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Protein-tyrosine phosphatase 1B expression is induced by inflammation in vivo.
Open accessAbstract
Protein-tyrosine phosphatase 1B (PTP1B) is a major negative regulator of insulin and leptin sensitivity. PTP1B overexpression in adipose tissue and skeletal muscle of humans and rodents may contribute to insulin resistance and obesity. The mechanisms mediating PTP1B overexpression in obese and diabetic states have been unclear. We find that adipose tissue inflammation and the pro-inflammatory cytokine tumor necrosis factor alpha (TNFalpha) regulate PTP1B expression in vivo. High fat feeding of mice increased PTP1B expression 1.5- to 7-fold in adipose tissue, liver, skeletal muscle, and arcuate nucleus of hypothalamus. PTP1B overexpression in high fat-fed mice coincided with increased adipose tissue expression of the macrophage marker CD68 and TNFalpha, which is implicated in causing obesity-induced insulin resistance. TNFalpha increased PTP1B mRNA and protein levels by 2- to 5-fold in a dose- and time-dependent manner in adipocyte and hepatocyte cell lines. TNFalpha administration in mice increased PTP1B mRNA 1.4- to 4-fold in adipose tissue, liver, skeletal muscle, and hypothalamic arcuate nucleus and PTP1B protein 2-fold in liver. Actinomycin D treatment blocked, and high dose salicylate treatment inhibited by 80%, TNFalpha-induced PTP1B expression in adipocyte cell lines, suggesting TNFalpha may induce PTP1B transcription via nuclear factor kappaB (NFkappaB) activation. Chromatin immunoprecipitation from adipocyte cell lines and liver of mice demonstrated TNFalpha-induced recruitment of NFkappaB subunit p65 to the PTP1B promoter in vitro and in vivo. In mice with diet-induced obesity, TNFalpha deficiency also partly blocked PTP1B overexpression in adipose tissue. Our data suggest that PTP1B overexpression in multiple tissues in obesity is regulated by inflammation and that PTP1B may be a target of anti-inflammatory therapies.
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“Consistent with this, the cellular effects of leptin have been amplified in cells lacking either SOCS3 or PT1b, a phosphotyrosine phosphatase.”
From Leptin at 14 y of age: an ongoing story (2009) · cites this paper as [47]
In the citing paper
“Importantly, mice with haploinsufficiency for either of these genes are resistant to obesity, remain lean on a high-fat diet, and retain leptin sensitivity (46,47).”
From Leptin at 14 y of age: an ongoing story (2009) · cites this paper as [47]
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Metadata
- Authors
- Zabolotny, J. M., Kim, Y.-B., Welsh, L. A., Kershaw, E. E., Neel, B. G., & Kahn, B. B.
- Affiliations
- Beth Israel Deaconess Medical Center (US)
- Corresponding author
- Zabolotny, Janice M.
- Venue
- Journal of Biological Chemistry
- Publisher
- Elsevier BV
- Published
- 2008-05
- Volume
- 283
- Issue
- 21
- Pages
- 14230-14241
- ISSN
- 0021-9258 (ISSN-L)
- PMC
- PMC2386946
- OpenAlex
- W2120790798
- Cited by
- 404
- References
- 76
- Citations by year
- 2026: 5 · 2025: 12 · 2024: 17 · 2023: 17 · 2022: 22 · 2021: 24 · 2020: 21 · 2019: 25 · 2018: 15 · 2017: 20 · 2016: 25 · 2015: 30 · 2014: 26 · 2013: 33 · 2012: 47
- FWCI
- 8.92
- Type
- journal article
- Language
- en
- Open access
- hybrid
- doi.org
- Licence
- Locations
- Journal of Biological Chemistry (publishedVersion, cc-by)
- PubMed Central (publishedVersion)
- PubMed (publishedVersion)
- Funders
- American Diabetes Association
- National Institutes of Health (DK057521, DK046200)
- National Cancer Institute (R01CA049152)
- National Institute of Diabetes and Digestive and Kidney Diseases (P30DK057521, R21DK073530, K01DK062212, P30DK046200, R01DK060839, R01DK060838, K08DK065833)
- Topics
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Protein Tyrosine Phosphatases
- Health Sciences › Medicine › Endocrinology, Diabetes and Metabolism › Adipokines, Inflammation, and Metabolic Diseases
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Peroxisome Proliferator-Activated Receptors
- Keywords
- PTP1B, adipose tissue inflammation, TNF-α, obesity, insulin resistance, leptin sensitivity, NF-κB, high-fat feeding, diet-induced obesity, CD68+ macrophages, hypothalamic arcuate nucleus, liver, skeletal muscle, anti-inflammatory therapy
- MeSH terms
- Animals, Animal Feed, Base Sequence, Cells, Cultured, Diabetes Mellitus, Inflammation, Insulin, Insulin Resistance, Molecular Sequence Data, Obesity, Transcription, Genetic, Tumor Necrosis Factor-alpha, Gene Expression Regulation, Enzymologic, Leptin, Mice, Rats, Protein Tyrosine Phosphatase, Non-Receptor Type 1
About these checks
Registry, retraction, Cites and statistics results are computed, not judged, with one exception: a printed reference that no index lists is read once by a model before it counts as a citation error. Claims are extracted by a model and kept only when their quote appears verbatim in the text; each cited source is then checked, with a model’s help, for whether it says what the claim relies on. Those verdicts can be wrong — read the claim’s quote and the cited source before relying on one.
Statistics and arithmetic are recomputed, not judged.
Confidence bands are shown only for fields calibrated on our annotated test set. None is calibrated yet, so no band is shown.
What counts as a claim ›How we measure confidence ›How we check this ›
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