LIVIVO - Das Suchportal für Lebenswissenschaften

switch to English language
Zurück zur letzten Suche Suchhistorie
Erweiterte Suche

Ihre letzten Suchen

  1. AU="Susan J. Burke"
  2. AU="Chen, Yuguang"
  3. AU="Zhao, Zhenghuan"
  4. AU="De Chiara, Anna Rosaria"
  5. AU="Savage, Anne"
  6. AU="Salamanca, Albert"
  7. AU="Zhong, Xiao-Song"
  8. AU="Deguchi, Masashi"
  9. AU="Żmuda, J"
  10. AU="Liao, Yanyan"
  11. AU="Zhu, Jin-Wei"
  12. AU="Khan, Azkia"
  13. AU="Folkman, Judah"
  14. AU=Bhatia Rajesh
  15. AU="Thobois, Stéphane"
  16. AU="Lai, Chien-Chih"
  17. AU="Ahn, Bo Young"
  18. AU="Jeje, Olamide"
  19. AU="Fine, Samson W"
  20. AU="Riemann, Burkhard"
  21. AU="Nazir, Ahsan"
  22. AU="Kawakita, Emi"
  23. AU="Wang, Junnian"
  24. AU="Nie, Chong"

Suchergebnis

Treffer 1 - 10 von insgesamt 14

Suchoptionen

  1. Artikel ; Online: Special Issue

    J. Jason Collier / Susan J. Burke

    Biomedicines, Vol 10, Iss 7, p

    Emerging Paradigms in Insulin Resistance

    2022  Band 1471

    Abstract: This Biomedicines Special Issue was designed to attract articles that focused on different facets of biology relating to insulin resistance, defined as reduced cellular and organismal response to the insulin hormone, and its underlying mechanisms [.] ...

    Abstract This Biomedicines Special Issue was designed to attract articles that focused on different facets of biology relating to insulin resistance, defined as reduced cellular and organismal response to the insulin hormone, and its underlying mechanisms [.]
    Schlagwörter n/a ; Biology (General) ; QH301-705.5
    Sprache Englisch
    Erscheinungsdatum 2022-06-01T00:00:00Z
    Verlag MDPI AG
    Dokumenttyp Artikel ; Online
    Datenquelle BASE - Bielefeld Academic Search Engine (Lebenswissenschaftliche Auswahl)

    Volltext online

    Zusatzmaterialien

    Kategorien

    Fernleihe an ZB MED

    Sie können sich den gewünschten Titel als lokale Nutzerin oder lokaler Nutzer von ZB MED direkt an den Standort Köln schicken lassen.

  2. Artikel ; Online: Pharmacological inhibition of lipolysis prevents adverse metabolic outcomes during glucocorticoid administration

    Melissa A. Linden / Susan J. Burke / Humza A. Pirzadah / Tai-Yu Huang / Heidi M. Batdorf / Walid K. Mohammed / Katarina A. Jones / Sujoy Ghosh / Shawn R. Campagna / J. Jason Collier / Robert C. Noland

    Molecular Metabolism, Vol 74, Iss , Pp 101751- (2023)

    2023  

    Abstract: Objective: Glucocorticoids are one of the most commonly prescribed classes of anti-inflammatory drugs; however, chronic treatment promotes iatrogenic (drug-induced) diabetes. As part of their physiological role, glucocorticoids stimulate lipolysis to ... ...

    Abstract Objective: Glucocorticoids are one of the most commonly prescribed classes of anti-inflammatory drugs; however, chronic treatment promotes iatrogenic (drug-induced) diabetes. As part of their physiological role, glucocorticoids stimulate lipolysis to spare glucose. We hypothesized that persistent stimulation of lipolysis during glucocorticoid therapy plays a causative role in the development of iatrogenic diabetes. Methods: Male C57BL/6J mice were given 100 μg/mL corticosterone (Cort) in the drinking water for two weeks and were fed either normal chow (TekLad 8640) or the same diet supplemented with an adipose triglyceride lipase inhibitor (Atglistatin - 2 g/kg diet) to inhibit the first step of lipolysis. Results: Herein, we report for the first time that glucocorticoid administration promotes a unique state of substrate excess and energetic overload in skeletal muscle that primarily results from the rampant mobilization of endogenous fuels. Inhibiting lipolysis protected mice from Cort-induced gains in fat mass, excess ectopic lipid accrual, hyperinsulinemia, and hyperglycemia. The role lipolysis plays in Cort-mediated pathology appears to differ between tissues. Within skeletal muscle, Cort-induced lipolysis facilitated diversion of glucose-derived carbons toward the pentose phosphate and hexosamine biosynthesis pathways but contributed to <3% of the Cort-induced genomic adaptations. In contrast, Cort stimulation of lipolysis accounted for ∼35% of the genomic changes in the liver but had minimal impact on hepatic metabolites reported. Conclusions: These data support the idea that activation of lipolysis plays a causal role in the progression toward iatrogenic diabetes during glucocorticoid therapy with differential impact on skeletal muscle and liver.
    Schlagwörter Glucocorticoid ; Substrate overload ; Lipolysis ; Adipose triglyceride lipase ; Iatrogenic diabetes ; Internal medicine ; RC31-1245
    Thema/Rubrik (Code) 572
    Sprache Englisch
    Erscheinungsdatum 2023-08-01T00:00:00Z
    Verlag Elsevier
    Dokumenttyp Artikel ; Online
    Datenquelle BASE - Bielefeld Academic Search Engine (Lebenswissenschaftliche Auswahl)

    Volltext online

    Zusatzmaterialien

    Kategorien

    Fernleihe an ZB MED

    Sie können sich den gewünschten Titel als lokale Nutzerin oder lokaler Nutzer von ZB MED direkt an den Standort Köln schicken lassen.

  3. Artikel ; Online: Transcriptional Regulation of Chemokine Genes

    Susan J. Burke / J. Jason Collier

    Biomolecules, Vol 5, Iss 2, Pp 1020-

    A Link to Pancreatic Islet Inflammation?

    2015  Band 1034

    Abstract: Enhanced expression of chemotactic cytokines (aka chemokines) within pancreatic islets likely contributes to islet inflammation by regulating the recruitment and activation of various leukocyte populations, including macrophages, neutrophils, and T- ... ...

    Abstract Enhanced expression of chemotactic cytokines (aka chemokines) within pancreatic islets likely contributes to islet inflammation by regulating the recruitment and activation of various leukocyte populations, including macrophages, neutrophils, and T-lymphocytes. Because of the powerful actions of these chemokines, precise transcriptional control is required. In this review, we highlight what is known about the signals and mechanisms that govern the transcription of genes encoding specific chemokine proteins in pancreatic islet β-cells, which include contributions from the NF-κB and STAT1 pathways. We further discuss increased chemokine expression in pancreatic islets during autoimmune-mediated and obesity-related development of diabetes.
    Schlagwörter chemokine ; diabetes ; inflammation ; islet ; transcription ; Biology (General) ; QH301-705.5 ; Science ; Q
    Sprache Englisch
    Erscheinungsdatum 2015-05-01T00:00:00Z
    Verlag Multidisciplinary Digital Publishing Institute
    Dokumenttyp Artikel ; Online
    Datenquelle BASE - Bielefeld Academic Search Engine (Lebenswissenschaftliche Auswahl)

    Volltext online

    Zusatzmaterialien

    Kategorien

    Fernleihe an ZB MED

    Sie können sich den gewünschten Titel als lokale Nutzerin oder lokaler Nutzer von ZB MED direkt an den Standort Köln schicken lassen.

  4. Artikel ; Online: Intact mitochondrial substrate efflux is essential for prevention of tubular injury in a sex-dependent manner

    Allison McCrimmon / Kerin M. Cahill / Claudia Kruger / Margaret E. Mangelli / Emily Bouffard / Timothy Dobroski / Kelly N. Michanczyk / Susan J. Burke / Robert C. Noland / Daria V. Ilatovskaya / Krisztian Stadler

    JCI Insight, Vol 7, Iss

    2022  Band 7

    Abstract: The importance of healthy mitochondrial function is implicated in the prevention of chronic kidney disease (CKD) and diabetic kidney disease (DKD). Sex differences also play important roles in DKD. Our previous studies revealed that mitochondrial ... ...

    Abstract The importance of healthy mitochondrial function is implicated in the prevention of chronic kidney disease (CKD) and diabetic kidney disease (DKD). Sex differences also play important roles in DKD. Our previous studies revealed that mitochondrial substrate overload (modeled by homozygous deletion of carnitine acetyl-transferase [CrAT]) in proximal tubules causes renal injury. Here, we demonstrate the importance of intact mitochondrial substrate efflux by titrating the amount of overload through the generation of a heterozygous CrAT-KO model (PT-CrATHET mouse). Intriguingly, these animals developed renal injury similarly to their homozygous counterparts. Mitochondria were structurally and functionally impaired in both sexes. Transcriptomic analyses, however, revealed striking sex differences. Male mice shut down fatty acid oxidation and several other metabolism-related pathways. Female mice had a significantly weaker transcriptional response in metabolism, but activation of inflammatory pathways was prominent. Proximal tubular cells from PT-CrATHET mice of both sexes exhibited a shift toward a more glycolytic phenotype, but female mice were still able to oxidize fatty acid–based substrates. Our results demonstrate that maintaining mitochondrial substrate metabolism balance is crucial to satisfying proximal tubular energy demand. Our findings have potentially broad implications, as both the glycolytic shift and the sexual dimorphisms discovered herein offer potentially new modalities for future interventions for treating kidney disease.
    Schlagwörter Metabolism ; Nephrology ; Medicine ; R
    Thema/Rubrik (Code) 570
    Sprache Englisch
    Erscheinungsdatum 2022-04-01T00:00:00Z
    Verlag American Society for Clinical investigation
    Dokumenttyp Artikel ; Online
    Datenquelle BASE - Bielefeld Academic Search Engine (Lebenswissenschaftliche Auswahl)

    Volltext online

    Zusatzmaterialien

    Kategorien

    Fernleihe an ZB MED

    Sie können sich den gewünschten Titel als lokale Nutzerin oder lokaler Nutzer von ZB MED direkt an den Standort Köln schicken lassen.

  5. Artikel ; Online: The Ubiquitin Ligase SIAH2 Negatively Regulates Glucocorticoid Receptor Activity and Abundance

    Susan J. Burke / Jessica L. Taylor / Heidi M. Batdorf / Robert C. Noland / David H. Burk / Yongmei Yu / Z. Elizabeth Floyd / J. Jason Collier

    Biomedicines, Vol 9, Iss 22, p

    2021  Band 22

    Abstract: Glucocorticoids are clinically essential drugs used routinely to control inflammation. However, a host of metabolic side effects manifests upon usage beyond a few days. In the present study, we tested the hypothesis that seven-in-absentia mammalian ... ...

    Abstract Glucocorticoids are clinically essential drugs used routinely to control inflammation. However, a host of metabolic side effects manifests upon usage beyond a few days. In the present study, we tested the hypothesis that seven-in-absentia mammalian homolog-2 (SIAH2), a ubiquitin ligase that regulates adipogenesis, is important for controlling adipocyte size, inflammation, and the ability of adipose tissue to expand in response to a glucocorticoid challenge. Using mice with global deletion of SIAH2 exposed or not to corticosterone, we found that adipocytes are larger in response to glucocorticoids in the absence of SIAH2. In addition, SIAH2 regulates glucocorticoid receptor (GR) transcriptional activity and total GR protein abundance. Moreover, these studies reveal that there is an increased expression of genes involved in fibrosis and inflammatory signaling pathways found in white adipose tissue in response to glucocorticoids in the absence of SIAH2. In summary, this is the first study to identify a role for SIAH2 to regulate transcriptional activity and abundance of the GR, which leads to alterations in adipose tissue size and gene expression during in vivo exposure to glucocorticoids.
    Schlagwörter adipose tissue ; glucocorticoid ; inflammation ; SIAH2 ; Biology (General) ; QH301-705.5
    Thema/Rubrik (Code) 570
    Sprache Englisch
    Erscheinungsdatum 2021-12-01T00:00:00Z
    Verlag MDPI AG
    Dokumenttyp Artikel ; Online
    Datenquelle BASE - Bielefeld Academic Search Engine (Lebenswissenschaftliche Auswahl)

    Volltext online

    Zusatzmaterialien

    Kategorien

    Fernleihe an ZB MED

    Sie können sich den gewünschten Titel als lokale Nutzerin oder lokaler Nutzer von ZB MED direkt an den Standort Köln schicken lassen.

  6. Artikel ; Online: Pioglitazone Reverses Markers of Islet Beta-Cell De-Differentiation in db/db Mice While Modulating Expression of Genes Controlling Inflammation and Browning in White Adipose Tissue from Insulin-Resistant Mice and Humans

    J. Jason Collier / Heidi M. Batdorf / Kaelan L. Merrifield / Thomas M. Martin / Ursula White / Eric Ravussin / David H. Burk / Chris R. Cooley / Michael D. Karlstad / Susan J. Burke

    Biomedicines, Vol 9, Iss 1189, p

    2021  Band 1189

    Abstract: Obesity, insulin resistance, and type 2 diabetes contribute to increased morbidity and mortality in humans. The db/db mouse is an important mouse model that displays many key features of the human disease. Herein, we used the drug pioglitazone, a ... ...

    Abstract Obesity, insulin resistance, and type 2 diabetes contribute to increased morbidity and mortality in humans. The db/db mouse is an important mouse model that displays many key features of the human disease. Herein, we used the drug pioglitazone, a thiazolidinedione with insulin-sensitizing properties, to investigate blood glucose levels, indicators of islet β-cell health and maturity, and gene expression in adipose tissue. Oral administration of pioglitazone lowered blood glucose levels in db/db mice with a corresponding increase in respiratory quotient, which indicates improved whole-body carbohydrate utilization. In addition, white adipose tissue from db/db mice and from humans treated with pioglitazone showed increased expression of glycerol kinase. Both db/db mice and humans given pioglitazone displayed increased expression of UCP-1 , a marker typically associated with brown adipose tissue. Moreover, pancreatic β-cells from db/db mice treated with pioglitazone had greater expression of insulin and Nkx6.1 as well as reduced abundance of the de-differentiation marker Aldh1a3. Collectively, these findings indicate that four weeks of pioglitazone therapy improved overall metabolic health in db/db mice. Our data are consistent with published reports of human subjects administered pioglitazone and with analysis of human adipose tissue taken from subjects treated with pioglitazone. In conclusion, the current study provides evidence that pioglitazone restores key markers of metabolic health and also showcases the utility of the db/db mouse to understand mechanisms associated with human metabolic disease and interventions that provide therapeutic benefit.
    Schlagwörter diabetes ; inflammation ; obesity ; thiazolidinedione ; Biology (General) ; QH301-705.5
    Thema/Rubrik (Code) 616
    Sprache Englisch
    Erscheinungsdatum 2021-09-01T00:00:00Z
    Verlag MDPI AG
    Dokumenttyp Artikel ; Online
    Datenquelle BASE - Bielefeld Academic Search Engine (Lebenswissenschaftliche Auswahl)

    Volltext online

    Zusatzmaterialien

    Kategorien

    Fernleihe an ZB MED

    Sie können sich den gewünschten Titel als lokale Nutzerin oder lokaler Nutzer von ZB MED direkt an den Standort Köln schicken lassen.

  7. Artikel ; Online: Lipid peroxidation regulates podocyte migration and cytoskeletal structure through redox sensitive RhoA signaling

    Claudia Kruger / Susan J. Burke / J. Jason Collier / Trang-Tiffany Nguyen / J. Michael Salbaum / Krisztian Stadler

    Redox Biology, Vol 16, Iss , Pp 248-

    2018  Band 254

    Abstract: Early podocyte loss is characteristic of chronic kidney diseases (CKD) in obesity and diabetes. Since treatments for hyperglycemia and hypertension do not prevent podocyte loss, there must be additional factors causing podocyte depletion. The role of ... ...

    Abstract Early podocyte loss is characteristic of chronic kidney diseases (CKD) in obesity and diabetes. Since treatments for hyperglycemia and hypertension do not prevent podocyte loss, there must be additional factors causing podocyte depletion. The role of oxidative stress has been implicated in CKD but it is not known how exactly free radicals affect podocyte physiology. To assess this relationship, we investigated the effects of lipid radicals on podocytes, as lipid peroxidation is a major form of oxidative stress in diabetes. We found that lipid radicals govern changes in podocyte homeostasis through redox sensitive RhoA signaling: lipid radicals inhibit migration and cause loss of F-actin fibers. These effects were prevented by mutating the redox sensitive cysteines of RhoA. We therefore suggest that in diseases associated with increased lipid peroxidation, lipid radicals can determine podocyte function with potentially pathogenic consequences for kidney physiology. Keywords: Lipid peroxidation, Reactive lipids, Podocyte, RhoA, Cysteine, Chronic kidney disease
    Schlagwörter Medicine (General) ; R5-920 ; Biology (General) ; QH301-705.5
    Thema/Rubrik (Code) 500
    Sprache Englisch
    Erscheinungsdatum 2018-06-01T00:00:00Z
    Verlag Elsevier
    Dokumenttyp Artikel ; Online
    Datenquelle BASE - Bielefeld Academic Search Engine (Lebenswissenschaftliche Auswahl)

    Volltext online

    Zusatzmaterialien

    Kategorien

    Fernleihe an ZB MED

    Sie können sich den gewünschten Titel als lokale Nutzerin oder lokaler Nutzer von ZB MED direkt an den Standort Köln schicken lassen.

  8. Artikel ; Online: Pancreatic, but not myeloid-cell, expression of interleukin-1alpha is required for maintenance of insulin secretion and whole body glucose homeostasis

    J. Jason Collier / Heidi M. Batdorf / Thomas M. Martin / Kristen E. Rohli / David H. Burk / Danhong Lu / Chris R. Cooley / Michael D. Karlstad / Joseph W. Jackson / Tim E. Sparer / Jingying Zhang / Randall L. Mynatt / Susan J. Burke

    Molecular Metabolism, Vol 44, Iss , Pp 101140- (2021)

    2021  

    Abstract: Objective: The expression of the interleukin-1 receptor type I (IL-1R) is enriched in pancreatic islet β-cells, signifying that ligands activating this pathway are important for the health and function of the insulin-secreting cell. Using isolated mouse, ...

    Abstract Objective: The expression of the interleukin-1 receptor type I (IL-1R) is enriched in pancreatic islet β-cells, signifying that ligands activating this pathway are important for the health and function of the insulin-secreting cell. Using isolated mouse, rat, and human islets, we identified the cytokine IL-1α as a highly inducible gene in response to IL-1R activation. In addition, IL-1α is elevated in mouse and rat models of obesity and Type 2 diabetes. Since less is known about the biology of IL-1α relative to IL-1β in pancreatic tissue, our objective was to investigate the contribution of IL-1α to pancreatic β-cell function and overall glucose homeostasis in vivo. Methods: We generated a novel mouse line with conditional IL-1α alleles and subsequently produced mice with either pancreatic- or myeloid lineage-specific deletion of IL-1α. Results: Using this in vivo approach, we discovered that pancreatic (IL-1αPdx1−/−), but not myeloid-cell, expression of IL-1α (IL-1αLysM−/−) was required for the maintenance of whole body glucose homeostasis in both male and female mice. Moreover, pancreatic deletion of IL-1α led to impaired glucose tolerance with no change in insulin sensitivity. This observation was consistent with our finding that glucose-stimulated insulin secretion was reduced in islets isolated from IL-1αPdx1−/− mice. Alternatively, IL-1αLysM−/− mice (male and female) did not have any detectable changes in glucose tolerance, respiratory quotient, physical activity, or food intake when compared with littermate controls. Conclusions: Taken together, we conclude that there is an important physiological role for pancreatic IL-1α to promote glucose homeostasis by supporting glucose-stimulated insulin secretion and islet β-cell mass in vivo.
    Schlagwörter Cytokines ; Cytokine receptors ; Inflammation ; Pancreatic islet ; Rodent ; Internal medicine ; RC31-1245
    Sprache Englisch
    Erscheinungsdatum 2021-02-01T00:00:00Z
    Verlag Elsevier
    Dokumenttyp Artikel ; Online
    Datenquelle BASE - Bielefeld Academic Search Engine (Lebenswissenschaftliche Auswahl)

    Volltext online

    Zusatzmaterialien

    Kategorien

    Fernleihe an ZB MED

    Sie können sich den gewünschten Titel als lokale Nutzerin oder lokaler Nutzer von ZB MED direkt an den Standort Köln schicken lassen.

  9. Artikel ; Online: FGF21 is required for protein restriction to extend lifespan and improve metabolic health in male mice

    Cristal M. Hill / Diana C. Albarado / Lucia G. Coco / Redin A. Spann / Md Shahjalal Khan / Emily Qualls-Creekmore / David H. Burk / Susan J. Burke / J. Jason Collier / Sangho Yu / David H. McDougal / Hans-Rudolf Berthoud / Heike Münzberg / Andrzej Bartke / Christopher D. Morrison

    Nature Communications, Vol 13, Iss 1, Pp 1-

    2022  Band 14

    Abstract: The restriction of dietary protein or amino acid intake is well established to extend lifespan in multiple species. Here, the authors show that the endocrine hormone FGF21 is necessary for dietary protein restriction to extend lifespan and improve ... ...

    Abstract The restriction of dietary protein or amino acid intake is well established to extend lifespan in multiple species. Here, the authors show that the endocrine hormone FGF21 is necessary for dietary protein restriction to extend lifespan and improve metabolic health in aged, male mice.
    Schlagwörter Science ; Q
    Sprache Englisch
    Erscheinungsdatum 2022-04-01T00:00:00Z
    Verlag Nature Portfolio
    Dokumenttyp Artikel ; Online
    Datenquelle BASE - Bielefeld Academic Search Engine (Lebenswissenschaftliche Auswahl)

    Volltext online

    Zusatzmaterialien

    Kategorien

    Fernleihe an ZB MED

    Sie können sich den gewünschten Titel als lokale Nutzerin oder lokaler Nutzer von ZB MED direkt an den Standort Köln schicken lassen.

  10. Artikel ; Online: FGF21 Signals Protein Status to the Brain and Adaptively Regulates Food Choice and Metabolism

    Cristal M. Hill / Thomas Laeger / Madeleine Dehner / Diana C. Albarado / Blaise Clarke / Desiree Wanders / Susan J. Burke / J. Jason Collier / Emily Qualls-Creekmore / Samantha M. Solon-Biet / Stephen J. Simpson / Hans-Rudolf Berthoud / Heike Münzberg / Christopher D. Morrison

    Cell Reports, Vol 27, Iss 10, Pp 2934-2947.e

    2019  Band 3

    Abstract: Summary: Reduced dietary protein intake induces adaptive physiological changes in macronutrient preference, energy expenditure, growth, and glucose homeostasis. We demonstrate that deletion of the FGF21 co-receptor βKlotho (Klb) from the brain produces ... ...

    Abstract Summary: Reduced dietary protein intake induces adaptive physiological changes in macronutrient preference, energy expenditure, growth, and glucose homeostasis. We demonstrate that deletion of the FGF21 co-receptor βKlotho (Klb) from the brain produces mice that are unable to mount a physiological response to protein restriction, an effect that is replicated by whole-body deletion of FGF21. Mice forced to consume a low-protein diet exhibit reduced growth, increased energy expenditure, and a resistance to diet-induced obesity, but the loss of FGF21 signaling in the brain completely abrogates that response. When given access to a higher protein alternative, protein-restricted mice exhibit a shift toward protein-containing foods, and central FGF21 signaling is essential for that response. FGF21 is an endocrine signal linking the liver and brain, which regulates adaptive, homeostatic changes in metabolism and feeding behavior during protein restriction. : Dietary protein restriction induces changes in macronutrient preference, energy expenditure, growth, and metabolism. Hill et al. show that deletion of the FGF21 co-receptor from the brain produces mice that are unable to mount a physiological response to dietary protein restriction. FGF21 acts in the brain to coordinate homeostatic responses to protein restriction. Keywords: dietary protein restriction, FGF21, Klb, central nervous system, macronutrient, nutrition
    Schlagwörter Biology (General) ; QH301-705.5
    Thema/Rubrik (Code) 612
    Sprache Englisch
    Erscheinungsdatum 2019-06-01T00:00:00Z
    Verlag Elsevier
    Dokumenttyp Artikel ; Online
    Datenquelle BASE - Bielefeld Academic Search Engine (Lebenswissenschaftliche Auswahl)

    Volltext online

    Zusatzmaterialien

    Kategorien

    Fernleihe an ZB MED

    Sie können sich den gewünschten Titel als lokale Nutzerin oder lokaler Nutzer von ZB MED direkt an den Standort Köln schicken lassen.

Zum Seitenanfang