Lipidomic Profiling Reveals the Reducing Lipid Accumulation Effect of Dietary Taurine in Groupers (Epinephelus coioides)

A lipidomic analysis was conducted to provide the first detailed overview of lipid molecule profiles in response to dietary lipid and taurine and associations of liver lipid-lowering effects of dietary taurine with lipid molecular species and the positional distributions of fatty acids in the liver of juvenile orange-spotted groupers (Epinephelus coioides). The results indicated that the liver was more sensitive to varied dietary lipid and taurine contents than the muscle with regard to lipid molecules. A total of 131 differential lipid molecules (DLMs) were observed in the liver of groupers when dietary taurine was increased from 0 to 1% at 15% lipid, among which all the up and down-regulated DLMs are phospholipids (PLs) and triglycerides (TGs), respectively. The liver content of TGs containing 18:2n-6 attached at the sn-2 and sn-3 positions on the glycerol backbone increased with increasing dietary lipid from 10 to 15% but decreased with increasing dietary taurine from 0 to 1%. Therefore, dietary taurine can not only reduce lipid accumulation through decreasing the contents of TGs containing 18:2n-6 at the sn-2 and sn-3 positions but also enhance the anti-inflammatory capacity and health status of groupers. This study will also provide a new insight into the function of taurine in farmed fish.

GROWTH OF JUVENILES OF THE FAT SNOOK, Centropomus parallelus, IN RESPONSE TO DIETARY LIPID, ENERGY AND PROTEIN

This study evaluated the growth of fat snook Centropomus parallelus in response to the dietary total lipids, gross energy (GE) and crude protein (CP) content. In the 1st experiment, five isonitrogenous diets with 541.7 ± 2.4 g kg-1 CP varied their lipid content in 113, 151, 160, 189 and 200 g kg-1 and GE in 18.8, 19.4, 20.4, 21.2 and 22.2 MJ kg-1, respectively. A total of 300 fish with 6.5 ± 2.4 g were stocked in 30 tanks of 1 m3 under 10 fish m-³ and reared for 96 days. There were no differences in fish final body weight (38.2 ± 12.5 g), daily weight gain (DWG, 0.35 ± 0.04 g day-1) and specific growth rate (SGR, 1.92 ± 0.11 day-1) among dietary treatments. Feed conversion ratio (FCR) was 1.76 ± 0.17 with a protein efficiency ratio of 1.06 ± 0.10. The viscerosomatic (VSI) and visceral fat indices (VFI) raised significantly with an increase in the dietary lipid while the hepatosomatic index (HSI) was unaffected. There was a significant reduction in feed intake as the dietary lipid content reached 189 g kg-1. In a 2nd study, five isolipidic diets (114.4 ± 1.9 g kg-1 lipids) with decreasing levels of CP and GE of 578, 535, 505, 465, and 430 g kg-1 and 20.5, 19.9, 19.4, 18.9, and 18.1 MJ kg-1, respectively, were evaluated. A total of 1,450 fish of 5.8 ± 2.1 g were reared in 30 tanks of 5.8 m³ under 10 fish m-3 for 93 days. Final survival reached 93.5 ± 5.5%. Fish DWG (0.27 ± 0.05 g day-1) and SGR (1.78 ± 0.11 % day-1) did not vary in response to dietary CP. Final body weight significantly reduced while HSI increased in fish fed the 430 g kg-1CP diet compared with fish fed the 578 g kg-1 CP diet. Results of this work indicated that fish between 5.8 g and 40.8 g wet body weight can maximize growth when fed diets containing 113.2 g kg-1 lipids, 540.5 g kg-1 CP and a 34.7 MJ kg-1 energy to protein ratio. Keywords: Centropomus parallelus, fat snook, protein, lipid, energy.

Intestinal SEC16B modulates obesity by controlling dietary lipid absorption

ABSTRACTGenome-wide association studies (GWAS) have identified genetic variants in SEC16 homolog B (SEC16B) locus to be associated with obesity and body mass index (BMI) in various populations. SEC16B encodes a scaffold protein located at endoplasmic reticulum (ER) exit sites that is implicated to participate in the trafficking of COPII vesicles in mammalian cells. However, the function of SEC16B in vivo, especially in lipid metabolism, has not been investigated. Here we demonstrated that intestinal SEC16B is required for dietary lipid absorption in mice. We showed that Sec16b intestinal knockout (IKO) mice, especially female mice, were protected from HFD-induced obesity. Loss of SEC16B in intestine dramatically reduced postprandial serum triglyceride output upon intragastric lipid load or during overnight fasting and high-fat diet (HFD) refeeding. Further studies showed that intestinal SEC16B deficiency impaired apoB lipidation and chylomicron secretion. These results revealed that SEC16B plays important roles in dietary lipid absorption, which may shed light on the association between variants in SEC16B and obesity in human.

Off-Target Effect of Lovastatin Disrupts Dietary Lipid Uptake and Dissemination through Pro-Drug Inhibition of the Mesenteric Lymphatic Smooth Muscle Cell Contractile Apparatus

Previously published, off-target effects of statins on skeletal smooth muscle function have linked structural characteristics within this drug class to myopathic effects. However, the effect of these drugs on lymphatic vascular smooth muscle cell function, and by proxy dietary cholesterol uptake, by the intestinal lymphatic network has not been investigated. Several of the most widely prescribed statins (Atorvastatin, Pravastatin, Lovastatin, and Simvastatin) were tested for their in-situ effects on smooth muscle contractility in rat mesenteric collecting lymphatic vessels. Lovastatin and Simvastatin had a concentration-dependent effect of initially increasing vessel contraction frequency before flatlining the vessel, a phenomenon which was found to be a lactone-ring dependent phenomenon and could be ameliorated through use of Lovastatin- or Simvastatin-hydroxyacid (HA). Simvastatin treatment further resulted in mitochondrial depolymerization within primary-isolated rat lymphatic smooth muscle cells (LMCs) while Lovastatin was found to be acting in a mitochondrial-independent manner, increasing the function of RhoKinase. Lovastatin’s effect on RhoKinase was investigated through pharmacological testing and in vitro analysis of increased MLC and MYPT1 phosphorylation within primary isolated LMCs. Finally, acute in vivo treatment of rats with Lovastatin, but not Lovastatin-HA, resulted in a significantly decreased dietary lipid absorption in vivo through induced disfunction of mesenteric lymph uptake and trafficking.