Circulating and local visfatin/Nampt/PBEF levels in spontaneously hypertensive rats, stroke-prone spontaneously hypertensive rats and Wistar-Kyoto rats

Abstract

Visfatin (also known as nicotinamide phosphoribosyltransferase and pre-B cell colony-enhancing factor) is a multifunctional protein. Visfatin has been reported to be involved in several biological processes in the cardiovascular system, . However, the role of visfatin in hypertension is still unclear. In this study, we examined the circulating and local adipose visfatin levels in spontaneously hypertensive rats (SHR), stroke-prone spontaneously hypertensive rats (SHR-SP), and in their normotensive control Wistar-Kyoto (WKY). SHR and SHR-SP rats exhibited lower body weight, lower fat tissue and hypolipidemia. No differences of serum visfatin levels were observed in SHR/SHR-SP and WKY. Serum visfatin levels did not correlate to serum glucose, lipids, insulin, and fat pad weights, but significantly correlated to weights of skeletal muscle. Visfatin expression in visceral fat tissue was slightly lower in SHR-SP compared with that in WKY. Moreover, there were no significant differences of visfatin expression in skeletal muscles among WKY, SHR and SHR-SP. Finally, visfatin protein was detected in L6 rat skeletal muscle cell culture medium, indicating that visfatin was secreted from skeletal muscle cells. Thus, our results may provide useful information for understanding the characteristic of visfatin in hypertensive models, and support the view that visfatin may be a myokine.

Fig. 1

a, b Blood pressure (BP) and c heart rate of Wistar-Kyoto rats (WKY, n = 8), spontaneously hypertensive rats (SHR, n = 8), and stroke-prone spontaneously hypertensive rats (SHR-SP, n = 8). **P < 0.01 versus WKY

Fig. 2

Serum biochemical parameters (a), body weight (BW) and fat tissue weights (b) of Wistar-Kyoto rats (WKY, n = 8), spontaneously hypertensive rats (SHR, n = 8), and stroke-prone spontaneously hypertensive rats (SHR-SP, n = 8). *P < 0.05, **P < 0.01 versus WKY. HDL High-density lipoprotein, LDL low-density lipoprotein, HOMA-IR homeostasis model assessment insulin resistance

Fig. 3

Serum visfatin levels of Wistar-Kyoto rats (WKY, n = 8), spontaneously hypertensive rats (SHR, n = 8), and stroke-prone spontaneously hypertensive rats (SHR-SP, n = 8)

Fig. 4

Scatter plots showing the relationships between serum visfatin levels and serum lipids levels (a), and between serum visfatin levels and body weights, fat pad weights and skeletal muscle weights (b) in of Wistar-Kyoto rats (WKY, n = 8), spontaneously hypertensive rats (SHR, n = 8), and stroke-prone spontaneously hypertensive rats (SHR-SP, n = 8). Data were analyzed by linear regression analysis. Abbreviations as in Fig. 2

Fig. 5

Western blotting showing visfatin expression in inguinal subcutaneous fat tissue and mesenteric visceral fat tissue in Wistar-Kyoto rats (WKY), spontaneously hypertensive rats (SHR), and stroke-prone spontaneously hypertensive rats (SHR-SP). *P < 0.05 versus WKY. GAPDH (glyceraldehyde 3-phosphate dehydrogenase) was used as a loading control

Fig. 6

Western blotting showing visfatin expression in skeletal muscle tissues and skeletal muscle cell culture medium. Visfatin protein (a) and mRNA (b) expression in gastrocnemius, soleus and extensor digitorum longus (EDL) in Wistar-Kyoto rats (WKY), spontaneously hypertensive rats (SHR), and stroke-prone spontaneously hypertensive rats (SHR-SP). NS Not significant versus WKY. GAPDH (glyceraldehyde 3-phosphate dehydrogenase) was used as a loading control. c Visfatin was detected in skeletal muscle tissue and L6 rat skeletal muscle cell culture medium. Recombinant mouse visfatin was used as a positive control