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Krill Oil Supplementation Reduces Exacerbated Hepatic Steatosis Induced by Thermoneutral Housing in Mice with Diet-Induced Obesity.

ABSTRACT: Preclinical evidence suggests that n-3 fatty acids EPA and DHA (Omega-3) supplemented as phospholipids (PLs) may be more effective than triacylglycerols (TAGs) in reducing hepatic steatosis. To further test the ability of Omega-3 PLs to alleviate liver steatosis, we used a model of exacerbated non-alcoholic fatty liver disease based on high-fat feeding at thermoneutral temperature. Male C57BL/6N mice were fed for 24 weeks a lard-based diet given either alone (LHF) or supplemented with Omega-3 (30 mg/g diet) as PLs (krill oil; ω3PL) or TAGs (Epax 3000TG concentrate; ω3TG), which had a similar total content of EPA and DHA and their ratio. Substantial levels of TAG accumulation (~250 mg/g) but relatively low inflammation/fibrosis levels were achieved in the livers of control LHF mice. Liver steatosis was reduced by >40% in the ω3PL but not ω3TG group, and plasma ALT levels were markedly reduced (by 68%) in ω3PL mice as well. Krill oil administration also improved hepatic insulin sensitivity, and its effects were associated with high plasma adiponectin levels (150% of LHF mice) along with superior bioavailability of EPA, increased content of alkaloids stachydrine and trigonelline, suppression of lipogenic gene expression, and decreased diacylglycerol levels in the liver. This study reveals that in addition to Omega-3 PLs, other constituents of krill oil, such as alkaloids, may contribute to its strong antisteatotic effects in the liver.

SUBMITTER: Sistilli G

PROVIDER: S-EPMC7912192 | biostudies-literature | 2021 Jan

REPOSITORIES: biostudies-literature

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Krill Oil Supplementation Reduces Exacerbated Hepatic Steatosis Induced by Thermoneutral Housing in Mice with Diet-Induced Obesity.

Sistilli Gabriella G Kalendova Veronika V Cajka Tomas T Irodenko Illaria I Bardova Kristina K Oseeva Marina M Zacek Petr P Kroupova Petra P Horakova Olga O Lackner Karoline K Gastaldelli Amalia A Kuda Ondrej O Kopecky Jan J Rossmeisl Martin M

Nutrients 20210129 2

Preclinical evidence suggests that n-3 fatty acids EPA and DHA (Omega-3) supplemented as phospholipids (PLs) may be more effective than triacylglycerols (TAGs) in reducing hepatic steatosis. To further test the ability of Omega-3 PLs to alleviate liver steatosis, we used a model of exacerbated non-alcoholic fatty liver disease based on high-fat feeding at thermoneutral temperature. Male C57BL/6N mice were fed for 24 weeks a lard-based diet given either alone (LHF) or supplemented with Omega-3 (3 ...[more]

PMID: 33572810

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Project description:BackgroundWe have previously reported that the free fatty acid extract (FFAE) of krill oil (KO) significantly inhibits the proliferation and migration, and induces apoptosis of colorectal cancer (CRC) cells. This study aimed to investigate the in vivo efficacy of various doses of KO supplementation on the inhibition of CRC tumour growth, molecular markers of proliferation, angiogenesis, apoptosis, the epidermal growth factor receptor (EGFR) and its downstream molecular signalling.MethodsMale Balb/c mice were randomly divided into four groups with five in each group. The control (untreated) group received standard chow diet; and other three groups received KO supplementation at 5%, 10%, and 15% of their daily dietary intake respectively for three weeks before and after the orthotopic implantation of CT-26 CRC cells in their caecum. The expression of cell proliferation marker Ki-67 and angiogenesis marker CD-31 were assessed by immunohistochemistry. The expression of EGFR, phosphorylated EGFR (pEGFR), protein kinase B (AKT), pAKT, extracellular signal-regulated kinase (ERK1/2), pERK1/2, cleaved caspase-7, cleaved poly (ADP-ribose) polymerase (PARP), and DNA/RNA damage were determined by western blot.ResultsKO supplementation reduced the CRC tumour growth in a dose-dependent manner; with 15% of KO being the most effective in reduction of tumour weight and volume (68.5% and 68.3% respectively, P < 0.001), inhibition of cell proliferation by 69.9% (P < 0.001) and microvessel density by 72.7% (P < 0.001). The suppressive effects of KO on EGFR and its downstream signalling, ERK1/2 and AKT, were consistent with our previous in vitro observations. Furthermore, KO exhibited pro-apoptotic effects on tumour cells as indicated by an increase in the expression of cleaved PARP by 3.9-fold and caspase-7 by 8.9-fold.ConclusionsThis study has demonstrated that KO supplementation reduces CRC tumour growth by inhibiting cancer cell proliferation and blood vessel formation and inducing apoptosis of tumour cells. These anti-cancer effects are associated with the downregulation of the EGFR signalling pathway and activation of caspase-7, PARP cleavage, and DNA/RNA damage.

Project description:BackgroundBioavailability of krill oil has been suggested to be higher than fish oil as much of the EPA and DHA in krill oil are bound to phospholipids (PL). Hence, PL content in krill oil might play an important role in incorporation of n-3 PUFA into the RBC, conferring properties that render it effective in reducing cardiovascular disease (CVD) risk. The objective of the present trial was to test the effect of different amounts of PL in krill oil on the bioavailability of EPA and DHA, assessed as the rate of increase of n-3 PUFA in plasma and RBC, in healthy volunteers.Methods and designIn a semi randomized crossover single blind design study, 20 healthy participants consumed various oils consisting of 1.5 g/day of low PL krill oil (LPL), 3 g/day of high PL krill oil (HPL) or 3 g/day of a placebo, corn oil, for 4 weeks each separated by 8 week washout periods. Both LPL and HPL delivered 600 mg of total n-3 PUFA/day along with 600 and 1200 mg/day of PL, respectively.ResultsChanges in plasma EPA, DPA, DHA, total n-3 PUFA, n-6:n-3 ratio and EPA + DHA concentrations between LPL and HPL krill oil supplementations were observed to be similar. Intake of both forms of krill oils increased the RBC level of EPA (p < 0.001) along with reduced n-6 PUFA (LPL: p < 0.001: HPL: p = 0.007) compared to control. HPL consumption increased (p < 0.001) RBC concentrations of EPA, DPA, total and n-3 PUFA compared with LPL. Furthermore, although LPL did not alter RBC n-6:n-3 ratio or the sum of EPA and DHA compared to control, HPL intake decreased (p < 0.001) n-6:n-3 ratio relative to control with elevated (p < 0.001) sum of EPA and DHA compared to control as well as to LPL krill oil consumption. HPL krill oil intake elevated (p < 0.005) plasma total and LDL cholesterol concentrations compared to control, while LPL krill oil did not alter total and LDL cholesterol, relative to control.ConclusionsThe results indicate that krill oil with higher PL levels could lead to enhanced bioavailability of n-3 PUFA compared to krill oil with lower PL levels.Trial registrationClinicaltrials.gov# NCT01323036.

Dataset Information

Krill Oil Supplementation Reduces Exacerbated Hepatic Steatosis Induced by Thermoneutral Housing in Mice with Diet-Induced Obesity.

Publications

Krill Oil Supplementation Reduces Exacerbated Hepatic Steatosis Induced by Thermoneutral Housing in Mice with Diet-Induced Obesity.

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