Kidney Week

Abstract: TH-PO942

Adiponectin and Its Receptors in Peripheral Muscle and Fat Tissues of CKD Patients

Session Information

• Molecular Mechanisms of CKD - I
  October 25, 2018 | Location: Exhibit Hall, San Diego Convention Center
  Abstract Time: 10:00 AM - 12:00 PM

Category: CKD (Non-Dialysis)

• 1903 CKD (Non-Dialysis): Mechanisms

Authors

• Milanesi, Samantha, University of Genoa, Genoa, Italy

Samantha Milanesi,

• Verzola, Daniela, University of Genoa, Genoa, Italy

Daniela Verzola,

• Saio, Michela, University of Genoa, Genoa, Italy

Michela Saio,

• Picciotto, Daniela, University of Genoa, Genoa, Italy

Daniela Picciotto,

• Brunori, Giuliano, Ospedale S. Chiara, Trento - Italy, Trento TN, Italy

Giuliano Brunori,

• Venturelli, Chiara, APSS TRENTO, Trento, Italy

Chiara Venturelli,

• Garibotto, Giacomo, University of Genoa, Genoa, Italy

Giacomo Garibotto,

Background

Inflammation contributes to protein-energy wasting (PEW) in CKD, but the role of adiponectin (APN), which has anti-inflammatory properties, is not known. APN is secreted preferentially by adipocytes, but also by skeletal muscle. APN binds two receptor isoforms, adiponectin receptor 1 (AR1) and adiponectin receptor 2 (AR2). The aim of this study was to examine the expression of APN and its receptors in skeletal muscle and adipose tissue in CKD patients.

Methods

Muscle biopsies were obtained from 29 CKD (eGFR 8±3 ml/min per 1.73m² , 15M/14F, age 69 yrs) patients and 14 controls (C) rectus abdominis muscle samples. In this cohort, visceral fat samples were also obtained in 16 CKD and 10 C subjects. The expressions of APN, AR1 and R2 were tested by rtPCR and immunohistochemistry.

Results

Skeletal Muscle: APN gene expression and protein were up-regulated, (by 6-3.5 folds with respect to C, p< 0.001), AR1 and R2 mRNAs were markedly downregulated (-90 %, p<0,001), while protein expression was unchanged in CKD vs. C. Adipose tissue: APN, AR1 and R2 mRNAs were upregulate (by 2-7 folds, p<0.05) in CKD vs. C. Muscle APN mRNA was directly related to TLR4 protein expression (r²=0.33, p=0.023); moreover, APN and IL-6 protein were directly related (r²=0.28, p<0.01). Only as a trend, APN protein was related to NF-kB pp65 (r²=0.179, p=0.056). Visceral Fat APN was directly related to plasma CRP ( r=0.62, p=0.028).

Conclusion

In conclusion, muscle and visceral fat APN and APN receptors expression pattern is markedly modified in CKD. The APN system appears to respond to chronic inflammation as a compensatory mechanism which helps to maintain body homeostasis.