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  • 1
    Online Resource
    Online Resource
    Liver Derived FGF21 Maintains Core Body Temperature During Acute Cold Exposure
    Springer Science and Business Media LLC ; 2019
    In:  Scientific Reports Vol. 9, No. 1 ( 2019-01-24)
    Details
    In: Scientific Reports, Springer Science and Business Media LLC, Vol. 9, No. 1 ( 2019-01-24)
    Abstract: Fibroblast Growth Factor 21 (FGF21) elicits an array of metabolic effects. However, the physiological role of FGF21 during thermal challenges is not clear. In this study, we assessed the tissue source of FGF21 and its site of action to regulate core body temperature in response to cold. Using mice lacking FGF21 specifically in the liver (FGF21 LivKO) or adipose tissues (FGF21 AdipoKO), we performed a series of cold exposure studies to examine the tissue specific induction of FGF21 in response to cold. We also examined the physiological site of FGF21 action during cold exposure by impairing FGF21 signaling to adipose tissues or the central nervous system (CNS) using genetic ablation of the FGF21 co-receptor β-klotho in adipose tissues (KLB AdipoKO) or pharmacological blockage of FGF21 signaling. We found that only liver-derived FGF21 enters circulation during acute cold exposure and is critical for thermoregulation. While FGF21 signaling directly to adipose tissues during cold is dispensable for thermoregulation, central FGF21 signaling is necessary for maximal sympathetic drive to brown adipose tissue to maintain thermoregulation during cold. These data demonstrate a previously unrecognized role for FGF21 in the maintenance of body temperature in response to cold.
    Type of Medium: Online Resource
    ISSN: 2045-2322
    URL: Article
    DOI: 10.1038/s41598-018-37198-y
    Language: English
    Publisher: Springer Science and Business Media LLC
    Publication Date: 2019
    detail.hit.zdb_id: 2615211-3
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  • 2
    Online Resource
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    MEKK2 regulates focal adhesion stability and motility in invasive breast cancer cells
    Elsevier BV ; 2014
    In:  Biochimica et Biophysica Acta (BBA) - Molecular Cell Research Vol. 1843, No. 5 ( 2014-05), p. 945-954
    Details
    In: Biochimica et Biophysica Acta (BBA) - Molecular Cell Research, Elsevier BV, Vol. 1843, No. 5 ( 2014-05), p. 945-954
    Type of Medium: Online Resource
    ISSN: 0167-4889
    URL: Article
    DOI: 10.1016/j.bbamcr.2014.01.029
    RVK:
    WA 15000
    Language: English
    Publisher: Elsevier BV
    Publication Date: 2014
    detail.hit.zdb_id: 2209512-3
    SSG: 12
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  • 3
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    Circulating FGF21 Is Liver Derived and Enhances Glucose Uptake During Refeeding and Overfeeding
    American Diabetes Association ; 2014
    In:  Diabetes Vol. 63, No. 12 ( 2014-12-01), p. 4057-4063
    Details
    In: Diabetes, American Diabetes Association, Vol. 63, No. 12 ( 2014-12-01), p. 4057-4063
    Abstract: Fibroblast growth factor (FGF)21 is an endocrine hormone that is expressed in multiple tissues and functions physiologically to maintain energy homeostasis. FGF21 is being pursued as a therapeutic target for diabetes and obesity because of its rapid and potent effects on improving insulin sensitivity. However, whether FGF21 enhances insulin sensitivity under physiologic conditions remains unclear. Here, we show that liver-derived FGF21 enters the circulation during fasting but also remains present and functional during the early stage of refeeding. After a prolonged fast, FGF21 acts as an insulin sensitizer to overcome the peripheral insulin resistance induced by fasting, thereby maximizing glucose uptake. Likewise, FGF21 is produced from the liver during overfeeding and mitigates peripheral insulin resistance. DIO FGF21 liver-specific knockout, but not FGF21 adipose-specific knockout, mice have increased insulin resistance and decreased brown adipose tissue–mediated glucose disposal. These data are compatible with the concept that FGF21 functions physiologically as an insulin sensitizer under conditions of acute refeeding and overfeeding.
    Type of Medium: Online Resource
    ISSN: 0012-1797 , 1939-327X
    URL: Article
    DOI: 10.2337/db14-0595
    Language: English
    Publisher: American Diabetes Association
    Publication Date: 2014
    detail.hit.zdb_id: 1501252-9
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  • 4
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    Fat and Iron Don't Mix
    Ovid Technologies (Wolters Kluwer Health) ; 2020
    In:  Immunometabolism Vol. 2, No. 4 ( 2020-10-08)
    Details
    In: Immunometabolism, Ovid Technologies (Wolters Kluwer Health), Vol. 2, No. 4 ( 2020-10-08)
    Abstract: Low-grade chronic adipose tissue (AT) inflammation is now recognized as a pivotal driver of the multi-organ dysfunction associated with obesity-related complications; and adipose tissue macrophages (ATMs) are key to the development of this inflammatory milieu. Along with their role in immunosurveillance, ATMs are central regulators of AT iron homeostasis. Under optimal conditions, ATMs maintain a proper homeostatic balance of iron in adipocytes; however, during obesity, this relationship is altered, and iron is repartitioned into adipocytes as opposed to ATMs. This adipocyte iron overload leads to systemic IR and the mechanism for these effects is still under investigation. Here, we comment on the most recent findings addressing the interplay between adipocyte and ATM iron handling, and metabolic dysfunction.
    Type of Medium: Online Resource
    ISSN: 2633-0407
    URL: Article
    DOI: 10.20900/immunometab20200034
    Language: English
    Publisher: Ovid Technologies (Wolters Kluwer Health)
    Publication Date: 2020
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  • 5
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    FGF21 Regulates Metabolism Through Adipose-Dependent and -Independent Mechanisms
    Elsevier BV ; 2017
    In:  Cell Metabolism Vol. 25, No. 4 ( 2017-04), p. 935-944.e4
    Details
    In: Cell Metabolism, Elsevier BV, Vol. 25, No. 4 ( 2017-04), p. 935-944.e4
    Type of Medium: Online Resource
    ISSN: 1550-4131
    URL: Article
    DOI: 10.1016/j.cmet.2017.03.005
    Language: English
    Publisher: Elsevier BV
    Publication Date: 2017
    detail.hit.zdb_id: 2174469-5
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  • 6
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    Prevalence, Resistance Mechanisms, and Susceptibility of Multidrug-Resistant Bloodstream Isolates of Pseudomonas aeruginosa
    American Society for Microbiology ; 2010
    In:  Antimicrobial Agents and Chemotherapy Vol. 54, No. 3 ( 2010-03), p. 1160-1164
    Details
    In: Antimicrobial Agents and Chemotherapy, American Society for Microbiology, Vol. 54, No. 3 ( 2010-03), p. 1160-1164
    Abstract: Pseudomonas aeruginosa is an important pathogen commonly implicated in nosocomial infections. The occurrence of multidrug-resistant (MDR) P. aeruginosa strains is increasing worldwide and limiting our therapeutic options. The MDR phenotype can be mediated by a variety of resistance mechanisms, and the corresponding relative biofitness is not well established. We examined the prevalence, resistance mechanisms, and susceptibility of MDR P. aeruginosa isolates (resistant to ≥3 classes of antipseudomonal agents [penicillins/cephalosporins, carbapenems, quinolones, and aminoglycosides]) obtained from a large, university-affiliated hospital. Among 235 nonrepeat bloodstream isolates screened between 2005 and 2007, 33 isolates (from 20 unique patients) were found to be MDR (crude prevalence rate, 14%). All isolates were resistant to carbapenems and quinolones, 91% were resistant to penicillins/cephalosporins, and 21% were resistant to the aminoglycosides. By using the first available isolate for each bacteremia episode ( n = 18), 13 distinct clones were revealed by repetitive-element-based PCR. Western blotting revealed eight isolates (44%) to have MexB overexpression. Production of a carbapenemase (VIM-2) was found in one isolate, and mutations in gyrA (T83I) and parC (S87L) were commonly found. Growth rates of most MDR isolates were similar to that of the wild type, and two isolates (11%) were found to be hypermutable. All available isolates were susceptible to polymyxin B, and only one isolate was nonsusceptible to colistin (MIC, 3 mg/liter), but all isolates were nonsusceptible to doripenem (MIC, 〉 2 mg/liter). Understanding and continuous monitoring of the prevalence and resistance mechanisms of MDR P. aeruginosa would enable us to formulate rational treatment strategies to combat nosocomial infections.
    Type of Medium: Online Resource
    ISSN: 0066-4804 , 1098-6596
    URL: Article
    DOI: 10.1128/AAC.01446-09
    RVK:
    XA 24552
    Language: English
    Publisher: American Society for Microbiology
    Publication Date: 2010
    detail.hit.zdb_id: 1496156-8
    SSG: 12
    SSG: 15,3
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  • 7
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    High CD8 T-Cell Receptor Clonality and Altered CDR3 Properties Are Associated With Elevated Isolevuglandins in Adipose Tissue During Diet-Induced Obesity
    American Diabetes Association ; 2018
    In:  Diabetes Vol. 67, No. 11 ( 2018-11-01), p. 2361-2376
    Details
    In: Diabetes, American Diabetes Association, Vol. 67, No. 11 ( 2018-11-01), p. 2361-2376
    Abstract: Adipose tissue (AT) CD4+ and CD8+ T cells contribute to obesity-associated insulin resistance. Prior studies identified conserved T-cell receptor (TCR) chain families in obese AT, but the presence and clonal expansion of specific TCR sequences in obesity has not been assessed. We characterized AT and liver CD8+ and CD4+ TCR repertoires of mice fed a low-fat diet (LFD) and high-fat diet (HFD) using deep sequencing of the TCRβ chain to quantify clonal expansion, gene usage, and CDR3 sequence. In AT CD8+ T cells, HFD reduced TCR diversity, increased the prevalence of public TCR clonotypes, and selected for TCR CDR3 regions enriched in positively charged and less polarized amino acids. Although TCR repertoire alone could distinguish between LFD- and HFD-fed mice, these properties of the CDR3 region of AT CD8+ T cells from HFD-fed mice led us to examine the role of negatively charged and nonpolar isolevuglandin (isoLG) adduct-containing antigen-presenting cells within AT. IsoLG-adducted protein species were significantly higher in AT macrophages of HFD-fed mice; isoLGs were elevated in M2-polarized macrophages, promoting CD8+ T-cell activation. Our findings demonstrate that clonal TCR expansion that favors positively charged CDR3s accompanies HFD-induced obesity, which may be an antigen-driven response to isoLG accumulation in macrophages.
    Type of Medium: Online Resource
    ISSN: 0012-1797 , 1939-327X
    URL: Article
    DOI: 10.2337/db18-0040
    Language: English
    Publisher: American Diabetes Association
    Publication Date: 2018
    detail.hit.zdb_id: 1501252-9
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  • 8
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    An Iron Refractory Phenotype in Obese Adipose Tissue Macrophages Leads to Adipocyte Iron Overload
    MDPI AG ; 2022
    In:  International Journal of Molecular Sciences Vol. 23, No. 13 ( 2022-07-03), p. 7417-
    Details
    In: International Journal of Molecular Sciences, MDPI AG, Vol. 23, No. 13 ( 2022-07-03), p. 7417-
    Abstract: Adipocyte iron overload is a maladaptation associated with obesity and insulin resistance. The objective of the current study was to determine whether and how adipose tissue macrophages (ATMs) regulate adipocyte iron concentrations and whether this is impacted by obesity. Using bone marrow-derived macrophages (BMDMs) polarized to M0, M1, M2, or metabolically activated (MMe) phenotypes, we showed that MMe BMDMs and ATMs from obese mice have reduced expression of several iron-related proteins. Furthermore, the bioenergetic response to iron in obese ATMs was hampered. ATMs from iron-injected lean mice increased their glycolytic and respiratory capacities, thus maintaining metabolic flexibility, while ATMs from obese mice did not. Using an isotope-based system, we found that iron exchange between BMDMs and adipocytes was regulated by macrophage phenotype. At the end of the co-culture, MMe macrophages transferred and received more iron from adipocytes than M0, M1, and M2 macrophages. This culminated in a decrease in total iron in MMe macrophages and an increase in total iron in adipocytes compared with M2 macrophages. Taken together, in the MMe condition, the redistribution of iron is biased toward macrophage iron deficiency and simultaneous adipocyte iron overload. These data suggest that obesity changes the communication of iron between adipocytes and macrophages and that rectifying this iron communication channel may be a novel therapeutic target to alleviate insulin resistance.
    Type of Medium: Online Resource
    ISSN: 1422-0067
    URL: Article
    DOI: 10.3390/ijms23137417
    Language: English
    Publisher: MDPI AG
    Publication Date: 2022
    detail.hit.zdb_id: 2019364-6
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  • 9
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    Metabolic and mitochondrial dysregulation in CD4+ T cells from HIV-positive women on combination anti-retroviral therapy
    Public Library of Science (PLoS) ; 2023
    In:  PLOS ONE Vol. 18, No. 10 ( 2023-10-10), p. e0286436-
    Details
    In: PLOS ONE, Public Library of Science (PLoS), Vol. 18, No. 10 ( 2023-10-10), p. e0286436-
    Abstract: For optimal functionality, immune cells require a robust and adaptable metabolic program that is fueled by dynamic mitochondrial activity. In this study, we investigate the metabolic alterations occurring in immune cells during HIV infection and antiretroviral therapy by analyzing the uptake of metabolic substrates and mitochondrial phenotypes. By delineating changes in immune cell metabolic programming during HIV, we may identify novel potential therapeutic targets to improve anti-viral immune responses. Methods After consent and voluntary participation was confirmed, whole blood was drawn from HIV uninfected women and women with chronic HIV infection on long-term combination antiretroviral therapy (HIV/cART). Peripheral blood mononuclear cells-derived immune cells were directly incubated with different fluorescently tagged metabolites and markers of mitochondrial activity: FITC-2-NBDG (2-[N-(7-nitrobenz-2-oxa-1,3-diazol-4-yl) amino]-2-deoxy-D-glucose), FITC-BODIPY (4,4-Difluoro-5,7-Dimethyl-4-Bora-3a,4a-Diaza-s-Indacene-3-Hexadecanoic Acid), FITC-MitoTracker Green and APC-MitoTracker Deep Red. The uptake of glucose and fats and the mitochondrial mass and potential were measured using flow cytometry. All values are reported quantitatively as geometric means of fluorescence intensity. Results During chronic HIV infection, cellular uptake of glucose increases in HIV + dendritic cells in particular. CD4 + T cells had the lowest uptake of glucose and fats compared to all other cells regardless of HIV status, while CD8 + T cells took up more fatty acids. Interestingly, despite the lower utilization of glucose and fats in CD4 + T cells, mitochondrial mass increased in HIV + CD4 + T cells compared to HIV negative CD4 + T-cells. HIV + CD4 + T cells also had the highest mitochondrial potential. Conclusions Significant disparities in the utilization of substrates by leukocytes during chronic HIV/cART exist. Innate immune cells increased utilization of sugars and fats while adaptive immune cells displayed lower glucose and fat utilization despite having a higher mitochondrial activity. Our findings suggest that cART treated HIV-infected CD4 + T cells be dysfunctional or may prefer alternative fuel sources not included in these studies. This underscores the importance of understanding the metabolic effects of HIV treatment on immune function.
    Type of Medium: Online Resource
    ISSN: 1932-6203
    URL: Article
    URL: Article
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    DOI: 10.1371/journal.pone.0286436
    DOI: 10.1371/journal.pone.0286436.g001
    DOI: 10.1371/journal.pone.0286436.g002
    DOI: 10.1371/journal.pone.0286436.g003
    DOI: 10.1371/journal.pone.0286436.g004
    DOI: 10.1371/journal.pone.0286436.t001
    DOI: 10.1371/journal.pone.0286436.s001
    DOI: 10.1371/journal.pone.0286436.s002
    DOI: 10.1371/journal.pone.0286436.s003
    DOI: 10.1371/journal.pone.0286436.s004
    Language: English
    Publisher: Public Library of Science (PLoS)
    Publication Date: 2023
    detail.hit.zdb_id: 2267670-3
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  • 10
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    The MEKK1 SWIM domain is a novel substrate receptor for c-Jun ubiquitylation
    Portland Press Ltd. ; 2012
    In:  Biochemical Journal Vol. 445, No. 3 ( 2012-08-01), p. 431-439
    Details
    In: Biochemical Journal, Portland Press Ltd., Vol. 445, No. 3 ( 2012-08-01), p. 431-439
    Abstract: MEKK1 [MAPK (mitogen-activated protein kinase)/ERK (extracellular-signal-regulated kinase) kinase kinase 1] is a MAP3K (MAPK kinase kinase) that regulates MAPK activation, and is the only known mammalian kinase that is also a ubiquitin ligase. MEKK1 contains a RING domain within its N-terminal regulatory region, and MEKK1 has been shown to ubiquitylate th e AP-1 (activator protein 1) transcription factor protein c-Jun, but the mechanism by which MEKK1 interacts with c-Jun to induce ubiquitylation has not been defined. Proximal to the RING domain is a SWIM (SWI2/SNF2 and MuDR) domain of undetermined function. In the present study, we demonstrate that the MEKK1 SWIM domain, but not the RING domain, directly associates with the c-Jun DNA-binding domain, and that the SWIM domain is required for MEKK1-dependent c-Jun ubiquitylation. We further show that this MEKK1 SWIM–Jun interaction is specific, as SWIM domains from other proteins failed to bind c-Jun. We reveal that, although the Jun and Fos DNA-binding domains are highly conserved, the MEKK1 SWIM domain does not bind Fos. Finally, we identify the sequence unique to Jun proteins required for specific interaction with the MEKK1 SWIM domain. Therefore we propose that the MEKK1 SWIM domain represents a novel substrate-binding domain necessary for direct interaction between c-Jun and MEKK1 that promotes MEKK1-dependent c-Jun ubiquitylation.
    Type of Medium: Online Resource
    ISSN: 0264-6021 , 1470-8728
    URL: Article
    DOI: 10.1042/BJ20120406
    RVK:
    WA 15000
    Language: English
    Publisher: Portland Press Ltd.
    Publication Date: 2012
    detail.hit.zdb_id: 1473095-9
    SSG: 12
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