteins ; ROCK1 protein, human (EC 2.7.11.1) ; rho-Associated Kinases (EC 2.7.11.1)
Language	English
Publishing date	2023-12-07
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	639186-2
ISSN	1530-6860 ; 0892-6638
ISSN (online)	1530-6860
ISSN	0892-6638
DOI	10.1096/fj.202201872RR
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Zs.A 2266: 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)
Zs.MO 296: Show issues

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Article ; Online: Membrane contact site detection (MCS-DETECT) reveals dual control of rough mitochondria-ER contacts.

Cardoen, Ben / Vandevoorde, Kurt R / Gao, Guang / Ortiz-Silva, Milene / Alan, Parsa / Liu, William / Tiliakou, Ellie / Vogl, A Wayne / Hamarneh, Ghassan / Nabi, Ivan R

The Journal of cell biology

2023 Volume 223, Issue 1

Abstract: Identification and morphological analysis of mitochondria-ER contacts (MERCs) by fluorescent microscopy is limited by subpixel resolution interorganelle distances. Here, the membrane contact site (MCS) detection algorithm, MCS-DETECT, reconstructs ... ...

Abstract	Identification and morphological analysis of mitochondria-ER contacts (MERCs) by fluorescent microscopy is limited by subpixel resolution interorganelle distances. Here, the membrane contact site (MCS) detection algorithm, MCS-DETECT, reconstructs subpixel resolution MERCs from 3D super-resolution image volumes. MCS-DETECT shows that elongated ribosome-studded riboMERCs, present in HT-1080 but not COS-7 cells, are morphologically distinct from smaller smooth contacts and larger contacts induced by mitochondria-ER linker expression in COS-7 cells. RiboMERC formation is associated with increased mitochondrial potential, reduced in Gp78 knockout HT-1080 cells and induced by Gp78 ubiquitin ligase activity in COS-7 and HeLa cells. Knockdown of riboMERC tether RRBP1 eliminates riboMERCs in both wild-type and Gp78 knockout HT-1080 cells. By MCS-DETECT, Gp78-dependent riboMERCs present complex tubular shapes that intercalate between and contact multiple mitochondria. MCS-DETECT of 3D whole-cell super-resolution image volumes, therefore, identifies novel dual control of tubular riboMERCs, whose formation is dependent on RRBP1 and size modulated by Gp78 E3 ubiquitin ligase activity.
MeSH term(s)	Humans ; Endoplasmic Reticulum/metabolism ; HeLa Cells ; Mitochondria/metabolism ; Mitochondrial Membranes/metabolism ; Ubiquitin-Protein Ligases/metabolism ; Ubiquitination ; COS Cells ; Animals ; Chlorocebus aethiops ; Ribosomes/metabolism
Chemical Substances	Ubiquitin-Protein Ligases (EC 2.3.2.27)
Language	English
Publishing date	2023-11-10
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	218154-x
ISSN	1540-8140 ; 0021-9525
ISSN (online)	1540-8140
ISSN	0021-9525
DOI	10.1083/jcb.202206109
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Article ; Online: Chloroquine attenuates diet-induced obesity and glucose intolerance through a mechanism that might involve FGF-21, but not UCP-1-mediated thermogenesis and inhibition of adipocyte autophagy.

Ortiz-Silva, Milene / Leonardi, Bianca F / Castro, Érique / Peixoto, Álbert S / Gilio, Gustavo R / Oliveira, Tiago E / Tomazelli, Caroline A / Andrade, Maynara L / Moreno, Mayara F / Belchior, Thiago / Magdalon, Juliana / Vieira, Thayna S / Donado-Pestana, Carlos M / Festuccia, William T

Molecular and cellular endocrinology

2023 Volume 578, Page(s) 112074

Abstract: Chloroquine diphosphate (CQ), a weak base used to inhibit autophagic flux and treat malaria and rheumatoid diseases, has been shown, through unknown mechanisms, to improve glucose and lipid homeostasis in patients and rodents. We investigate herein the ... ...

Abstract	Chloroquine diphosphate (CQ), a weak base used to inhibit autophagic flux and treat malaria and rheumatoid diseases, has been shown, through unknown mechanisms, to improve glucose and lipid homeostasis in patients and rodents. We investigate herein the molecular mechanisms underlying these CQ beneficial metabolic actions in diet-induced obese mice. For this, C57BL6/J mice fed with either a chow or a high-fat diet (HFD) and uncoupling protein 1 (UCP-1) KO and adipocyte Atg7-deficient mice fed with a HFD were treated or not with CQ (60 mg/kg of body weight/day) during 8 weeks and evaluated for body weight, adiposity, glucose homeostasis and brown and white adipose tissues (BAT and WAT) UCP-1 content. CQ reduced body weight gain and adipose tissue and liver masses in mice fed with a HFD, without altering food intake, oxygen consumption, respiratory exchange ratio, spontaneous motor activity and feces caloric content. CQ attenuated the insulin intolerance, hyperglycemia, hyperinsulinemia, hypertriglyceridemia and hypercholesterolemia induced by HFD intake, such effects that were associated with increases in serum and liver fibroblast growth factor 21 (FGF-21) and BAT and WAT UCP-1 content. Interestingly, CQ beneficial metabolic actions of reducing body weight and adiposity and improving glucose homeostasis were preserved in HFD-fed UCP-1 KO and adipocyte Atg7 deficient mice. CQ reduces body weight gain and adiposity and improves glucose homeostasis in diet-induced obese mice through mechanisms that might involve FGF-21, but not UCP1-mediated nonshivering thermogenesis or inhibition of adipocyte autophagy.
Language	English
Publishing date	2023-09-22
Publishing country	Ireland
Document type	Journal Article
ZDB-ID	187438-x
ISSN	1872-8057 ; 0303-7207
ISSN (online)	1872-8057
ISSN	0303-7207
DOI	10.1016/j.mce.2023.112074
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Article ; Online: Hepatocellular carcinoma induced by hepatocyte Pten deletion reduces BAT UCP-1 and thermogenic capacity in mice, despite increasing serum FGF-21 and iWAT browning.

Peixoto, Álbert S / Moreno, Mayara F / Castro, Érique / Perandini, Luiz A / Belchior, Thiago / Oliveira, Tiago E / Vieira, Thayna S / Gilio, Gustavo R / Tomazelli, Caroline A / Leonardi, Bianca F / Ortiz-Silva, Milene / Silva Junior, Luciano P / Moretti, Eduardo H / Steiner, Alexandre A / Festuccia, William T

Journal of physiology and biochemistry

2023 Volume 79, Issue 4, Page(s) 731–743

Abstract: Hepatocellular carcinoma (HCC) markedly enhances liver secretion of fibroblast growth factor 21 (FGF-21), a hepatokine that increases brown and subcutaneous inguinal white adipose tissues (BAT and iWAT, respectively) uncoupling protein 1 (UCP-1) content, ...

Abstract	Hepatocellular carcinoma (HCC) markedly enhances liver secretion of fibroblast growth factor 21 (FGF-21), a hepatokine that increases brown and subcutaneous inguinal white adipose tissues (BAT and iWAT, respectively) uncoupling protein 1 (UCP-1) content, thermogenesis and energy expenditure. Herein, we tested the hypothesis that an enhanced BAT and iWAT UCP-1-mediated thermogenesis induced by high levels of FGF-21 is involved in HCC-associated catabolic state and fat mass reduction. For this, we evaluated body weight and composition, liver mass and morphology, serum and tissue levels of FGF-21, BAT and iWAT UCP-1 content, and thermogenic capacity in mice with Pten deletion in hepatocytes that display a well-defined progression from steatosis to steatohepatitis (NASH) and HCC upon aging. Hepatocyte Pten deficiency promoted a progressive increase in liver lipid deposition, mass, and inflammation, culminating with NASH at 24 weeks and hepatomegaly and HCC at 48 weeks of age. NASH and HCC were associated with elevated liver and serum FGF-21 content and iWAT UCP-1 expression (browning), but reduced serum insulin, leptin, and adiponectin levels and BAT UCP-1 content and expression of sympathetically regulated gene glycerol kinase (GyK), lipoprotein lipase (LPL), and fatty acid transporter protein 1 (FATP-1), which altogether resulted in an impaired whole-body thermogenic capacity in response to CL-316,243. In conclusion, FGF-21 pro-thermogenic actions in BAT are context-dependent, not occurring in NASH and HCC, and UCP-1-mediated thermogenesis is not a major energy-expending process involved in the catabolic state associated with HCC induced by Pten deletion in hepatocytes.
MeSH term(s)	Mice ; Animals ; Carcinoma, Hepatocellular/metabolism ; Uncoupling Protein 1/genetics ; Uncoupling Protein 1/metabolism ; Adipose Tissue, Brown/metabolism ; Non-alcoholic Fatty Liver Disease/metabolism ; Liver Neoplasms/metabolism ; Hepatocytes ; Thermogenesis/genetics ; Adipose Tissue, White/metabolism
Chemical Substances	fibroblast growth factor 21 ; Uncoupling Protein 1
Language	English
Publishing date	2023-07-05
Publishing country	Spain
Document type	Journal Article
ZDB-ID	1325104-1
ISSN	1877-8755 ; 0034-9402 ; 1138-7548
ISSN (online)	1877-8755
ISSN	0034-9402 ; 1138-7548
DOI	10.1007/s13105-023-00970-4
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Article: Human Cachexia Induces Changes in Mitochondria, Autophagy and Apoptosis in the Skeletal Muscle.

de Castro, Gabriela S / Simoes, Estefania / Lima, Joanna D C C / Ortiz-Silva, Milene / Festuccia, William T / Tokeshi, Flávio / Alcântara, Paulo S / Otoch, José P / Coletti, Dario / Seelaender, Marilia

Cancers

2019 Volume 11, Issue 9

Abstract: Cachexia is a wasting syndrome characterized by the continuous loss of skeletal muscle mass due to imbalance between protein synthesis and degradation, which is related with poor prognosis and compromised quality of life. Dysfunctional mitochondria are ... ...

Abstract	Cachexia is a wasting syndrome characterized by the continuous loss of skeletal muscle mass due to imbalance between protein synthesis and degradation, which is related with poor prognosis and compromised quality of life. Dysfunctional mitochondria are associated with lower muscle strength and muscle atrophy in cancer patients, yet poorly described in human cachexia. We herein investigated mitochondrial morphology, autophagy and apoptosis in the skeletal muscle of patients with gastrointestinal cancer-associated cachexia (CC), as compared with a weight-stable cancer group (WSC). CC showed prominent weight loss and increased circulating levels of serum C-reactive protein, lower body mass index and decreased circulating hemoglobin, when compared to WSC. Electron microscopy analysis revealed an increase in intermyofibrillar mitochondrial area in CC, as compared to WSC. Relative gene expression of Fission 1, a protein related to mitochondrial fission, was increased in CC, as compared to WSC. LC3 II, autophagy-related (ATG) 5 and 7 essential proteins for autophagosome formation, presented higher content in the cachectic group. Protein levels of phosphorylated p53 (Ser46), activated caspase 8 (Asp384) and 9 (Asp315) were also increased in the skeletal muscle of CC. Overall, our results demonstrate that human cancer-associated cachexia leads to exacerbated muscle-stress response that may culminate in muscle loss, which is in part due to disruption of mitochondrial morphology, dysfunctional autophagy and increased apoptosis. To the best of our knowledge, this is the first report showing quantitative morphological alterations in skeletal muscle mitochondria in cachectic patients.
Language	English
Publishing date	2019-08-28
Publishing country	Switzerland
Document type	Journal Article
ZDB-ID	2527080-1
ISSN	2072-6694
ISSN	2072-6694
DOI	10.3390/cancers11091264
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Article: PPARγ-induced upregulation of subcutaneous fat adiponectin secretion, glyceroneogenesis and BCAA oxidation requires mTORC1 activity

Biochimica et biophysica acta. 2021 Aug., v. 1866, no. 8

2021

Abstract: The nutrient sensors peroxisome proliferator-activated receptor γ (PPARγ) and mechanistic target of rapamycin complex 1 (mTORC1) closely interact in the regulation of adipocyte lipid storage. The precise mechanisms underlying this interaction and whether ...

Abstract	The nutrient sensors peroxisome proliferator-activated receptor γ (PPARγ) and mechanistic target of rapamycin complex 1 (mTORC1) closely interact in the regulation of adipocyte lipid storage. The precise mechanisms underlying this interaction and whether this extends to other metabolic processes and the endocrine function of adipocytes are still unknown. We investigated herein the involvement of mTORC1 as a mediator of the actions of the PPARγ ligand rosiglitazone in subcutaneous inguinal white adipose tissue (iWAT) mass, endocrine function, lipidome, transcriptome and branched-chain amino acid (BCAA) metabolism. Mice bearing regulatory associated protein of mTOR (Raptor) deletion and therefore mTORC1 deficiency exclusively in adipocytes and littermate controls were fed a high-fat diet supplemented or not with the PPARγ agonist rosiglitazone (30 mg/kg/day) for 8 weeks and evaluated for iWAT mass, lipidome, transcriptome (Rnaseq), respiration and BCAA metabolism. Adipocyte mTORC1 deficiency not only impaired iWAT adiponectin transcription, synthesis and secretion, PEPCK mRNA levels, triacylglycerol synthesis and BCAA oxidation and mRNA levels of related proteins but also completely blocked the upregulation in these processes induced by pharmacological PPARγ activation with rosiglitazone. Mechanistically, adipocyte mTORC1 deficiency impairs PPARγ transcriptional activity by reducing PPARγ protein content, as well as by downregulating C/EBPα, a co-partner and facilitator of PPARγ. In conclusion, mTORC1 and PPARγ are essential partners involved in the regulation of subcutaneous adipose tissue adiponectin production and secretion and BCAA oxidative metabolism.
Keywords	adipocytes ; adiponectin ; aerobiosis ; agonists ; amino acids ; glyceroneogenesis ; high fat diet ; ligands ; oxidation ; protein content ; rapamycin ; subcutaneous fat ; transcription (genetics) ; transcriptome ; triacylglycerols ; white adipose tissue
Language	English
Dates of publication	2021-08
Publishing place	Elsevier B.V.
Document type	Article
Note	NAL-AP-2-clean
ISSN	1388-1981
DOI	10.1016/j.bbalip.2021.158967
Database	NAL-Catalogue (AGRICOLA)

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Article ; Online: Akt activation by insulin treatment attenuates cachexia in Walker-256 tumor-bearing rats.

de Fatima Silva, Flaviane / de Morais, Hely / Ortiz Silva, Milene / da Silva, Francemilson Goulart / Vianna Croffi, Rafael / Serrano-Nascimento, Caroline / Rodrigues Graciano, Maria Fernanda / Rafael Carpinelli, Angelo / Barbosa Bazotte, Roberto / de Souza, Helenir Medri

Journal of cellular biochemistry

2020 Volume 121, Issue 11, Page(s) 4558–4568

Abstract: Cancer-bearing often exhibits hypoinsulinemia, insulin (INS) resistance and glutamine depletion associated with cachexia. However, INS and glutamine effects on cachexia metabolic abnormalities, particularly on tumor-affected proteins related to INS ... ...

Abstract	Cancer-bearing often exhibits hypoinsulinemia, insulin (INS) resistance and glutamine depletion associated with cachexia. However, INS and glutamine effects on cachexia metabolic abnormalities, particularly on tumor-affected proteins related to INS resistance, are poorly known. The main purpose of this study was to investigate the effects of INS and glutamine dipeptide (GDP) treatments on phospho-protein kinase B (p-Akt), and phospho-hormone sensitive lipase (p-HSL) in Walker-256 tumor-bearing rats. INS (NPH, 40 UI/kg, subcutaneous), GDP (1.5 g/kg, oral), INS+GDP or vehicle (control rats) were administered for 13 days, once a day, starting at the day of inoculation of tumor cells. The experiments were performed 4 hours after the last treatment to evaluate acute effects of INS and GDP, besides the chronic effects. INS and/or INS+GDP treatments, which markedly increased the insulinemia, increased the p-Akt: total Akt ratio and prevented the increased p-HSL
MeSH term(s)	Animals ; Blood Glucose/analysis ; Cachexia/drug therapy ; Cachexia/etiology ; Cachexia/metabolism ; Cachexia/pathology ; Carcinoma 256, Walker/complications ; Carcinoma 256, Walker/pathology ; Drug Therapy, Combination ; Glutamine/pharmacology ; Hypoglycemic Agents/pharmacology ; Insulin/pharmacology ; Insulin Resistance ; Male ; Proto-Oncogene Proteins c-akt/genetics ; Proto-Oncogene Proteins c-akt/metabolism ; Rats ; Rats, Wistar
Chemical Substances	Blood Glucose ; Hypoglycemic Agents ; Insulin ; Glutamine (0RH81L854J) ; Proto-Oncogene Proteins c-akt (EC 2.7.11.1)
Language	English
Publishing date	2020-02-14
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	392402-6
ISSN	1097-4644 ; 0730-2312
ISSN (online)	1097-4644
ISSN	0730-2312
DOI	10.1002/jcb.29682
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Zs.A 1114: Show issues

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Article ; Online: PPARγ-induced upregulation of subcutaneous fat adiponectin secretion, glyceroneogenesis and BCAA oxidation requires mTORC1 activity.

Biochimica et biophysica acta. Molecular and cell biology of lipids

2021 Volume 1866, Issue 8, Page(s) 158967

Abstract	The nutrient sensors peroxisome proliferator-activated receptor γ (PPARγ) and mechanistic target of rapamycin complex 1 (mTORC1) closely interact in the regulation of adipocyte lipid storage. The precise mechanisms underlying this interaction and whether this extends to other metabolic processes and the endocrine function of adipocytes are still unknown. We investigated herein the involvement of mTORC1 as a mediator of the actions of the PPARγ ligand rosiglitazone in subcutaneous inguinal white adipose tissue (iWAT) mass, endocrine function, lipidome, transcriptome and branched-chain amino acid (BCAA) metabolism. Mice bearing regulatory associated protein of mTOR (Raptor) deletion and therefore mTORC1 deficiency exclusively in adipocytes and littermate controls were fed a high-fat diet supplemented or not with the PPARγ agonist rosiglitazone (30 mg/kg/day) for 8 weeks and evaluated for iWAT mass, lipidome, transcriptome (Rnaseq), respiration and BCAA metabolism. Adipocyte mTORC1 deficiency not only impaired iWAT adiponectin transcription, synthesis and secretion, PEPCK mRNA levels, triacylglycerol synthesis and BCAA oxidation and mRNA levels of related proteins but also completely blocked the upregulation in these processes induced by pharmacological PPARγ activation with rosiglitazone. Mechanistically, adipocyte mTORC1 deficiency impairs PPARγ transcriptional activity by reducing PPARγ protein content, as well as by downregulating C/EBPα, a co-partner and facilitator of PPARγ. In conclusion, mTORC1 and PPARγ are essential partners involved in the regulation of subcutaneous adipose tissue adiponectin production and secretion and BCAA oxidative metabolism.
MeSH term(s)	Adiponectin/metabolism ; Amino Acids, Branched-Chain/metabolism ; Animals ; Glycerol/metabolism ; Mechanistic Target of Rapamycin Complex 1/metabolism ; Mice ; Oxidation-Reduction ; PPAR gamma/metabolism ; Subcutaneous Fat/metabolism ; Up-Regulation
Chemical Substances	Adiponectin ; Amino Acids, Branched-Chain ; PPAR gamma ; Mechanistic Target of Rapamycin Complex 1 (EC 2.7.11.1) ; Glycerol (PDC6A3C0OX)
Language	English
Publishing date	2021-05-15
Publishing country	Netherlands
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	60-7
ISSN	1879-2618 ; 1879-2596 ; 1879-260X ; 1872-8006 ; 1879-2642 ; 1879-2650 ; 0006-3002 ; 0005-2728 ; 0005-2736 ; 0304-4165 ; 0167-4838 ; 1388-1981 ; 0167-4889 ; 0167-4781 ; 0304-419X ; 1570-9639 ; 0925-4439 ; 1874-9399
ISSN (online)	1879-2618 ; 1879-2596 ; 1879-260X ; 1872-8006 ; 1879-2642 ; 1879-2650
ISSN	0006-3002 ; 0005-2728 ; 0005-2736 ; 0304-4165 ; 0167-4838 ; 1388-1981 ; 0167-4889 ; 0167-4781 ; 0304-419X ; 1570-9639 ; 0925-4439 ; 1874-9399
DOI	10.1016/j.bbalip.2021.158967
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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
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Article ; Online: Effects of metformin on insulin resistance and metabolic disorders in tumor-bearing rats with advanced cachexia.

de Fatima Silva, Flaviane / Ortiz-Silva, Milene / Galia, Winny Beatriz de Souza / Cassolla, Priscila / da Silva, Francemilson Goulart / Graciano, Maria Fernanda Rodrigues / Carpinelli, Angelo Rafael / de Souza, Helenir Medri

Canadian journal of physiology and pharmacology

2018 Volume 96, Issue 5, Page(s) 498–505

Abstract: Metformin (MET) is widely used in the correction of insulin (INS) resistance and metabolic abnormalities in type 2 diabetes. However, its effect on INS resistance and metabolic disorders associated with cancer cachexia is not established. We investigated ...

Abstract	Metformin (MET) is widely used in the correction of insulin (INS) resistance and metabolic abnormalities in type 2 diabetes. However, its effect on INS resistance and metabolic disorders associated with cancer cachexia is not established. We investigated the MET effects, isolated or associated with INS, on INS resistance and metabolic changes induced by Walker-256 tumor in rats with advanced cachexia. MET (500 mg·kg
MeSH term(s)	Animals ; Cachexia/complications ; Cachexia/drug therapy ; Cachexia/metabolism ; Cachexia/pathology ; Insulin/metabolism ; Insulin Resistance ; Male ; Metformin/pharmacology ; Metformin/therapeutic use ; Neoplasms/complications ; Proto-Oncogene Proteins c-akt/metabolism ; Rats ; Rats, Wistar ; Signal Transduction/drug effects
Chemical Substances	Insulin ; Metformin (9100L32L2N) ; Proto-Oncogene Proteins c-akt (EC 2.7.11.1)
Language	English
Publishing date	2018-01-05
Publishing country	Canada
Document type	Journal Article
ZDB-ID	127527-6
ISSN	1205-7541 ; 0008-4212
ISSN (online)	1205-7541
ISSN	0008-4212
DOI	10.1139/cjpp-2017-0171
Database	MEDical Literature Analysis and Retrieval System OnLINE

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