Jacqueline M. Stephens

ORCID: 0000-0002-3796-9531
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About
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Research Areas
  • Adipokines, Inflammation, and Metabolic Diseases
  • Adipose Tissue and Metabolism
  • Cytokine Signaling Pathways and Interactions
  • Immune Cell Function and Interaction
  • Regulation of Appetite and Obesity
  • Growth Hormone and Insulin-like Growth Factors
  • Peroxisome Proliferator-Activated Receptors
  • Metabolism, Diabetes, and Cancer
  • Exercise and Physiological Responses
  • Diet and metabolism studies
  • Cardiovascular Disease and Adiposity
  • Phytochemicals and Antioxidant Activities
  • Cancer, Hypoxia, and Metabolism
  • NF-κB Signaling Pathways
  • RNA modifications and cancer
  • RNA Research and Splicing
  • Lipid metabolism and disorders
  • Ubiquitin and proteasome pathways
  • Pancreatic function and diabetes
  • Diet, Metabolism, and Disease
  • Muscle metabolism and nutrition
  • Natural Compound Pharmacology Studies
  • Diabetes and associated disorders
  • interferon and immune responses
  • Mitochondrial Function and Pathology

Louisiana State University
2016-2025

Pennington Biomedical Research Center
2016-2025

Louisiana State University System
2010-2022

National Institutes of Health
2020

Yale University
2020

Harvard University
2020

Rockefeller University
2020

Louisiana State University Health Sciences Center New Orleans
2018

Indiana State University
2016

Association on Higher Education And Disability
2009

A number of studies have demonstrated that tumor necrosis factor-α (TNF-α) is associated with profound insulin resistance in adipocytes and may also play a critical role the obesity non-insulin-dependent diabetes mellitus. Reports on mechanism TNF-α action been somewhat contradictory. GLUT4 down-regulation has implicated as possible cause reduced kinase function receptor. Here we examine effects factor protein components thought to be involved insulin-stimulated glucose transport adipocytes,...

10.1074/jbc.272.2.971 article EN cc-by Journal of Biological Chemistry 1997-01-01

Emerging evidence suggests that increases in activated T cell populations adipose tissue may contribute toward obesity-associated metabolic syndrome. The present study investigates three unanswered questions: 1) Do adipose-resident cells (ARTs) from lean and obese mice have altered cytokine production response to TCR ligation?; 2) the extralymphoid ARTs possess a unique repertoire compared with lymphoid-resident whether obesity alters diversity specific depots?; 3) Does short-term...

10.4049/jimmunol.1000021 article EN The Journal of Immunology 2010-06-26

Fully differentiated 3T3-L1 adipocytes were chronically exposed to 5 nM tumor necrosis factor-alpha (TNF). This resulted in the development of an insulin resistance based on inability stimulate hexose uptake. Western blot analysis for glucose transporter protein isolated membrane fractions indicated a total depletion GLUT4 (insulin-responsive transporter) cells treated with TNF. Plasma content GLUT1 (growth-related was similar both control and TNF-treated cells; however, intracellular...

10.1016/s0021-9258(18)54714-1 article EN cc-by Journal of Biological Chemistry 1991-11-01

Glucose transport in skeletal muscle is mediated by two distinct transporter isoforms, designated muscle/adipose glucose (Glut4) and erythrocyte/HepG2/brain (Glut1), which differ both abundance membrane distribution. The present study was designed to investigate whether differences insulin responsiveness of red white might be due differential expression the isoforms. transport, as well Glut1 Glut4 protein mRNA levels, were determined portions quadriceps gastrocnemius muscles male...

10.1042/bj2700397 article EN Biochemical Journal 1990-09-01

We have previously demonstrated the ability of tumor necrosis factor-alpha (TNF) to down-regulate expression GLUT4 (insulin-responsive glucose transporter) and C/EBP-alpha (CCAAT/enhancer-binding protein) (Stephens J. M., Pekala, P. H. (1991) Biol. Chem. 266, 21839-21845). As has been suggested control expression, we examined time course for attenuation transcription these genes. Run-on assays indicate a coordinate transcriptional repression both genes (as well as 422/aP2 gene, adipocyte...

10.1016/s0021-9258(18)42251-x article EN cc-by Journal of Biological Chemistry 1992-07-01

Interferon-gamma (IFNgamma) treatment of adipocytes results in a down-regulation the peroxisome proliferator-activated receptor gamma (PPARgamma). The decrease PPARgamma expression is mediated by inhibition synthesis and increased degradation PPARgamma. In this study, we demonstrate that both PPARgamma1 PPARgamma2 are targeted to proteasome under basal conditions more labile than PPARgamma2. IFNgamma-induced increase turnover blocked accompanied an PPARgamma-polyubiquitin conjugates....

10.1074/jbc.m108473200 article EN cc-by Journal of Biological Chemistry 2002-02-01

Moringa oleifera (moringa) is tropical plant traditionally used as an antidiabetic food. It produces structurally unique and chemically stable moringa isothiocyanates (MICs) that were evaluated for their therapeutic use in vivo.C57BL/6L mice fed very high fat diet (VHFD) supplemented with 5% concentrate (MC, delivering 66 mg/kg/d of MICs) accumulated mass, had improved glucose tolerance insulin signaling, did not develop fatty liver disease compared to VHFD-fed mice. MC-fed group also...

10.1002/mnfr.201400679 article EN Molecular Nutrition & Food Research 2015-01-24

Significance Many theories regarding the causes of insulin resistance in skeletal muscle center on ability to oxidize fat, with evidence supporting either decreased or increased fatty acid oxidation (FAO) as causal resistance. Inhibition transport into mitochondria specifically mouse results a rather remarkable phenotype. Despite an accumulation lipids muscle, sensitivity is maintained. The responds FAO by adapting metabolism use other fuel sources, and reliance upon peroxisomal fat...

10.1073/pnas.1418560112 article EN Proceedings of the National Academy of Sciences 2015-06-08

Obesity is a condition characterized by excess adipose tissue that results from positive energy balance and the most common metabolic disorder in industrialized world. The obesity epidemic shows no sign of slowing, it increasingly global problem. Serious clinical problems associated with include an increased risk for type 2 diabetes, atherosclerosis, cancer. Hence, understanding origin development adipocytes will be critical to analysis treatment diseases. Historically, albeit incorrectly,...

10.1371/journal.pbio.1001436 article EN cc-by PLoS Biology 2012-11-27

STATs (Signal Transducers and Activators of Transcription) comprise a family transcription factors that reside in the cytoplasm resting cells. In response to variety stimuli, become tyrosine-phosphorylated translocate nucleus where they mediate transcriptional regulation. We have used 3T3-L1 murine cell line examine expression STAT proteins as function their differentiation into adipocytes. The 1, 3, 5, but not 6, is markedly elevated adipocytes compared with fibroblast precursors. Exposure...

10.1074/jbc.271.18.10441 article EN cc-by Journal of Biological Chemistry 1996-05-01

Interferon-γ (IFN-γ) is known primarily for its roles in immunological responses but also has been shown to affect fat metabolism and adipocyte gene expression. To further investigate the effects of IFN-γ on cells, we examined this cytokine expression transcription factors 3T3-L1 adipocytes. Although regulated several factors, treatment resulted a rapid reduction both peroxisome proliferator-activated receptor (PPAR) protein mRNA. A 48-h exposure decrease CCAAT/enhancer-binding α sterol...

10.1074/jbc.m007894200 article EN cc-by Journal of Biological Chemistry 2001-03-01

The differentiation of adipocytes is regulated by the activity a variety transcription factors, including peroxidase proliferator-activated receptor (PPAR)-γ and C/EBPα. Our current study demonstrates that ectopic expression STAT5A, such as PPAR-γ C/EBPα, promotes adipogenesis in two nonprecursor fibroblast cell lines. Using morphologic biochemical criteria, we have demonstrated STAT5A combination STAT5B are sufficient to induce early late adipogenic markers BALB/c NIH-3T3 cells. Yet, alone...

10.2337/diabetes.52.2.308 article EN Diabetes 2003-02-01

Lipocalin-2 (LCN2) is secreted from adipocytes, and its expression up-regulated in obese diabetic mice humans. LCN2 secretion have been shown to be induced by two proinflammatory cytokines, IFNγ TNFα, cultured murine human adipocytes. In these studies, we demonstrated that TNFα vivo. Although observed a strong induction of white adipose tissue (WAT) depots, the varied among different insulin-sensitive tissues. Knockdown experiments also STAT1 required for IFNγ-induced lipocalin-2 Similarly,...

10.1074/jbc.m113.532234 article EN cc-by Journal of Biological Chemistry 2014-01-06
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