PTP1B and SHP2 in POMC neurons reciprocally regulate energy balance in mice
Open accessAbstract
Protein tyrosine phosphatase 1B (PTP1B) and SH2 domain-containing protein tyrosine phosphatase-2 (SHP2) have been shown in mice to regulate metabolism via the central nervous system, but the specific neurons mediating these effects are unknown. Here, we have shown that proopiomelanocortin (POMC) neuron-specific deficiency in PTP1B or SHP2 in mice results in reciprocal effects on weight gain, adiposity, and energy balance induced by high-fat diet. Mice with POMC neuron-specific deletion of the gene encoding PTP1B (referred to herein as POMC-Ptp1b-/- mice) had reduced adiposity, improved leptin sensitivity, and increased energy expenditure compared with wild-type mice, whereas mice with POMC neuron-specific deletion of the gene encoding SHP2 (referred to herein as POMC-Shp2-/- mice) had elevated adiposity, decreased leptin sensitivity, and reduced energy expenditure. POMC-Ptp1b-/- mice showed substantially improved glucose homeostasis on a high-fat diet, and hyperinsulinemic-euglycemic clamp studies revealed that insulin sensitivity in these mice was improved on a standard chow diet in the absence of any weight difference. In contrast, POMC-Shp2-/- mice displayed impaired glucose tolerance only secondary to their increased weight gain. Interestingly, hypothalamic Pomc mRNA and alpha-melanocyte-stimulating hormone (alphaMSH) peptide levels were markedly reduced in POMC-Shp2-/- mice. These studies implicate PTP1B and SHP2 as important components of POMC neuron regulation of energy balance and point to what we believe to be a novel role for SHP2 in the normal function of the melanocortin system.
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Neuronal or POMC-specific PTP1B knockout mice are protected from diet-induced obesity and exhibit increased leptin sensitivity.
“neuronal (17) or POMC-specific (7) PTP1B knockout mice are protected from DIO and exhibit increased leptin sensitivity.”
From Leptin and the Central Nervous System Control of Glucose Metabolism (2011) · cites this paper as [7]
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Retracted
- Authors
- Banno, R., Zimmer, D., De Jonghe, B. C., Atienza, M., Rak, K., Yang, W., & Bence, K. K.
- Affiliations
- University of Pennsylvania (US)
- Brown University (US)
- Corresponding author
- Bence, Kendra K.
- Venue
- Journal of Clinical Investigation
- Published
- 2010-03-01
- Volume
- 120
- Issue
- 3
- Pages
- 720-734
- ISSN
- 0021-9738 (ISSN-L)
- PMC
- PMC2827947
- OpenAlex
- W2118743996
- Cited by
- 214
- References
- 111
- Citations by year
- 2026: 2 · 2025: 7 · 2024: 7 · 2023: 5 · 2022: 11 · 2021: 10 · 2020: 4 · 2019: 12 · 2018: 15 · 2017: 13 · 2016: 11 · 2015: 12 · 2014: 26 · 2013: 23 · 2012: 26
- FWCI
- 11.33
- Type
- journal article
- Language
- en
- Open access
- bronze
- doi.org
- Locations
- Journal of Clinical Investigation (publishedVersion)
- PubMed Central (publishedVersion)
- PubMed (publishedVersion)
- Funders
- National Institutes of Health
- National Cancer Institute (R01-CA-49152, R01CA049152)
- National Institute of Diabetes and Digestive and Kidney Diseases (R01DK082417, P30DK019525)
- Topics
- Life Sciences › Neuroscience › Endocrine and Autonomic Systems › Regulation of Appetite and Obesity
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Protein Tyrosine Phosphatases
- Health Sciences › Medicine › Epidemiology › Adipokines, Inflammation, and Metabolic Diseases
- Keywords
- PTP1B, SHP2, proopiomelanocortin neurons, energy balance, leptin sensitivity, energy expenditure, adiposity, high-fat diet, glucose homeostasis, insulin sensitivity, melanocortin system, alpha-melanocyte-stimulating hormone, hypothalamus, weight gain
- MeSH terms
- Animals, Energy Metabolism, Hypothalamus, Insulin, Neurons, Pro-Opiomelanocortin, RNA, Messenger, Weight Gain, Mice, Knockout, Adiposity, Mice, Protein Tyrosine Phosphatase, Non-Receptor Type 1, Protein Tyrosine Phosphatase, Non-Receptor Type 11
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