ArticleCell communication and signaling : CCS2025
Strengthening monocarboxylate transporters by adiponectin receptor agonist ameliorates diabetic peripheral neuropathy.
Article in Cell communication and signaling : CCS, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.
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Who cites it
4 citing papers in PubMed.
- Review
- Bioenergetic failure in diabetic peripheral neuropathy: from glucotoxicity to multidimensional metabolic imbalance.Journal of neurology · 2026Review
- Harnessing spatiotemporal melatonin delivery from engineered platforms for targeted microenvironment remodeling in peripheral neuropathy.Materials today. Bio · 2026Review
- Relationship between serum LDH levels and diabetic peripheral neuropathy in type 2 diabetic patients.Frontiers in endocrinology · 2025Article
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Authors and funding
11 authors.
Funding
Abstract
backgroundDisruption of energy support to peripheral nerves leads to dysfunction and degeneration of both neuronal axons and Schwann cells (SCs).
methodsWe evaluated the effects of the adiponectin receptor (AdipoR) agonist, AdipoRon on diabetic peripheral neuropathy (DPN) using db/db mice, murine ND7/23 cells, and human SCs.
resultsAdipoRon improved sensorimotor function and restored nerve phenotypes in the sciatic nerve and paw skin of db/db mice by reducing systemic oxidative stress and insulin resistance. AdipoRon restored impaired oxidative stress response, apoptosis, and autophagy activity through increased AdipoR1/R2-intracellular Ca++-CaMKKβ expression as well as LKB1/AMPK-PPARα/PGC-1α/Nrf2 phosphorylation. It also decreased mTOR phosphorylation, which is related to the preservation of mitochondria in axons and SCs, and improved MCT1/2/4 expression and lactate and ATP/AMP levels in the sciatic nerve of db/db mice. In ND7/23 cells and SCs, AdipoRon decreased oxidative stress and apoptosis while increasing autophagy by suppressing high glucose- and palmitate-induced cellular and mitochondrial oxidative stress, activating the same signaling as in the sciatic nerve. These protective changes were induced by providing energy substrate, lactate and ATP, through the increased expression of MCT1/2/4, facilitating metabolic communication between neurons and SCs.
conclusionAdipoRon may play an important role in preventing DPN by ameliorating oxidative stress, apoptosis, and autophagy, strengthening metabolic support for neurons and SCs under diabetic conditions.
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