Fish Oil Decreases Hepatic Lipogenic Genes in Rats Fasted and Refed on a High Fructose Diet

Abstract

Fasting and then refeeding on a high-carbohydrate diet increases serum and hepatic triacylglycerol (TAG) concentrations compared to standard diets. Fructose is a lipogenic monosaccharide which stimulates de novo fatty acid synthesis. Omega-3 (n-3) fatty acids stimulate hepatic β-oxidation, partitioning fatty acids away from TAG synthesis. This study investigated whether dietary n-3 fatty acids from fish oil (FO) improve the hepatic lipid metabolic response seen in rats fasted and then refed on a high-fructose diet. During the post-prandial (fed) period, rats fed a FO rich diet showed an increase in hepatic peroxisome proliferator-activated receptor α (PPAR-α) gene expression and decreased expression of carbohydrate responsive element binding protein (ChREBP), fatty acid synthase (FAS) and microsomal triglyceride transfer protein (MTTP). Feeding a FO rich diet for 7 days prior to 48 h of fasting resulted in lower hepatic TAG, lower PPAR-α expression and maintenance of hepatic n-3 fatty acid content. Refeeding on a high fructose diet promoted an increase in hepatic and serum TAG and in hepatic PPAR-α, ChREBP and MTTP expression. FO did not prevent the increase in serum and hepatic TAG after fructose refeeding, but did decrease hepatic expression of lipogenic genes and increased the n-3 fatty acid content of the liver. n-3 Fatty acids can modify some components of the hepatic lipid metabolic response to later feeding with a high fructose diet.

Stachyose combined with tea polyphenols mitigated metabolic disorders in high fructose diet-fed mice as studied by GC-MS metabolomics approach

“…Castro et al found that long-term intake of HF significantly increased oleic acid levels in the liver and adipose tissue (de Castro, Cardoso, Calder, Jordão, & Vannucchi, 2015b;de Castro et al, 2015a). Our study revealed a significant increase in serum elaidic acid levels in mice after 8 weeks of drinking with HF water.…”

Zingiber officinaleextract and omega‐3 fatty acids ameliorate endoplasmic reticulum stress in a nonalcoholic fatty liver rat model

“…The therapeutic effect demonstrated by Z. officinale or omega‐3 is coherent with other studies that evaluated both therapies or their individual components against metabolic syndrome disorders such as type2 diabetes, obesity, IR, and NAFLD. These effects have been studied to be through regulation of lipogenesis, β‐oxidation besides their antioxidant and anti‐inflammatory activity (de Castro, Cardoso, Calder, Jordão, & Vannucchi, ; Huang, Deng, Meng, & Ma, ; Lai et al, ; Li et al, ; Molinar‐Toribio et al, ; Singh, Akanksha, Singh, Maurya, Srivastava, ). Here, we demonstrated a novel pathway by which the therapeutic approaches treat NAFLD by modulation of ER stress proposed to be responsible for NAFLD progression through different mechanisms (Ferré & Foufelle, ; Jo et al, ; Lee et al, ).…”

Fatty Acid Binding Protein‐1 (FABP1) and the Human FABP1 T94A Variant: Roles in the Endocannabinoid System and Dyslipidemias

“…While EPA and DHA induce PPARα transcription activity of LCFA oxidative genes, they concomitantly accelerate degradation and/or reduce nuclear distribution of SREBP1c and ChREBP. This decreases SREBP1c (213–215) and ChREBP (241–245) transcription of lipogenic genes which thereby decreases hepatic TAG and NAFLD in human subjects not segregated by FABP1 genotype. Another possibility is suggested by cannabinoid receptor (e.g.…”

“…In any case, FABP1 (7, 13, 14, 16, 40–42) and the nuclear receptors it impacts, i.e. PPARα (41, 42, 47, 246–248), SREBP1c (213–215), and ChREBP (241–245), continue to be current active therapeutic targets for lipid lowering.…”