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Marta Porniece @martaapp.bsky.social · 15/10/2025

8️⃣ Huge thanks to my amazing students Jessie & Charlotte 🙌 and to Stephen X Zhang & @markandermann.bsky.social from @harvardmed.bsky.social & NYU Center for Neural Science for their guidance in analysis, conceptualization, and making sense of it all.

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Marta Porniece @martaapp.bsky.social · 15/10/2025

7️⃣ These findings highlight functional alterations in hypothalamic satiety-promoting neurons and reveal the neural consequences of an obesogenic environment.

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Marta Porniece @martaapp.bsky.social · 15/10/2025

6️⃣ 💡 Interestingly, switching from NCD → HFD didn’t further impair PVH-MC4R neurons, suggesting resilience once these circuits are established.

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Marta Porniece @martaapp.bsky.social · 15/10/2025

5️⃣ Importantly, switching obese mice back to a “healthy” diet partially restored feeding behavior, but not neural activity, showing lasting effects of high-fat diet on brain circuits controlling appetite.

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Marta Porniece @martaapp.bsky.social · 15/10/2025

4️⃣ 🥬 In lean mice, feeding-evoked responses gradually grow as a meal progresses → signals satiety & meal termination. 🍔 In hig- fat-diet-fed mice, responses start too strong and stay flat, suggesting impaired satiety signal integration.

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Marta Porniece @martaapp.bsky.social · 15/10/2025

3️⃣ 🧩 We found that PVH-MC4R neurons integrate satiety signals during feeding, but this process becomes disrupted in diet induced obesity and can’t be fully rescued by dietary intervention.

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Marta Porniece @martaapp.bsky.social · 15/10/2025

2️⃣ These questions drove us to study how these neurons integrate satiety signals (brain “calorie counting”) and drive motivation to eat. 🍽️

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Marta Porniece @martaapp.bsky.social · 15/10/2025

1️⃣ 🥳 Thrilled to share that my postdoc work has finally hit the press! www.nature.com/articles/s41... When we started, we didn’t really know what PVH-MC4R neurons do in obesity. Are they still signaling or “dead”? (e.g., does the chronically high leptin alter α-MSH–MC4R signaling?) 🧵👇

nature.com

Obesity dysregulates feeding-evoked response dynamics in hypothalamic satiety neurons - Scientific Reports

Scientific Reports - Obesity dysregulates feeding-evoked response dynamics in hypothalamic satiety neurons

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Marta Porniece @martaapp.bsky.social · 28/05/2025

🙏 Huge thanks to our fantastic co-authors, especially Charlotte & Jessica, for their incredible help. Grateful to Stephen & @markandermann.bsky.social for their key contributions to experimental design and writing. Thanks to Maria Lehtinen for postdoc guidance and Andermann Lab for their insights.

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Marta Porniece @martaapp.bsky.social · 28/05/2025

🧬 Our data suggest that in obesity, feeding responses in PVHMC4R neurons fail to "reset" between meals, possibly due to persistently high leptin and disrupted AgRP/α-MSH signaling. 🎯Future work should assess peptide transmission onto PVHMC4R neurons to pinpoint mechanisms and refine interventions.

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Marta Porniece @martaapp.bsky.social · 28/05/2025

🔄 Can switching from a high-fat to a healthy diet reverse brain changes in obesity? Switching high-fat-diet fed mice to normal chow diet partially restored early-meal PVHMC4R responses and the licking vigor, but the gradual increase in responses was blunted.

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Marta Porniece @martaapp.bsky.social · 28/05/2025

⚖️ The strengthened responses were not driven by reduced motivation to consume palatable food - they consumed less despite food restriction and caloric matching to controls. 🧠 This behavioral suppression points to premature satiation rather than motivation deficits.

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Marta Porniece @martaapp.bsky.social · 28/05/2025

🍽️ In lean mice, feeding-related responses in PVH-MC4R neurons gradually strengthen during a meal, reflecting growing satiety. 🧠 In mice fed a HFD for many weeks, responses are already strong at meal onset and don’t further increase over the meal, suggesting a disruption in encoding of satiety state.

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