Leptin Signaling in the Arcuate Nucleus Reduces Insulin’s Capacity to Suppress Hepatic Glucose Production in Obese Mice
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Insulin action in the hypothalamus results in the suppression of hepatic glucose production (HGP). Obesity is often associated with a diminished response to insulin, leading to impaired suppression of HGP in obese mice. Here, we demonstrate that blocking central leptin signaling in diet-induced obese (DIO) mice restores the liver's ability to suppress glucose production. Leptin increases the expression of the insulin receptor phosphatase PTP1B, which is highly expressed in the hypothalamus of DIO mice. We demonstrate that the central pharmacological inhibition or ARH-targeted deletion of PTP1B restores the suppression of HGP in obese mice. Additionally, mice that lack PTP1B in AgRP neurons exhibit enhanced ARH insulin signaling and have improved glucose tolerance and insulin sensitivity. Overall, our findings indicate that obesity-induced increases in PTP1B diminish insulin action in the hypothalamus, resulting in unconstrained HGP and contributing to hyperglycemia in obesity.
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In obesity conditions, pathological leptin signaling contributes to sustained hepatic glucose production due to abnormal activation of ARC neurons.
“In obesity conditions, pathological leptin signaling also contributes to sustained hepatic glucose production, due to abnormal activation of ARC neurons 128.”
From Inter‐organ communication: a gatekeeper for metabolic health (2019) · cites this paper as [128]
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- Authors
- Balland, E., Chen, W., Dodd, G. T., Conductier, G., Coppari, R., Tiganis, T., & Cowley, M. A.
- Affiliations
- Monash University (AU)
- University of Geneva (CH)
- Corresponding author
- Tiganis, Tony
- Cowley, Michael A.
- Venue
- Cell Reports
- Publisher
- Elsevier BV
- Published
- 2019-01
- Volume
- 26
- Issue
- 2
- Pages
- 346-355.e3
- ISSN
- 2211-1247 (ISSN-L)
- OpenAlex
- W2908997056
- Cited by
- 44
- References
- 54
- Citations by year
- 2026: 2 · 2025: 4 · 2024: 5 · 2023: 5 · 2022: 5 · 2021: 5 · 2020: 9 · 2019: 9
- FWCI
- 3.87
- Type
- journal article
- Language
- en
- Open access
- gold
- doi.org
- Licence
- Locations
- Cell Reports (publishedVersion, cc-by-nc-nd)
- PubMed (publishedVersion)
- Archive ouverte UNIGE (University of Geneva) (publishedVersion, other-oa)
- Monash University Research Portal (Monash University) (submittedVersion, cc-by-nc-nd)
- DOAJ (DOAJ: Directory of Open Access Journals) (submittedVersion, cc-by-sa)
- Archive ouverte UNIGE (University of Geneva) (submittedVersion, cc-by-nc-nd)
- Funders
- Fondation pour la Recherche Medicale (FRM SPE20140129012)
- Diabetes Australia (DART Grant 2016)
- NHMRC (1079422, 1103037, 1100240, 1065641, 1103193)
- Topics
- Life Sciences › Neuroscience › Endocrine and Autonomic Systems › Regulation of Appetite and Obesity
- Health Sciences › Medicine › Epidemiology › Adipokines, Inflammation, and Metabolic Diseases
- Health Sciences › Medicine › Surgery › Pancreatic function and diabetes
- Keywords
- leptin signaling, arcuate nucleus, hepatic glucose production, insulin resistance, PTP1B, diet-induced obesity, AgRP neurons, hypothalamus, glucose tolerance, hyperglycemia, insulin sensitivity
- MeSH terms
- Animals, Arcuate Nucleus of Hypothalamus, Gluconeogenesis, Insulin, Liver, Male, Mice, Inbred C57BL, Obesity, Signal Transduction, Leptin, Mice, Protein Tyrosine Phosphatase, Non-Receptor Type 1, Diet, High-Fat
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