Cited by 229Chronic Kidney Disease and DiabetesAdipokines, Inflammation, and Metabolic DiseasesRenal Diseases and Glomerulopathies

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The Adiponectin Receptor Agonist AdipoRon Ameliorates Diabetic Nephropathy in a Model of Type 2 Diabetes

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Kim, Yaeni, Lim, Ji Hee, Kim, Min Young, Kim, Eun Nim, Yoon, Hye Eun, Shin, Seok Joon, Choi, Bum Soon, Kim, Yong-Soo, Chang, Yoon Sik, Park, Cheol Whee·2018·Journal of the American Society of Nephrology

DOI 10.1681/asn.2017060627PMC PMC5875945

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Abstract

Adiponectin exerts renoprotective effects against diabetic nephropathy (DN) by activating the AMP-activated protein kinase (AMPK)/peroxisome proliferative-activated receptor– α (PPAR α ) pathway through adiponectin receptors (AdipoRs). AdipoRon is an orally active synthetic adiponectin receptor agonist. We investigated the expression of AdipoRs and the associated intracellular pathways in 27 patients with type 2 diabetes and examined the effects of AdipoRon on DN development in male C57BLKS/J db/db mice, glomerular endothelial cells (GECs), and podocytes. The extent of glomerulosclerosis and tubulointerstitial fibrosis correlated with renal function deterioration in human kidneys. Expression of AdipoR1, AdipoR2, and Ca 2+ /calmodulin-dependent protein kinase kinase– β (CaMKK β ) and numbers of phosphorylated liver kinase B1 (LKB1)– and AMPK-positive cells significantly decreased in the glomeruli of early stage human DN. AdipoRon treatment restored diabetes-induced renal alterations in db/db mice. AdipoRon exerted renoprotective effects by directly activating intrarenal AdipoR1 and AdipoR2, which increased CaMKK β , phosphorylated Ser 431 LKB1, phosphorylated Thr 172 AMPK, and PPAR α expression independently of the systemic effects of adiponectin. AdipoRon-induced improvement in diabetes-induced oxidative stress and inhibition of apoptosis in the kidneys ameliorated relevant intracellular pathways associated with lipid accumulation and endothelial dysfunction. In high-glucose–treated human GECs and murine podocytes, AdipoRon increased intracellular Ca 2+ levels that activated a CaMKK β /phosphorylated Ser 431 LKB1/phosphorylated Thr 172 AMPK/PPAR α pathway and downstream signaling, thus decreasing high-glucose–induced oxidative stress and apoptosis and improving endothelial dysfunction. AdipoRon further produced cardioprotective effects through the same pathway demonstrated in the kidney. Our results show that AdipoRon ameliorates GEC and podocyte injury by activating the intracellular Ca 2+ /LKB1-AMPK/PPAR α pathway, suggesting its efficacy for treating type 2 diabetes–associated DN.

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Authors: Kim, Y., Lim, J. H., Kim, M. Y., Kim, E. N., Yoon, H. E., Shin, S. J., Choi, B. S., Kim, Y.-S., Chang, Y. S., & Park, C. W.
Affiliations: The Catholic University of Korea Incheon St. Mary's Hospital (KR)
The Catholic University of Korea Seoul St. Mary's Hospital (KR)
The Catholic University of Korea Yeouido St. Mary's Hospital (KR)
Corresponding author: Park, Cheol Whee
ORCID: Kim, Yaeni
Kim, Eun Nim
Yoon, Hye Eun
Shin, Seok Joon
Choi, Bum Soon
Kim, Yong-Soo
Park, Cheol Whee
Venue: Journal of the American Society of Nephrology
Publisher: Ovid Technologies (Wolters Kluwer Health)
Published: 2018-01-12
Volume: 29
Issue: 4
Pages: 1108-1127
ISSN: 1046-6673 (ISSN-L)
1533-3450
DOI: 10.1681/asn.2017060627
PMC: PMC5875945
OpenAlex: W2783996679
Cited by: 229
References: 40
Citations by year: 2026: 19 · 2025: 31 · 2024: 41 · 2023: 28 · 2022: 30 · 2021: 23 · 2020: 28 · 2019: 22 · 2018: 7
FWCI: 16.38
Type: journal article
Language: en
Open access: green
www.ncbi.nlm.nih.gov
Locations: Journal of the American Society of Nephrology (publishedVersion)
Europe PMC (PubMed Central) (publishedVersion)
PubMed Central (publishedVersion)
PubMed (publishedVersion)
Funders: Yonsei University
Topics: Health Sciences › Medicine › Nephrology › Chronic Kidney Disease and Diabetes
Health Sciences › Medicine › Endocrinology, Diabetes and Metabolism › Adipokines, Inflammation, and Metabolic Diseases
Health Sciences › Medicine › Nephrology › Renal Diseases and Glomerulopathies
Keywords: AdipoRon, adiponectin receptor agonist, diabetic nephropathy, type 2 diabetes, AMPK, PPARα, CaMKKβ, LKB1, AdipoR1, AdipoR2, glomerular endothelial cells, podocytes, oxidative stress, apoptosis, endothelial dysfunction, intracellular calcium, cardioprotection, db/db mice
MeSH terms: Animals, Cells, Cultured, Diabetes Mellitus, Type 2, Diabetic Nephropathies, Glucose, Humans, Male, Mice, Inbred C57BL, Mice, Obese, Phosphorylation, Piperidines, Protein Processing, Post-Translational, Apoptosis, Protein Serine-Threonine Kinases, Oxidative Stress, Endothelial Cells, PPAR alpha, Podocytes, Mice, Adiponectin, Receptors, Leptin, Receptors, Adiponectin, Calcium-Calmodulin-Dependent Protein Kinase Kinase, AMP-Activated Protein Kinases

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The Adiponectin Receptor Agonist AdipoRon Ameliorates Diabetic Nephropathy in a Model of Type 2 Diabetes

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