G
Gyorgy Baffy
Researcher at Brigham and Women's Hospital
Publications - 83
Citations - 4981
Gyorgy Baffy is an academic researcher from Brigham and Women's Hospital. The author has contributed to research in topics: Nonalcoholic fatty liver disease & Cirrhosis. The author has an hindex of 27, co-authored 76 publications receiving 4465 citations. Previous affiliations of Gyorgy Baffy include Rhode Island Hospital & Harvard University.
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Journal ArticleDOI
Uncoupling Protein-2 Negatively Regulates Insulin Secretion and Is a Major Link between Obesity, β Cell Dysfunction, and Type 2 Diabetes
Chen-Yu Zhang,Gyorgy Baffy,Gyorgy Baffy,Pascale Perret,Stefan Krauss,Odile D. Peroni,Danica Grujic,Thilo Hagen,Antonio Vidal-Puig,Olivier Boss,Young-Bum Kim,Xin Xiao Zheng,Michael B. Wheeler,Gerald I. Shulman,Catherine B. Chan,Bradford B. Lowell +15 more
TL;DR: Results establish UCP2 as a key component of β cell glucose sensing, and as a critical link between obesity, β cell dysfunction, and type 2 diabetes.
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Hepatocellular carcinoma in non-alcoholic fatty liver disease: An emerging menace
TL;DR: Current evidence as it pertains to the epidemiology, pathogenesis, and prevention of NAFLD-associated HCC, including metformin and PPAR gamma agonists, is summarized.
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Apoptosis induced by withdrawal of interleukin-3 (IL-3) from an IL-3-dependent hematopoietic cell line is associated with repartitioning of intracellular calcium and is blocked by enforced Bcl-2 oncoprotein production.
TL;DR: Investigation of the regulation of intracellular pools of Ca2+ in an interleukin-3 (IL-3)-dependent hematopoietic cell line 32D found no difference in 32D-NEO cells before and after IL-3 withdrawal, suggesting that the observed alterations in mitochondrial and nonmitochondrial Ca2+.
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Kupffer cells in non-alcoholic fatty liver disease: the emerging view.
TL;DR: Altered lipid homeostasis in NAFLD may unfavourably affect TLR4 receptor complex assembly and sorting, interfere with signalling flux redistribution, promote amplification loops, and impair negative regulation including alternative activation of Kupffer cells.
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The mitochondrial uncoupling protein-2 promotes chemoresistance in cancer cells.
TL;DR: This work shows this critical adaptive response in cancer cells to be linked to uncoupling protein-2 (UCP2), a mitochondrial suppressor of reactive oxygen species (ROS), which is present in drug-resistant lines of various cancer cells and in human colon cancer.