Hormonal
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.
This research highlights that obesity is not just about calories in vs. calories out, but involves specific brain signaling pathways (like aPKC in POMC neurons) that regulate hunger. Disrupting these pathways can lead to increased food intake and weight gain, even if the diet is high-fat. This suggests that targeting these neural mechanisms could be a potential therapeutic strategy for obesity.
Here we show that central nervous system (CNS) action of the PI3K signaling intermediate atypical protein kinase C (aPKC) constrains food intake, weight gain, and glucose intolerance in both rats and mice.
Why this rating
High-quality animal models (knockout mice, pharmacological inhibition) with consistent results across acute and chronic studies.
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
More from this paper
- Pharmacological inhibition of central aPKC activity acutely increases food intake and worsens glucose tolerance in chow-fed rodents.Good
- Deletion of PKC-l in POMC neurons causes central leptin resistance, characterized by reduced melanocortin content and impaired leptin-induced neuronal activation.Good
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