Pannexin 1 attenuates hepatic steatosis and insulin resistance via AMPK-autophagy axis activation

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Key Points

This research investigates how Pannexin 1 regulates lipid accumulation and insulin sensitivity through the AMPK-autophagy axis.
Utilized Panx1 knockout mice and wild-type controls subjected to a high-fat diet to study metabolic dysfunction.
Conducted in vitro experiments on Hepa1-6 hepatocytes with Palmitic and Oleic acid treatments.
Employed multiple analytical techniques including histology, molecular assays, and autophagy modulation to establish mechanistic insights.
Panx1 knockout significantly exacerbated high-fat diet-induced metabolic dysfunction, increasing body weight, glucose intolerance, and hepatic lipid accumulation.
Panx1 overexpression led to decreased hepatic steatosis, improved insulin sensitivity, and reduced serum lipids.
Autophagy was confirmed as crucial for Panx1's metabolic effects, with pharmacological modulation validating its role in insulin signaling.

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Demonstrates Pannexin 1's regulatory role in hepatic lipid metabolism and insulin sensitivity, suggesting a potential therapeutic target for MASLD.

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Zhu et al. (2026) studied this question.

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