@article {542831,
	title = {Increased energy expenditure, decreased adiposity, and tissue-specific insulin sensitivity in protein-tyrosine phosphatase 1B-deficient mice.},
	journal = {Mol Cell Biol},
	volume = {20},
	number = {15},
	year = {2000},
	month = {2000 Aug},
	pages = {5479-89},
	abstract = {Protein-tyrosine phosphatase 1B (PTP-1B) is a major protein-tyrosine phosphatase that has been implicated in the regulation of insulin action, as well as in other signal transduction pathways. To investigate the role of PTP-1B in vivo, we generated homozygotic PTP-1B-null mice by targeted gene disruption. PTP-1B-deficient mice have remarkably low adiposity and are protected from diet-induced obesity. Decreased adiposity is due to a marked reduction in fat cell mass without a decrease in adipocyte number. Leanness in PTP-1B-deficient mice is accompanied by increased basal metabolic rate and total energy expenditure, without marked alteration of uncoupling protein mRNA expression. In addition, insulin-stimulated whole-body glucose disposal is enhanced significantly in PTP-1B-deficient animals, as shown by hyperinsulinemic-euglycemic clamp studies. Remarkably, increased insulin sensitivity in PTP-1B-deficient mice is tissue specific, as insulin-stimulated glucose uptake is elevated in skeletal muscle, whereas adipose tissue is unaffected. Our results identify PTP-1B as a major regulator of energy balance, insulin sensitivity, and body fat stores in vivo.},
	keywords = {Adipose Tissue, Animals, Body Weight, Carrier Proteins, Energy Metabolism, Female, Glucose, Glucose Tolerance Test, Homeostasis, Hyperinsulinism, Insulin Resistance, Ion Channels, Leptin, Male, Membrane Proteins, Membrane Transport Proteins, Mice, Mice, Inbred C57BL, Mice, Mutant Strains, Mitochondrial Proteins, Muscle, Skeletal, Protein Tyrosine Phosphatase, Non-Receptor Type 1, Protein Tyrosine Phosphatases, Proteins, RNA, Messenger},
	issn = {0270-7306},
	author = {Klaman, L D and Boss, O and Peroni, O D and Kim, J K and Martino, J L and Zabolotny, J M and Moghal, N and Lubkin, M and Kim, Y B and Sharpe, A. H. and Stricker-Krongrad, A and Shulman, G I and Neel, B G and Kahn, B B}
}
