Krill Oil Inhibits NLRP3 Inflammasome Activation in the Prevention of the Pathological Injuries of Diabetic Cardiomyopathy

Diabetic cardiomyopathy (DCM) is a common complication of diabetes mellitus (DM), resulting in high mortality. Myocardial fibrosis, cardiomyocyte apoptosis and inflammatory cell infiltration are hallmarks of DCM, leading to cardiac dysfunction. To date, few effective approaches have been developed for the intervention of DCM. In the present study, we investigate the effect of krill oil (KO) on the prevention of DCM using a mouse model of DM induced by streptozotocin and a high-fat diet. The diabetic mice developed pathological features, including cardiac fibrosis, apoptosis and inflammatory cell infiltration, the effects of which were remarkably prevented by KO. Mechanistically, KO reversed the DM-induced cardiac expression of profibrotic and proinflammatory genes and attenuated DM-enhanced cardiac oxidative stress. Notably, KO exhibited a potent inhibitory effect on NLR family pyrin domain containing 3 (NLRP3) inflammasome that plays an important role in DCM. Further investigation showed that KO significantly upregulated the expression of Sirtuin 3 (SIRT3) and peroxisome proliferator-activated receptor-γ coactivator 1α (PGC-1α), which are negative regulators of NLRP3. The present study reports for the first time the preventive effect of KO on the pathological injuries of DCM, providing SIRT3, PGC-1α and NLRP3 as molecular targets of KO. This work suggests that KO supplementation may be a viable approach in clinical prevention of DCM.

Partial Replacement of Dietary Fat with Krill Oil or Coconut Oil Alleviates Dyslipidemia by Partly Modulating Lipid Metabolism in Lipopolysaccharide-Injected Rats on a High-Fat Diet

This study investigated the effects of partial replacement of dietary fat with krill oil (KO) or coconut oil (CO) on dyslipidemia and lipid metabolism in rats fed with a high-fat diet (HFD). Sprague Dawley rats were divided into three groups as follows: HFD, HFD + KO, and HFD + CO. The rats were fed each diet for 10 weeks and then intraperitoneally injected with phosphate-buffered saline (PBS) or lipopolysaccharide (LPS) (1 mg/kg). The KO- and CO-fed rats exhibited lower levels of serum lipids and aspartate aminotransferases than those of the HFD-fed rats. Rats fed with HFD + KO displayed significantly lower hepatic histological scores and hepatic triglyceride (TG) content than rats fed with HFD. The KO supplementation also downregulated the adipogenic gene expression in the liver. When treated with LPS, the HFD + KO and HFD + CO groups reduced the adipocyte size in the epididymal white adipose tissues (EAT) relative to the HFD group. These results suggest that KO and CO could improve lipid metabolism dysfunction.

The Effect of Krill Oil on Longevity and Locomotion: A Pilot Study

Krill oil as a dietary supplement is popular for consumers. Several experimental and clinical trials have suggested that krill oil is beneficial for longevity and locomotion, but the underlying mechanisms...

Development and Validation of a Simple Method to Quantify Contents of Phospholipids in Krill Oil by Fourier-Transform Infrared Spectroscopy

This study focuses on developing a quantification method for phosphatidylcholine (PC) and total phospholipid (PL) in krill oil using Fourier-transform infrared (FT-IR) spectroscopy. Signals derived from the choline and phosphate groups were selected as indicator variables for determining PC and total PL content; calibration curves with a correlation coefficient of >0.988 were constructed with calibration samples prepared by mixing krill oil raw material and fish oil in different ratios. The limit of detection (LOD, 0.35–3.29%) of the method was suitable for the designed assay with good accuracy (97.90–100.33%). The relative standard deviations for repeatability (0.90–2.31%) were acceptable. Therefore, both the methods using absorbance and that using second-derivative were confirmed to be suitable for quantitative analysis. When applying this method to test samples, including supplements, the PC content and total PL content were in good agreement with an average difference of 2–3% compared to the 31P NMR method. These results confirmed that the FT-IR method can be used as a convenient and rapid alternative to the 31P NMR method for quantifying PLs in krill oil.

The Possible Hepatoprotecive Effects of ''Krill Oil and Silymarin against Carbon Tetrachloride (CCl4)-Induced Rats Model of Liver Fibrosis: In Vivo Study''

Liver fibrosis is considered now as one of the most spread disease worldwide. It is attributed to different underlying causative agents such as viral infections, ethanol-induced liver steatosis, and non-ethanol-induced hepatic steatosis, autoimmune and inherited disorders. Hepatic fibrosis was known to behave as tissue repair mechanism in which the initiation occurred through complicated series of interrelated and regulated signaling. These signals involved interactions between different types of cells. Among these cells are hepatocytes, non-parenchymal cells such as hepatic stellate cells (HSCs), liver sinusoidal endothelial cells, Kupffer cells, biliary epithelial cells, liver associated lymphocytes, and the non-resident infiltrating immune cells. current work was aimed to investigate the possible potential hepatopretective effects of krill oil alone and in combination with silymarin against Carbone tetrachloride-induced liver fibrosis/injury in white albino rats. Moreover, fifty white albino rats of both genders were utilized in this study. During such study liver fibrosis/damage was induced by intraperitoneal (I.P) injection of Carbone tetrachloride (CCl4) 50% in olive oil 1ml/kg twice weekly for 6 consecutive weeks in the induction group. Krill oil alone and in combination with silymarin was administered orally concurrently with I.P CCl4 for 6 consecutive weeks in the treatment groups. At the end of treatment period all animals were killed ,serum and tissue samples were collected for subsequent analyses. Serum levels of aminotransferases (ALT,AST), albumin , total serum bilirubin (T.S.B), and total anti-oxidant capacity were measured spectrophotometrically. In addition tissue level (content) of liver hudroxyproline content (Hyp) was determined by ELISA and relative liver weight percentage (R.L.W%) was also estimated.Results were significantly revealed that krill oil potentiate the hepatoprotective effects of silymarin against Carbone tetrachloride-induced liver fibrosis/injury.

Krill-Oil-Dependent Increases in HS-Omega-3 Index, Plasma Choline and Antioxidant Capacity in Well-Conditioned Power Training Athletes

There is evidence that both omega-3 polyunsaturated fatty acids (n-3 PUFAs) and choline can influence sports performance, but information establishing their combined effects when given in the form of krill oil during power training protocols is missing. The purpose of this study was therefore to characterize n-3 PUFA and choline profiles after a one-hour period of high-intensity physical workout after 12 weeks of supplementation. Thirty-five healthy power training athletes received either 2.5 g/day of Neptune krill oilTM (550 mg EPA/DHA and 150 mg choline) or olive oil (placebo) in a randomized double-blind design. After 12 weeks, only the krill oil group showed a significant HS-Omega-3 Index increase from 4.82 to 6.77% and a reduction in the ARA/EPA ratio (from 50.72 to 13.61%) (p < 0.001). The krill oil group showed significantly higher recovery of choline concentrations relative to the placebo group from the end of the first to the beginning of the second exercise test (p = 0.04) and an 8% decrease in total antioxidant capacity post-exercise versus 21% in the placebo group (p = 0.35). In conclusion, krill oil can be used as a nutritional strategy for increasing the HS-Omega-3 Index, recover choline concentrations and address oxidative stress after intense power trainings.