Research
Hormonal
Deletion of PKC-l in POMC neurons causes central leptin resistance, characterized by reduced melanocortin content and impaired leptin-induced neuronal activation.
Leptin resistance can be caused by defects in the downstream signaling of POMC neurons, specifically involving aPKC. This leads to reduced production of satiety signals (melanocortin), contributing to obesity.
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selective deletion of the aPKC isoform Pkc-l in proopiomelanocortin (POMC) neurons disrupts leptin action, reduces melanocortin content in the paraventricular nucleus, and markedly increases susceptibility to obesity, glucose intolerance, and insulin resistance specifically in HFD-fed male mice.
Why this rating
High-quality animal models with detailed mechanistic analysis.
Source
Deletion of Protein Kinase C λ in POMC Neurons Predisposes to Diet-Induced Obesity
Mauricio D. Dorfman et al. · Diabetes · 2017
DOI 10.2337/db16-0482
mechanism_onlyCited 22×
Read the paper DOI resolved against Crossref · corpus check 2026-06-10
More from this paper
- Central nervous system atypical protein kinase C (aPKC) activity, specifically the PKC-l isoform in POMC neurons, is required to constrain food intake and prevent diet-induced obesity and glucose intolerance.Good
- Pharmacological inhibition of central aPKC activity acutely increases food intake and worsens glucose tolerance in chow-fed rodents.Good
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