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Ruth Gordillo

Researcher at University of Texas Southwestern Medical Center

Publications -  73
Citations -  3882

Ruth Gordillo is an academic researcher from University of Texas Southwestern Medical Center. The author has contributed to research in topics: Adipose tissue & Adipocyte. The author has an hindex of 25, co-authored 67 publications receiving 2851 citations. Previous affiliations of Ruth Gordillo include University of Extremadura & University of California, Los Angeles.

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An FGF21-Adiponectin-Ceramide Axis Controls Energy Expenditure and Insulin Action in Mice

TL;DR: It is shown that FGF21 rapidly and robustly stimulates adiponectin secretion in rodents while diminishing accumulation of ceramides in obese animals, and that F GF21 critically depends on adip onectin to exert its glycemic and insulin sensitizing effects.
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Theory of asymmetric organocatalysis of Aldol and related reactions: rationalizations and predictions.

TL;DR: Computational studies have led to models to understand some classic and contemporary asymmetric reactions involving organocatalysts, and Quantitative predictions for several new catalysts and reactions are provided.
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Targeted Induction of Ceramide Degradation Leads to Improved Systemic Metabolism and Reduced Hepatic Steatosis

TL;DR: Observations suggest the existence of a rapidly acting "cross-talk" between liver and adipose tissue sphingolipids, critically regulating glucose metabolism and hepatic lipid uptake.
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An Endothelial-to-Adipocyte Extracellular Vesicle Axis Governed by Metabolic State

TL;DR: It is shown that neighboring endothelial cells (ECs) transfer cav1-containing EVs to adipocytes in vivo, which reciprocate by releasing EVs to ECs, which facilitates transfer of plasma constituents from ECs to the adipocyte.
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Specific Hepatic Sphingolipids Relate to Insulin Resistance, Oxidative Stress, and Inflammation in Nonalcoholic Steatohepatitis.

TL;DR: Sphingolipid species are not only increased in insulin-resistant humans with NASH but also correlate with hepatic oxidative stress and inflammation, suggesting that these lipids may play a role during progression of simple steatosis to NASH in humans.