Effect of Partial Substitution of Fish Meal with Sunflower Meal on Feed Utilization, Intestinal Digestive Enzyme, Hematological Indexes, Intestinal, and Liver Morphology on Juvenile Turbot (Scophthal musmaximus L.)

A 70-day feeding trial was conducted to evaluate effects of partial substitution of fish meal (FM) by sunflower meal (SFM) on juvenile turbot (Scophthal musmaximus L.). Five isonitrogenous and isoenergetic diets were formulated with 0%, 15%, 25%, 35%, and 45% replacement of FM protein with protein from SFM. Triplicate groups of juvenile turbot (30 fish per group), were hand-fed twice daily to apparent satiation. Final body weight (FBW), specific growth rate (SGR), and weight gain rate (WGR), were not significantly influenced by type of plant protein at the 15% level (P>0.05), while higher levels showed significant reduction of FBW, SGR, WGR. Feed efficiency ratio (FER) and feed intake (FI) were significantly influenced when FM protein was replaced up to 45% (P0.05). In the SFM diet groups, all superoxide dismutase (SOD) values were significantly higher than the control (P0.05) in microvilli height between diets; parenchyma structure of liver was severely damaged; smaller hepatocyte areas and areas with high levels of hepatocyte vacuolization and disorganization were present. All results indicated that SFM protein can partially replace FM protein in juvenile turbot diets without adverse effects

TET2 facilitates PPARγ agonist–mediated gene regulation and insulin sensitization in adipocytes

Emerging evidence indicates that epigenetic mechanisms like DNA methylation directly contribute to metabolic regulation. For example, we previously demonstrated that de novo DNA methyltransferase Dnmt3a plays a causal role in the development of adipocyte insulin resistance. Recent studies suggest that DNA demethylation plays an important role in the developmental process of adipocytes. However, little is known about whether DNA demethylase ten-eleven translocation (TET) proteins regulate the metabolic functions of adipocytes.MethodsThe expression of Tet genes was assessed in the fractionated adipocytes of chow- and high fat diet-fed C57/Bl6 mice using qPCR and western blotting. The effect of Tet2 gain- or loss-of-function in fully mature 3T3-L1 adipocytes in the presence/absence of Rosiglitazone (Rosi) and TNF-α on insulin sensitivity was using the insulin-stimulated glucose uptake and insulin signaling assays. Gene expression and DNA methylation analyses of PPARγ target genes was performed in the same setting. In addition, PPARγ reporter assays, co-immunoprecipitation assays, PPARγ ChIP-PCR analyses were performed.ResultsWe found that adipose expression of TET2, alone among its family members, was significantly reduced in diet-induced insulin resistance. TET2 gain-of-function was sufficient to promote insulin sensitivity while loss-of-function was necessary to facilitate insulin sensitization in response to the PPARγ agonist Rosiglitazone (Rosi) in cultured adipocytes. Consistent with this, TET2 was required for Rosi-dependent gene activation of certain PPARγ targets accompanied by changes in DNA demethylation at the promoter regions. Furthermore, TET2 was necessary to sustain PPARγ binding to target loci upon activation with Rosi via physical interaction with PPARγ.ConclusionsOur data demonstrate that TET2 works as an epigenetic regulator of Rosi-mediated insulin sensitization and transcriptional regulation in adipocytes