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Here we present the presence of adiponectin and adiponectin receptors [type 1 (adipoR1) and type 2 (adipoR2)] in rainbow trout (Oncorhynchus mykiss) tissues and cell cultures together with the response to different scenarios. In response to fasting, adiponectin expression was up-regulated in adipose tissue, while the expression of its receptors increased in white and red muscle. Insulin injection decreased adipoR1 expression in white and red muscles. We deduce that the adipoRs in trout muscle show opposite responses to increasing insulin plasma levels, which may maintain sensitivity to insulin in this tissue. Adiponectin expression was inhibited by the inflammatory effect of lipopolysaccharide (LPS) in adipose tissue and red muscle. Moreover, results indicate that LPS may lead to mobilization of fat reserves, increasing adipoR1 expression in adipose tissue. The effects of LPS could be mediated through tumour necrosis factor α (TNFα), at least in red muscle. Insulin, growth hormone and TNFα all diminished expression of adipoR2 in adipocytes and adipoR1 in myotubes, while insulin increased the expression of adipoR2 in the muscle cells. Adiponectin activates Akt in rainbow trout myotubes, which may lead to an increase in fatty acid uptake and oxidation. Overall, our results show that the adiponectin system responds differently to various physiological challenges and that it is hormonally controlled in vivo and in vitro. To the best of our knowledge, this is the first time this has been demonstrated in teleosts, and it may be a valuable contribution to our understanding of adipokines in fish.

The present study aimed to analyze adiposity heterogeneity and the role of liver X receptor (LXRalpha) and peroxisome proliferator-activated receptors (PPARs) as targets of tumour necrosis factor-alpha (TNFalpha) in gilthead sea bream (Sparus aurata L.). The screening of 20 fish at the beginning of the warm season identified two major groups with fat and lean phenotypes. Fat fish showed increased liver and mesenteric fat depots. This increased adiposity was concurrent in the adipose tissue to enhanced expression of lipoprotein lipase (LPL) whereas mRNA levels of the hormone-sensitive lipase (HSL) remained almost unchanged. The resulting LPL/HSL ratio was thereby highest in fat fish, which suggests that this group of fish has not reached its peak fat storage capacity. This is not surprising given the increased expression of PPARgamma in the absence of a counter-regulatory raise of TNFalpha. However, this lipolytic cytokine exerted dual effects in primary adipocyte cultures that differ within and between lean and fat fish. One set of fat fish did not respond to TNFalpha treatment whereas a second set exhibited a lipolytic response (increased glycerol release) that was apparently mediated by the downregulated expression of PPARbeta. In lean fish, TNFalpha exerted a strong and non-transcriptionally mediated lipolytic action. Alternatively, TNFalpha would inhibit lipid deposition via the downregulated expression of adipogenic nuclear factors (PPARgamma and LXRalpha). TNFalpha targets are therefore different in fish with lean and fat phenotypes, which is indicative of the complex network involved in the regulation of fish lipid metabolism.