Effect of Bombyx mori on the Liver Protection of Non-Alcoholic Fatty Liver Disease Based on In Vitro and In Vivo Models

Abstract

Edible insects, Bombyx mori (silkworm; SW), which feed on mulberry leaves, have been consumed by humans for a long time as supplements or traditional medication. Non-alcoholic fatty liver disease (NAFLD) is a liver metabolic disorder that affects many people worldwide. We examined the hepatoprotective effects of SW using in vitro and high-fat and high-fructose (HFHF) diet-induced obese in vivo model mice by real-time PCR, immunoblot analysis, and fecal microbiota analysis. SW significantly reduced lipid accumulation and expression of the lipogenic genes in HepG2 cells and the livers of HFHF-induced mice. SW caused significant reductions in triglycerides, and total cholesterol in serum and upregulation of fatty acid oxidation markers compared to the HFHF group. Besides, SW significantly induced phosphorylation of AMPK and ACC in both models, suggesting roles in AMPK activation and the ACC signaling pathway. Furthermore, the gut microbiota analysis demonstrated that SW treatment reduced Firmicutes to Bacteroidetes ratios and the relative abundance of the Lachnospiraceae family compared to HFHF-induced obese mice. These results provide a novel therapeutic agent of hepatoprotective effects of SW for non-alcoholic hepatic steatosis that targets hepatic AMPK and ACC-mediated lipid metabolism.

Ethanol Extract of Liriope platyphylla Root Attenuates Non-Alcoholic Fatty Liver Disease in High-Fat Diet-Induced Obese Mice via Regulation of Lipogenesis and Lipid Uptake

“…CD36 and FATP5 are expressed and regulated by PPARγ [ 11 , 50 ]. A HFD can induce PPARγ expression, which accelerates lipid accumulation and leads to hepatic steatosis in mouse liver cells [ 51 ]. Treatment with LPE reduced the protein expression of PPARγ both in vivo and in vitro.…”

Ethyl 2-[2,3,4-Trimethoxy-6-(1-Octanoyl)Phenyl] Acetate (TMPA) Ameliorates Lipid Accumulation by Disturbing the Combination of LKB1 with Nur77 and Activating the AMPK Pathway in HepG2 Cells and Mice Primary Hepatocytes

“…It is generally accepted that ACC is a central enzyme that is crucial as source of fatty acids from nonlipid precursors by de novo lipogenesis. 16 CPT1A is an essential ratelimiting enzyme involved in the breakdown of fatty acids (β-oxidation), and effectively translocates fatty acids into the mitochondria. The regulation of CPT1A is closely associated with malonyl-CoA, downstream of ACC, which negatively regulates CPT1A expression and may be positively regulated by ACC.…”

“…Moreover, high expression of ACC and SREBP-1 will accelerate the production of fatty acids. 16,29 The increase in SREBP-1 levels can also positively regulate the expression of ACC. Our results showed no significant differences in SREBP-1 or ACC, but we observed an increase in p-ACC.…”

“…14 During lipid metabolism in the liver, activated AMPKα can phosphorylate 3-hydroxy-3-methylglutaryl-CoA reductase (HMGCR) at Ser872 15 and acetyl-CoA carboaxylase (ACC) at S79, and subsequently inhibits the activation of HMGCR and ACC, which is crucial for lipid production. 12,16 In addition, ACC is a potent allosteric inhibitor of carnitine palmitoyltransferase 1 (CPT1A), which imports long chain fatty acyl-CoA into the mitochondria and promotes fatty acid βoxidation. Therefore, the suppression of ACC promotes the activation of CPT1A and then reduces the deposition of FFAs.…”

Current Issues in Molecular Biology Journal Enters a New Era

“…the bioinformatics-based assessment of the prognostic value of general transcription factor III in colorectal cancer [29]. -how an edible insect, Bombyx mori, protects the liver, thus leaving open the door to finding novel therapeutic molecular approaches to combatting non-alcoholic fatty liver diseases [30]. -the wide variety of anthocyanin levels, whose health benefit potential is well recognized, in selected species and cultivars of berry fruits [31].…”