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Your search keyword '"Amy E. Troy"' showing total 2 results
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2 results on '"Amy E. Troy"'

1. PPAR gamma is required for the differentiation of adipose tissue in vivo and in vitro

Author

Evan D. Rosen, Gary Bradwin, Kathryn J. Moore, Bruce M. Spiegelman, Richard M. Mortensen, David S. Milstone, Pasha Sarraf, and Amy E Troy

Subjects
Male, medicine.medical_specialty, Gene Dosage, Peroxisome proliferator-activated receptor, Adipose tissue, Receptors, Cytoplasmic and Nuclear, Biology, Mice, Sebaceous Glands, In vivo, Internal medicine, medicine, Null cell, Animals, RNA, Antisense, RNA, Messenger, Molecular Biology, Transcription factor, In Situ Hybridization, Skin, chemistry.chemical_classification, Mice, Knockout, Chimera, Stem Cells, Cell Differentiation, Cell Biology, Fat cell differentiation, Cell biology, Endocrinology, Glucose, Nuclear receptor, chemistry, Adipose Tissue, Adipogenesis, Gene Targeting, Female, Transcription Factors
Abstract

The process of adipogenesis is known to involve the interplay of several transcription factors. Activation of one of these factors, the nuclear hormone receptor PPAR gamma, is known to promote fat cell differentiation in vitro. Whether PPAR gamma is required for this process in vivo has remained an open question because a viable loss-of-function model for PPAR gamma has been lacking. We demonstrate here that mice chimeric for wild-type and PPAR gamma null cells show little or no contribution of null cells to adipose tissue, whereas most other organs examined do not require PPAR gamma for proper development. In vitro, the differentiation of ES cells into fat is shown to be dependent on PPAR gamma gene dosage. These data provide direct evidence that PPAR gamma is essential for the formation of fat.

Published
1999

2. Cross-regulation of C/EBP alpha and PPAR gamma controls the transcriptional pathway of adipogenesis and insulin sensitivity

Author

Zhidan Wu, Bruce M. Spiegelman, Regina P. Brun, Stefanie Hauser, Guillaume Adelmant, Catherine McKeon, Evan D. Rosen, Amy E Troy, and Gretchen J. Darlington

Subjects
medicine.medical_specialty, Adipose tissue, chemistry.chemical_compound, Mice, Internal medicine, Gene expression, medicine, Transcriptional regulation, Animals, Insulin, Phosphorylation, Promoter Regions, Genetic, Molecular Biology, Mice, Knockout, biology, Ccaat-enhancer-binding proteins, Glucose transporter, Tyrosine phosphorylation, Cell Differentiation, Cell Biology, Fibroblasts, Lipid Metabolism, Phosphoproteins, Receptor, Insulin, Cell biology, Insulin receptor, Endocrinology, Enhancer Elements, Genetic, Glucose, chemistry, Adipose Tissue, Adipogenesis, biology.protein, Insulin Receptor Substrate Proteins, Insulin Resistance, Protein Processing, Post-Translational
Abstract

Mice deficient in C/EBP alpha have defective development of adipose tissue, but the precise role of C/EBP alpha has not been defined. Fibroblasts from C/EBP alpha(-/-) mice undergo adipose differentiation through expression and activation of PPAR gamma, though several clear defects are apparent. C/EBP alpha-deficient adipocytes accumulates less lipid, and they do not induce endogenous PPAR gamma, indicating that cross-regulation between C/EBP alpha and PPAR gamma is important in maintaining the differentiated state. The cells also show a complete absence of insulin-stimulated glucose transport, secondary to reduced gene expression and tyrosine phosphorylation for the insulin receptor and IRS-1. These results define multiple roles for C/EBP alpha in adipogenesis and show that cross-regulation between PPAR gamma and C/EBP alpha is a key component of the transcriptional control of this cell lineage.

Published
1999

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