Adiponectin Paradox More Evident in Non-Obese Than in Obese Patients with Diabetic Microvascular Complications.
adiponectin
diabetic complications
obesity
Journal
Diabetes, metabolic syndrome and obesity : targets and therapy
ISSN: 1178-7007
Titre abrégé: Diabetes Metab Syndr Obes
Pays: New Zealand
ID NLM: 101515585
Informations de publication
Date de publication:
2023
2023
Historique:
received:
02
09
2022
accepted:
11
01
2023
entrez:
10
2
2023
pubmed:
11
2
2023
medline:
11
2
2023
Statut:
epublish
Résumé
Adiponectin is generally regarded as a beneficial molecule, protecting against insulin resistance and atherosclerosis, and its serum levels are low in individuals with obesity as well as in those with type 2 diabetes (T2DM). However, several clinical studies have shown associations between high adiponectin values and major health concerns. These conflicting findings are termed the "adiponectin paradox". Similarly, these paradoxical adiponectin elevations were observed in patients with diabetic microvascular complications. This cross-sectional study aimed to identify differences in factors, including adiponectin, related to diabetic vascular complications between non-obese and obese patients. Study patients with T2DM were non-obese (n=197) or obese (n=197), matched by a propensity score model adjusted with age and gender. Independent factors for each of the microvascular complications were determined using multivariate logistic regression analyses. The prevalence of nephropathy was high in obese T2DM patients. In addition to long diabetes duration, elevated adiponectin was a common characteristic of patients with microvascular complications. Logistic regression analyses for microvascular complications revealed adiponectin to be highly related to retinopathy (odds ratio [OR], 1.138; 95%confidence intervals [CI], 1.004-1.289, p<0.001), nephropathy (OR, 1.192; CI, 1.077-1.319, p<0.001) and neuropathy (OR, 1.217; CI, 1.071-1.384, p<0.001), in non-obese patients. In contrast, the association between adiponectin values and complications was modest in obese patients. Adiponectin regulation in response to vascular damage differed between non-obese and obese patients, suggesting that adiponectin regulation is compromised by fat accumulation. Assuming that paradoxical elevation of adiponectin in vascular damage is a compensatory response, we speculate that responsive upregulation might be insufficient in obese patients. These newly-recognized differences in adiponectin values might lead to novel insights into adiponectin regulation and our understanding of the adiponectin paradox.
Identifiants
pubmed: 36760589
doi: 10.2147/DMSO.S387744
pii: 387744
pmc: PMC9882416
doi:
Types de publication
Journal Article
Langues
eng
Pagination
201-212Informations de copyright
© 2023 Satoh et al.
Déclaration de conflit d'intérêts
None of the authors has any conflicts of interest to disclose for this work.
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