Cited by 214Regulation of Appetite and ObesityProtein Tyrosine PhosphatasesAdipokines, Inflammation, and Metabolic Diseases

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PTP1B and SHP2 in POMC neurons reciprocally regulate energy balance in mice

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Banno, Ryoichi, Zimmer, Derek, De Jonghe, Bart C., Atienza, Marybless, Rak, Kimberly, Yang, Wentian, Bence, Kendra K.·2010·Journal of Clinical Investigation

DOI 10.1172/jci39620PMC PMC2827947

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Abstract

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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Self-citation

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.
ORCID: Banno, Ryoichi
Rak, Kimberly
Yang, Wentian
Bence, Kendra K.
Venue: Journal of Clinical Investigation
Publisher: American Society for Clinical Investigation
Published: 2010-03-01
Volume: 120
Issue: 3
Pages: 720-734
ISSN: 0021-9738 (ISSN-L)
DOI: 10.1172/jci39620
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 › Endocrinology, Diabetes and Metabolism › 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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PTP1B and SHP2 in POMC neurons reciprocally regulate energy balance in mice

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