Krill Products: An Overview of Animal Studies
Abstract
:1. Introduction
Composition | KO (g/100 g Oil) | KP (g/100 g Powder or Extracted Fat) | KPC (g/100 g KPC or Extracted Fat) |
---|---|---|---|
Protein | - | 38 | 78 |
Total lipids | 89 | 51 | 8 |
Triglycerides | 34 | 45 * | - |
Total PLs | 43 | 43 * | - |
PC | 35 | 40 * | - |
Total omega-3 | 25 | 20 * | 27 * |
EPA | 13 | 10 * | 12 * |
DHA | 7 | 5 * | 13 * |
Total omega-6 | 2 | 2 * | 4 * |
Saturated FA | 23 | 25 * | 37 * |
Total MUFAs | 15 | 20 * | 21 * |
2. Documentation of Krill Oil Health Benefits in Animal Studies
Classification of health benefits | Study | Animal model | Diets | Duration of Supplementation | Effect of KO/KPC and KP |
---|---|---|---|---|---|
Effect of KO | |||||
Obesity | Zhu et al., 2008 [34] | SD rats (obesity model) n = 60 | Different doses: High fat with 16.7, 33.3, 99.9 or 199.8 g/L KO | 4 weeks | decreased levels of serum TAG, TC and LDL-C |
reduced body weight | |||||
Obesity | Batetta et al., 2009 [23] | Zucker rats (obesity model) n = 18 | Control diet with 0.5 g EPA+DHA/100 g diet (from either KO or FO) | 4 weeks | decreased levels of plasma LDL-C |
increased levels of plasma TAG | |||||
reduced TAG in liver and heart | |||||
decreased AEA and 2-AG in VAT and AEA in liver and heart | |||||
reduced TNFα secretion from macrophages (associated with lower levels of AA in membrane PLs) | |||||
Obesity | Tandy et al., 2009 [30] | C57BL/6 mice (obesity model) n = 46 | Different doses: Normal diet or high fat diet with 1.25%, 2.5% or 5.0% KO | 8 weeks | reduced hepatic steatosis and plasma glucose and TC (not TAG) |
increased adiponectin | |||||
reduced hepatic TNFα expression and down-regulation of several hepatic genes involved in FA synthesis and catabolism | |||||
Obesity | Di Marzo et al., 2010 [28] | Zucker rats (obesity model) n = 18 | Control diet with 0.5 g EPA+DHA/100 g diet (from either KO or FO) | 4 weeks | increased EPA and DHA levels in brain |
decreased 2-AG levels in brain | |||||
Obesity | Piscitelli et al., 2011 [29] | C57BL/6 mice (obesity model) n = 6–10 per group | Different doses: Normal diet or high fat diet with 1.25, 2.5 or 5% KO | 8 weeks | reduction of AEA and/or 2-AG levels in heart, kidneys, gastrocnemius muscle, inguinal and epididymal adipose tissue |
Obesity | Ferramosca et al., 2012 [24] | SD rats n = 120 | Control, High fat control, High fat 2.5% KO | 12 weeks | decreased levels of hepatic TAG and cholesterol |
reduced plasma TAG and glucose levels | |||||
reduced hepatic FA synthesis | |||||
increased hepatic FA oxidation | |||||
increased mitochondrial respiration efficiency | |||||
reduction in body weight | |||||
Obesity | Tillander et al., 2014 [31] | C57BL/6J mice | High fat control (n = 9) High fat FO (5.8%) (n = 6) High fat KO (5.7%) (n = 6) | 6 weeks | decreased plasma levels of NEFA |
down regulation of cholesterol and fatty acid synthesis (mRNA level) | |||||
Obesity | Ivanova et al., 2014 [32] | New Zealand white rabbits n = 24 | Castrated control, Non-castrated control, Castrated KO (daily dose of 600 mg omega-3), Castrated FO (daily dose of 600 mg omega-3) | 2 months | decreased fasting glucose for both FO and KO |
modified gene expression of key enzymes in β-oxidation, lipogenesis in liver and skeletal muscle | |||||
Inflammation | Ierna et al., 2010 [27] | DBA/1 mice (arthritis model) n = 42 | Control diet with 0.44 g EPA+DHA/100 g diet from KO or 0.47 g EPA+DHA/100 g diet from FO). Induction of arthritis Day 25, boost Day 47 | 68 days | reduction in paw swelling |
reduction in histopathology scores (joint section) | |||||
Inflammation | Grimstad et al., 2012 [21] | Wistar rats (colitis model) n = 30 | Control, Control + DSS, Control + DSS + KO, Induction of colitis by DSS on Day 23 | 30 days | improved colon length |
increased level of (PG)E3 and Pparg1 α expression | |||||
Cardiovascular | Fosshaug et al., 2011 [25] | Wistar rats (myocardial infarction model) | Control n = 14 pre-treated (2 weeks) with KO n = 18 not pre-treated with KO n = 17 Induction of myocardial infarction by left coronary artery ligation | 7 weeks | Pre-treated KO group: - attenuated LV dilation - reduced heart and lung weights - reduced mRNA levels of LV stress and matrix remodeling markers |
Not pre-treated KO group: - increased LV | |||||
Brain | Gamoh et al., 2011 [35] | Wistar rats | Control (n = 15) High dose krill PL (420 mg EPA+DHA) (n = 14) Low dose krill PL (301 mg EPA+DHA) (n = 13) | 6 weeks | improved spatial-memory related learning ability |
increased levels of EPA, DPA and DHA and decreased level of AA in the brain | |||||
decreased levels of lipid peroxide and reactive oxygen species | |||||
increased cell generation in dentate gyrus | |||||
Brain | Wibrand et al., 2013 [22] | Wistar rats | Control (n = 12) Imipramine (n = 12) KO 1.25% (n = 14) KO 2.50% (n = 14) | 7 weeks | improved learning and memory processes |
anti-depressant-like effects | |||||
Liver | Ferramosca et al., 2012 [36] | Wistar rats n = 18 | Control, 2.5% KO, 2.5% FO | 6 weeks | decreased levels of plasma TAG and TC |
inhibition of hepatic lipogenesis (reduced activity of CIC, ACC and FAS) | |||||
Gene expression | Burri et al., 2011 [37] | CBA/J micen = 30 | Control diet with 1.5% KO or 1.1% FO | 3 months | down-regulation of: hepatic glucose pathways, lipid and cholesterol synthesis (FO up-regulated cholesterol synthesis pathway) |
Kidney | Gigliotti et al., 2013 [33] | Female SD rats n = 60 | 12% corn oil (n = 10) 12% flaxseed (n = 10) 12% menhaden oil (n = 10) 12% KO (n = 10) 12% salmon oil (n = 10) 12% tuna oil (n = 10) | 8 weeks | increased kidney weight |
increased calcium content of the kidneys | |||||
increased urinary phosphorous excretion | |||||
Safety | Robertson et al., 2014 [20] | Wistar rats n = 80 | Control, 1.7% KO, 3.3% KO, 5% KO | 13 weeks | NOAEL is 5% KO |
Effect of KPC and KP | |||||
Inflammation | Bjørndal et al., 2012 [38] | C57BL/6 mice constitutively expressing hTNFα gene (n = 20) | High fat control; High fat 3% KP | 6 weeks | decreased plasma and liver TAG levels |
down-regulation of hepatic genes involved in lipogenesis | |||||
reduction of TNFα in liver | |||||
Kidney | Gigliotti et al., 2008 [40] | Female SD rats n = 30 | 10% KPC, 10% casein | 4 weeks | reduced kidney weight |
reduced total mineral content of the kidneys | |||||
no differences in kidney function | |||||
Kidney, Bone | Gigliotti et al., 2011 [41] | Female SD rats n = 20 | 10% KPC, 10% casein | 4 weeks | reduced kidney injury (lower urinary NAG activity, reduced kidney mineralization, tendency for higher GRFs and lower proteinuria) and Ca deposition |
no effect on bone mass or strength | |||||
Gene expression | Bjørndal et al., 2013 [41] | CBA/J mice n = 20 | Low fat control Low fat 3% KP | 3 months | large number of pathways are modulated |
down regulated pathways: β-oxidation, glucose metabolism and amino acid catabolism | |||||
Safety | Bridges et al., 2010 [42] | Female SD rats n = 20 | 10% KPC, 10% casein | 4 weeks | increased DHA concentration in brain, and increased EPA and DHA concentration in fat pads and liver |
decreased pro-inflammatory 2-series prostaglandin and thromboxan metabolites | |||||
Safety | Berge et al., 2014 [43] | Wistar rats | Control, 9.67% KP | 13 weeks | NOAEL is 9.67% KP |
2.1. Different tissue FA Distribution When Carried in PL Versus TAG Ester Forms
2.2. Krill Oil—Endocannabinoid System
2.3. Krill Oil—Body and Tissue Weights
2.4. Krill Oil—Glucose Tolerance
2.5. Krill Oil—Chronic Inflammation, Rheumatoid Arthritis and Ulcerative Colitis
2.6. Krill Oil—Cardiovascular Risk Markers and Myocardial Infarction
2.7. Krill Oil— Cognitive Function/Depression
2.8. Krill Oil—Gene Expression
2.9. Krill Powder
Metabolic Pathway | Krill Oil | Krill Powder | ||
---|---|---|---|---|
High-fat | Low-fat | High-fat | Low-fat | |
Lipid synthesis | ↓ | ↓ | ↓ | - |
Cholesterol metabolism | ↓ | ↓ | ↓ | - |
β-oxidation | ↑ | ↓ | ↑ | ↓ |
Mitochondrial respiration | ? | ↑ | ? | ↑ |
Amino acid catabolism | ? | - | ? | ↓ |
Glucose synthesis | ↓ | ↓ | ↓ | ↓ |
3. Discussion
4. Conclusions
Abbreviations
AEA | N-arachidonoyl-ethanolamine |
2-AG | 2-arachidonoylglycerol |
ALA | α-linolenic acid |
ALSAT | aversive light stimulus avoidance test |
ARA | arachidonic acid |
CIC | mitochondrial citrate carrier |
CNS | central nervous system |
CVD | cardiovascular disease |
DAI | disease activity index |
DHA | docosahexaenoic acid |
DSS | dextran sulfate sodium |
EC | endocannabinoids |
EPA | eicosapentaenoic acid |
FA | fatty acid |
FO | fish oil |
HDL | high-density lipoprotein |
IMIP | Imipramine |
KO | krill oil |
LDL | low-density lipoprotein |
LPS | lipopolysaccharide |
LV | left ventricular |
lyso-PC | lysophosphatidylcholine |
MI | myocardial infarction |
NAFLD | non-alcoholic fatty liver disease |
NHANES | national health and nutrition examination survey |
NEFA | non-esterified fatty acid |
NOAEL | no observed adverse effect level |
n-3 PUFA | omega-3 polyunsaturated fatty acid |
PC | phosphatidylcholine |
PE | phosphatidylethanolamine |
PL | phospholipid |
PPARα | peroxisome proliferator-activated receptor alpha |
RME | Reference Memory Error |
TAG | triacylglyceride |
TNFα | tumor necrosis factor-alpha |
WME | Working Memory Error |
Acknowledgements
Conflicts of Interest
References
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Burri, L.; Johnsen, L. Krill Products: An Overview of Animal Studies. Nutrients 2015, 7, 3300-3321. https://doi.org/10.3390/nu7053300
Burri L, Johnsen L. Krill Products: An Overview of Animal Studies. Nutrients. 2015; 7(5):3300-3321. https://doi.org/10.3390/nu7053300
Chicago/Turabian StyleBurri, Lena, and Line Johnsen. 2015. "Krill Products: An Overview of Animal Studies" Nutrients 7, no. 5: 3300-3321. https://doi.org/10.3390/nu7053300