Research
Hormonal
Pharmacological inhibition of central aPKC activity acutely increases food intake and worsens glucose tolerance in chow-fed rodents.
Blocking a specific brain enzyme (aPKC) can cause immediate overeating and poor blood sugar control, even in lean animals. This underscores the importance of this enzyme in regulating hunger and metabolism.
GoodSupportsHIGH confidence
Pharmacological inhibition of CNS aPKC activity acutely increases food intake and worsens glucose tolerance in chow-fed rodents and causes excess weight gain during high-fat diet (HFD) feeding.
Why this rating
Consistent results across acute and chronic pharmacological studies in rats and mice.
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
- 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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