J
Jacqueline M. Stephens
Researcher at Pennington Biomedical Research Center
Publications - 48
Citations - 6884
Jacqueline M. Stephens is an academic researcher from Pennington Biomedical Research Center. The author has contributed to research in topics: Adipose tissue & Adipocyte. The author has an hindex of 28, co-authored 37 publications receiving 6081 citations. Previous affiliations of Jacqueline M. Stephens include Boston University & Boston Medical Center.
Papers
More filters
Journal ArticleDOI
The NLRP3 inflammasome instigates obesity-induced inflammation and insulin resistance
Bolormaa Vandanmagsar,Yun-Hee Youm,Anthony Ravussin,Jose E. Galgani,Krisztian Stadler,Randall L. Mynatt,Eric Ravussin,Jacqueline M. Stephens,Vishwa Deep Dixit +8 more
TL;DR: It is established that calorie restriction and exercise-mediated weight loss in obese individuals with type 2 diabetes is associated with a reduction in adipose tissue expression of Nlrp3 as well as with decreased inflammation and improved insulin sensitivity, and that the NlrP3 inflammasome senses obesity-associated danger signals and contributes to obesity-induced inflammation and insulin resistance.
Journal ArticleDOI
Tumor Necrosis Factor-α-induced Insulin Resistance in 3T3-L1 Adipocytes Is Accompanied by a Loss of Insulin Receptor Substrate-1 and GLUT4 Expression without a Loss of Insulin Receptor-mediated Signal Transduction
TL;DR: The insulin resistance of glucose transport in 3T3-L1 adipocytes exposed to TNF-α for 72-96 h results from a reduced amount in requisite proteins involved in insulin action, consistent with earlier studies indicating that T NF-α reduces the transcriptional activity of the GLUT4 gene in murine adipocytes, and reduced mRNA transcription of a number of relevant genes.
Journal ArticleDOI
Transcriptional repression of the GLUT4 and C/EBP genes in 3T3-L1 adipocytes by tumor necrosis factor-alpha.
TL;DR: The lack of response to insulin appeared due to a suppression ofGLUT4 expression as well as a decreased intracellular content of GLUT1, which was judged to be regulated at least in part at the level of transcription.
Journal ArticleDOI
Obesity Increases the Production of Proinflammatory Mediators from Adipose Tissue T Cells and Compromises TCR Repertoire Diversity: Implications for Systemic Inflammation and Insulin Resistance
Hyunwon Yang,Yun-Hee Youm,Bolormaa Vandanmagsar,Anthony Ravussin,Jeffrey M. Gimble,Frank L. Greenway,Jacqueline M. Stephens,Randall L. Mynatt,Vishwa Deep Dixit +8 more
TL;DR: It is established that ARTs have a restricted TCR-Vβ repertoire, and T cells contribute toward the complex proinflammatory microenvironment of adipose tissue in obesity.
Journal ArticleDOI
Identification of adropin as a secreted factor linking dietary macronutrient intake with energy homeostasis and lipid metabolism.
K. Ganesh Kumar,James L. Trevaskis,Daniel D. Lam,Gregory M. Sutton,Robert A. Koza,Vladimir N. Chouljenko,Konstantin G. Kousoulas,Pamela M. Rogers,Robert A. Kesterson,Marie S. Thearle,Anthony W. Ferrante,Randall L. Mynatt,Thomas P. Burris,Jesse Z. Dong,Heather A. Halem,Michael D. Culler,Lora K. Heisler,Jacqueline M. Stephens,Andrew A. Butler +18 more
TL;DR: Adropinregulated expression of hepatic lipogenic genes and adipose tissue peroxisome proliferator-activated receptor gamma, a major regulator of lipogenesis, may be a factor governing glucose and lipid homeostasis, which protects against hepatosteatosis and hyperinsulinemia associated with obesity.