scholarly journals Magma Seawater Inhibits Hepatic Lipid Accumulation through Suppression of Lipogenic Enzymes Regulated by SREBPs in Thioacetamide-Injected Rats

Marine Drugs ◽  
2019 ◽  
Vol 17 (6) ◽  
pp. 317 ◽  
Author(s):  
Minji Woo ◽  
Jeong Sook Noh ◽  
Mi Jeong Kim ◽  
Yeong Ok Song ◽  
Hyunjoo Lee
Keyword(s):  
Lipid Accumulation ◽  
Fatty Acid Synthase ◽  
Regulatory Element ◽  
Thiobarbituric Acid ◽  
Control Group ◽  
Chow Diet ◽  
Lipogenic Enzymes ◽  
Hepatic Lipid ◽  
Antioxidative Status ◽  
Hepatic Lipid Accumulation

Thioacetamide (TAA) is known to induce lipid accumulation in the liver. In the present study, we investigated the effects of magma seawater (MS) rich in minerals on hepatic lipid metabolism by evaluating lipogenic enzymes regulated by sterol regulatory element-binding proteins (SREBPs). Rats (n = 10 per group) were intraperitoneally injected with TAA (200 mg/kg bw) thrice a week for seven weeks in combination with a respective experimental diet. Rats in the TAA-treated group received either a chow diet (Control group) or a chow diet containing MS (TMS group, 2.05%) or silymarin (TSM group, 0.05%). Rats in the normal group were injected with PBS as a vehicle and received a chow diet. Rats in the TMS group showed significantly lower hepatic lipid concentrations than rats in the control group (p < 0.05). Hepatic protein expression levels of fatty acid synthase, SREBP-1, 3-hydroxy-3-methylglutaryl-coenzyme A reductase, and SREBP-2 were significantly downregulated in the TMS group, whereas carnitine palmitoyltransferase 1 levels were upregulated (p < 0.05). Hepatic thiobarbituric acid reactive substances levels were lower in the TMS group, whereas protein levels of glutathione peroxidase and catalase were elevated (p < 0.05). The effects of MS were comparable to those of silymarin. Our results evidently showed that MS inhibits hepatic lipid accumulation by suppressing lipid synthesis, accompanied by lipid oxidation and elevation of antioxidative status.

miR-23a/b-3p promotes hepatic lipid accumulation by regulating Srebp-1c and Fas

2021 ◽  
Author(s):  
Linfang Li ◽  
Xiaoyi Zhang ◽  
Hangjiang Ren ◽  
Xiuqing Huang ◽  
Tao Shen ◽  
...  
Keyword(s):  
Lipid Accumulation ◽  
Fatty Acid Synthase ◽  
Leptin Receptor ◽  
Regulatory Element ◽  
Hepatic Lipid ◽  
Hepatic Lipid Accumulation ◽  
Protein Levels ◽  
Triglyceride Accumulation ◽  
Element Binding Protein ◽  
Sterol Regulatory Element

miR-23a-3p and miR-23b-3p are members of the miR-23~27~24-2 superfamily. The role of miR-23a/b-3p in regulating hepatic lipid accumulation is still unknown. Here, we found that increased miR-23a-3p and miR-23b-3p levels were accompanied by an increase in the protein levels of the sterol regulatory element-binding protein-1 (SREBP-1) and fatty acid synthase (FAS) in the steatotic livers of mice fed a high-fat diet (HFD) and leptin-receptor-deficient type 2 diabetic mice (db/db). Importantly, overexpression of miR-23a/b-3p in Hep1-6 cells elevated the intracellular triglyceride level and upregulated the expression of Srebp-1c and Fas. Taken together, these results suggested that miR-23a/b-3p enhanced mRNA stability by binding the 5'-UTR of Srebp-1c and Fas mRNA, thereby promoting triglyceride accumulation in hepatocytes.

scholarly journals Curcumin attenuates insulin resistance and hepatic lipid accumulation in a rat model of intra-uterine growth restriction through insulin signalling pathway and sterol regulatory element binding proteins

2019 ◽  
Vol 122 (6) ◽  
pp. 616-624 ◽  
Author(s):  
Yu Niu ◽  
Jintian He ◽  
Hussain Ahmad ◽  
Chao Wang ◽  
Xiang Zhong ◽  
...  
Keyword(s):  
Insulin Resistance ◽  
Lipid Accumulation ◽  
Insulin Signalling ◽  
Regulatory Element ◽  
Hepatic Lipid ◽  
Hepatic Lipid Accumulation ◽  
Uterine Growth ◽  
Element Binding Protein ◽  
Sterol Regulatory Element ◽  
Intra Uterine Growth Restriction

AbstractThe objective of the present study was to investigate the effect of curcumin on insulin resistance (IR) and hepatic lipid accumulation in intra-uterine growth restriction (IUGR). Rats with a normal birth weight (NBW) or IUGR were fed basic diets (NBW and IUGR groups) or basic diets supplemented with curcumin (NBW-C and IUGR-C groups) from 6 to 12 weeks. Rats in the IUGR group showed higher levels of glucose and homeostasis model assessment for insulin resistance index (HOMA-IR) (P< 0·05) than in the NBW group. The livers of IUGR rats exhibited higher (P< 0·05) concentration of TAG and lower (P< 0·05) activities of lipolysis enzymes compared with the normal rats. In response to dietary curcumin supplementation, concentrations of serum insulin, glucose and HOMA-IR, pyruvate, TAG, total cholesterol and NEFA in the liver were decreased (P< 0·05). The concentrations of glycogen and activities of lipolysis enzymes in the liver were increased (P< 0·05) in the IUGR-C group compared with the IUGR group. These results were associated with lower (P< 0·05) phosphorylated insulin receptor substrate 1, protein kinase B or Akt, glycogen synthase kinase 3β and expressions of sterol regulatory element binding protein 1 and fatty acid synthase (FASN); decreased expressions forCd36, sterol regulatory element binding protein 1c (Srebf1) andFasn; increased (P< 0·05) expression of PPARα; and expressions forPparaand hormone-sensitive lipase in the liver of IUGR-C rats than the IUGR rats. Maternal malnutrition caused IR and lipid accumulation in the liver. Curcumin supplementation prevented IR by regulating insulin signalling pathways and attenuated hepatic lipid accumulation.

scholarly journals R. verniciflua and E. ulmoides Extract (ILF-RE) Protects against Chronic CCl4-Induced Liver Damage by Enhancing Antioxidation

Nutrients ◽  
2019 ◽  
Vol 11 (2) ◽  
pp. 382 ◽  
Author(s):  
Hwa-Young Lee ◽  
Geum-Hwa Lee ◽  
Young Yoon ◽  
Han-Jung Chae
Keyword(s):  
Oxidative Stress ◽  
Er Stress ◽  
Liver Damage ◽  
Lipid Accumulation ◽  
Fatty Acid Synthase ◽  
Regulatory Element ◽  
Protective Effects ◽  
Gamma Glutamyl Transpeptidase ◽  
Hepatic Lipid Accumulation ◽  
Lipogenic Genes

This study aimed to characterize the protective effects of R. verniciflua extract (ILF-R) and E. ulmoides extract (ILF-E), the combination called ILF-RE, against chronic CCl4-induced liver oxidative injury in rats, as well as to investigate the mechanism underlying hepatoprotection by ILF-RE against CCl4-induced hepatic dysfunction. Chronic hepatic stress was induced via intraperitoneal (IP) administration of a mixture of CCl4 (0.2 mL/100 g body weight) and olive oil [1:1(v/v)] twice a week for 4 weeks to rats. ILF-RE was administered orally at 40, 80, and 120 mg/kg to rats for 4 weeks. Alanine transaminase (ALT), aspartate transaminase (AST), gamma-glutamyl transpeptidase (GGT), and lipid peroxidation assays were performed, and total triglyceride, cholesterol, and LDL-cholesterol levels were quantified. Furthermore, ER stress and lipogenesis-related gene expression including sterol regulatory element-binding transcription factor 1 (SREBP-1), fatty acid synthase (FAS), and P-AMPK were assessed. ILF-RE markedly protected against liver damage by inhibiting oxidative stress and increasing antioxidant enzyme activity including glutathione (GSH), glutathione peroxidase (GPx), superoxide dismutase (SOD), and catalase. Furthermore, hepatic dyslipidemia was regulated after ILF-RE administration. Moreover, hepatic lipid accumulation and its associated lipogenic genes, including those encoding SREBP-1 and FAS, were regulated after ILF-RE administration. This was accompanied by regulation of ER stress response signaling, suggesting a mechanism underlying ILF-RE-mediated hepatoprotection against lipid accumulation. The present results indicate that ILF-RE exerts hepatoprotective effects against chronic CCl4-induced dysfunction by suppressing hepatic oxidative stress and lipogenesis, suggesting that ILF-RE is a potential preventive/therapeutic natural product in treating hepatoxicity and associated dysfunction.

scholarly journals Urinary Medium-Chained Acyl-Carnitines Sign High Caloric Intake whereas Short-Chained Acyl-Carnitines Sign High -Protein Diet within a High-Fat, Hypercaloric Diet in a Randomized Crossover Design Dietary Trial

Nutrients ◽  
2021 ◽  
Vol 13 (4) ◽  
pp. 1191
Author(s):  
Nadezda V. Khodorova ◽  
Annemarie Rietman ◽  
Douglas N. Rutledge ◽  
Jessica Schwarz ◽  
Julien Piedcoq ◽  
...  
Keyword(s):  
Lipid Accumulation ◽  
Control Diet ◽  
Crossover Design ◽  
Short Chain ◽  
Control Group ◽  
High Fat ◽  
Hepatic Lipid ◽  
Hepatic Lipid Accumulation ◽  
Early Biomarkers ◽  
Hypercaloric Diet

The western dietary pattern is known for its frequent meals rich in saturated fat and protein, resulting in a postprandial state for a large part of the day. Therefore, our aim was to investigate the postprandial glucose and lipid metabolism in response to high (HP) or normal (NP) protein, high-fat hypercaloric diet and to identify early biomarkers of protein intake and hepatic lipid accumulation. In a crossover design, 17 healthy subjects were randomly assigned to consume a HP or NP hypercaloric diet for two weeks. In parallel, a control group (CD; n = 10) consumed a weight-maintaining control diet. Biomarkers of postprandial lipid and glucose metabolism were measured in 24 h urine and in plasma before and following a meal challenge. The metabolic profile of urine but not plasma, showed increased excretion of 13C, carnitine and short chain acyl-carnitines after adaptation to the HP diet. Urinary excretion of decatrienoylcarnitine and octenoylcarnitine increased after adaptation to the NP diet. Our results suggest that the higher excretion of short-chain urinary acyl-carnitines could facilitate the elimination of excess fat of the HP diet and thereby reduce hepatic fat accumulation previously reported, whereas the higher excretion medium-chains acyl-carnitine could be early biomarkers of hepatic lipid accumulation.

scholarly journals Gestational Hypercholesterolemia Programs NAFLD in a Sex-Specific Manner in ApoE-Deficient Mice (P11-140-19)

2019 ◽  
Vol 3 (Supplement_1) ◽  
Author(s):  
Jerad Dumolt ◽  
Mulchand Patel ◽  
Todd Rideout
Keyword(s):  
Fatty Acid Synthase ◽  
Regulatory Element ◽  
Female Offspring ◽  
Positive Control ◽  
Male Offspring ◽  
Chow Diet ◽  
Lipid Profiling ◽  
Nonalcoholic Fatty Liver ◽  
Hepatic Lipid ◽  
Specific Manner

Abstract Objectives Two separate studies were conducted to determine if gestational hypercholesterolemia alters fetal hepatic lipid metabolism (study 1) and programs nonalcoholic fatty liver disease (NAFLD) in a sex-specific manner in adult offspring (study 2). Methods Study 1: 12 female apoE−/− mice were randomly assigned to two different chow-based diets throughout gestation: chow (CON; control) or chow diet with cholesterol (CH; 0.15%). On gestation day 18, fetuses were euthanized and samples amalgamated for evaluation of serum, hepatic, and placental lipid profiling and transcriptional changes in hepatic microRNA (miRNA). Study 2: 18 female apoE−/− mice were randomly assigned to the same diets as above but throughout both the gestation and lactation periods. At birth, litters were cross-fostered with surrogate CON and CH dams to generate three experimental groups (n = 6/group; gestation exposure-lactation exposure): (CON-CON; control), (CH-CH; positive control), and (CH-CON). On postnatal day 21, one male and one female from each litter were weaned on to a chow diet until adulthood (postnatal day 84) and euthanized for serum and hepatic lipid profiling. Results Study 1: Fetuses from CH dams possessed increased (P < 0.05) hepatic triglycerides (TG) which was accompanied with a down regulation (P < 0.05) of the hepatic lipogenic genes fatty acid synthase (-1.8 fold, FAS), acetyl-CoA carboxylase (-1.6 fold, ACC), and sterol regulatory element-binding protein 1c (-1.2 fold, SREBP1c). Furthermore, fetal livers from CH mothers showed increased miRNA-27a (+ 1.9 fold) and reduced miRNA-200c expression (-1.8 fold) (P < 0.05). Study 2: Compared to CON-CON, CH-CH and CH-CON male offspring demonstrated increased (P < 0.05) serum TG and hepatic cholesterol and TG concentrations. With the exception of increased (P < 0.05) serum TG in CH-CH adult female offspring, which was normalized in CH-CON females, no differences (P > 0.05) in serum and hepatic lipids were observed in female offspring between treatment groups. Conclusions In apoE−/- mice, exposure to excessive cholesterol during gestation alters fetal hepatic lipid and miRNA status and programs NALFD in a sex-specific manner in adult male offspring only. Funding Sources Supported by the National Institute for Complementary and Alternative Medicine.

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