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Anjana V. Yeldandi

Researcher at Northwestern University

Publications -  97
Citations -  6068

Anjana V. Yeldandi is an academic researcher from Northwestern University. The author has contributed to research in topics: Peroxisome & Peroxisome Proliferation. The author has an hindex of 38, co-authored 90 publications receiving 5471 citations. Previous affiliations of Anjana V. Yeldandi include University of Chicago.

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Adipocyte-specific Gene Expression and Adipogenic Steatosis in the Mouse Liver Due to Peroxisome Proliferator-activated Receptor γ1 (PPARγ1) Overexpression

TL;DR: It is suggested that a high level of PPARγ in mouse liver is sufficient for the induction of adipogenic transformation of hepatocytes with adipose tissue-specific gene expression and lipid accumulation.
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Defect in Peroxisome Proliferator-activated Receptor α-inducible Fatty Acid Oxidation Determines the Severity of Hepatic Steatosis in Response to Fasting *

TL;DR: Observations point to the critical importance of PPARα in the transcriptional regulatory responses to fasting and in determining the severity of hepatic steatosis.
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Steatohepatitis, spontaneous peroxisome proliferation and liver tumors in mice lacking peroxisomal fatty acyl-coa oxidase:implications for peroxisome proliferator-activated receptor alpha natural ligand metabolism

TL;DR: It is shown that mice deficient in AOX exhibit steatohepatitis, increased hepatic H2O2 levels, and hepatocellular regeneration, leading to a complete reversal of fatty change by 6 to 8 months of age, implicating acyl-CoA and other putative substrates for AOX, as biological ligands for PPARα.
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Peroxisomal and mitochondrial fatty acid beta-oxidation in mice nullizygous for both peroxisome proliferator-activated receptor alpha and peroxisomal fatty acyl-CoA oxidase. Genotype correlation with fatty liver phenotype.

TL;DR: This paper showed that mice nullizygous for both PPARalpha and AOX (PPARalpha-/- AOX-/-) failed to exhibit spontaneous peroxisome proliferation and induction of PPARα-regulated genes by biological ligands unmetabolized in the absence of AOX.