scholarly journals Wheat Flour, Enriched with γ-Oryzanol, Phytosterol, and Ferulic Acid, Alleviates Lipid and Glucose Metabolism in High-Fat-Fructose-Fed Rats

Nutrients ◽  
2019 ◽  
Vol 11 (7) ◽  
pp. 1697
Author(s):  
Xiao-Xuan Guo ◽  
Zhu Zeng ◽  
Yong-Zhong Qian ◽  
Jing Qiu ◽  
Kai Wang ◽  
...  
Keyword(s):  
Insulin Resistance ◽  
Glucose Metabolism ◽  
Western Blot ◽  
Ferulic Acid ◽  
Wheat Flour ◽  
Lipid Accumulation ◽  
Functional Food ◽  
Metabolic Dysfunction ◽  
High Fat ◽  
Hepatic Lipid Accumulation

(1) Background: Modern dietary patterns with a high intake of fat and fructose, as well as refined carbohydrates, closely relate to lipid/glucose metabolic disorders. The main objective of this study is to provide new thoughts in designing functional food with some lipid/glucose metabolism regulating effects for obese people. (2) Methods: The alleviating abilities of γ-oryzanol, phytosterol or ferulic acid-enriched wheat flour on lipid/glucose metabolic dysfunction were evaluated in male SD rats induced by a high-fat-fructose diet. The underlying mechanisms were clarified using western blot. (3) Results: In an in vitro cell model, γ-oryzanol, phytosterol and ferulic acid regulate lipid/glucose metabolism by increasing the phosphorylation of AMPK and Akt, and PI3K expression, as well as decreasing expressions of DGAT1 and SCD. The in vivo study shows that ferulic acid and γ-oryzanol-enriched flours are beneficial for managing body weight, improving glucose metabolism, hyperlipidemia and hepatic lipid accumulation. Phytosterol-enriched flour exerted remarkable effects in regulating hyperinsulinemia, insulin resistance and hyperuricemia. Western blot analysis of proteins from liver samples reveals that these enriched flours alleviated hepatic lipid accumulation and insulin resistance through their elevation in the phosphorylation of AMPK and Akt. (4) Conclusions: Our study indicates that these enriched flours can serve as a health-promoting functional food to regulate obesity-related lipid/glucose metabolic dysfunction in rats.

Supplementation of a High-Fat Diet with Chlorogenic Acid Is Associated with Insulin Resistance and Hepatic Lipid Accumulation in Mice

2013 ◽  
Vol 61 (18) ◽  
pp. 4371-4378 ◽  
Author(s):  
Aidilla Mubarak ◽  
Jonathan M. Hodgson ◽  
Michael J. Considine ◽  
Kevin D. Croft ◽  
Vance B. Matthews
Keyword(s):  
Insulin Resistance ◽  
Chlorogenic Acid ◽  
Lipid Accumulation ◽  
High Fat Diet ◽  
High Fat ◽  
Hepatic Lipid ◽  
Hepatic Lipid Accumulation

scholarly journals Lemon Balm Extract ALS-L1023 Regulates Obesity and Improves Insulin Sensitivity via Activation of Hepatic PPARα in High-Fat Diet-Fed Obese C57BL/6J Mice

2020 ◽  
Vol 21 (12) ◽  
pp. 4256
Author(s):  
Dongju Lee ◽  
Yujin Shin ◽  
Jong Seong Roh ◽  
Jiwon Ahn ◽  
Sunhyo Jeoong ◽  
...  
Keyword(s):  
Insulin Resistance ◽  
Weight Gain ◽  
Insulin Sensitivity ◽  
Lipid Accumulation ◽  
High Fat Diet ◽  
Obese Mice ◽  
High Fat ◽  
Lemon Balm ◽  
Hepatic Lipid ◽  
Hepatic Lipid Accumulation

Our previous studies demonstrated that peroxisome proliferator-activated receptor α (PPARα) activation reduces weight gain and improves insulin sensitivity in obese mice. Since excess lipid accumulation in non-adipose tissues is suggested to be responsible for the development of insulin resistance, this study was undertaken to examine whether the lemon balm extract ALS-L1023 regulates hepatic lipid accumulation, obesity, and insulin resistance and to determine whether its mechanism of action involves PPARα. Administration of ALS-L1023 to high-fat-diet-induced obese mice caused reductions in body weight gain, visceral fat mass, and visceral adipocyte size without changes of food consumption profiles. ALS-L1023 improved hyperglycemia, hyperinsulinemia, glucose and insulin tolerance, and normalized insulin-positive β-cell area in obese mice. ALS-L1023 decreased hepatic lipid accumulation and concomitantly increased the expression of PPARα target genes responsible for fatty acid β-oxidation in livers. In accordance with the in vivo data, ALS-L1023 reduced lipid accumulation and stimulated PPARα reporter gene expression in HepG2 cells. These effects of ALS-L1023 were comparable to those of the PPARα ligand fenofibrate, while the PPARα antagonist GW6471 inhibited the actions of ALS-L1023 on lipid accumulation and PPARα luciferase activity in HepG2 cells. Higher phosphorylated protein kinase B (pAkt)/Akt ratios and lower expression of gluconeogenesis genes were observed in the livers of ALS-L1023-treated mice. These results indicate that ALS-L1023 may inhibit obesity and improve insulin sensitivity in part through inhibition of hepatic lipid accumulation via hepatic PPARα activation.

scholarly journals The Root of Polygonum multiflorum Thunb. Alleviates Non-Alcoholic Steatosis and Insulin Resistance in High Fat Diet-Fed Mice

Nutrients ◽  
2020 ◽  
Vol 12 (8) ◽  
pp. 2353
Author(s):  
Soonwoong Jung ◽  
Hyeonwi Son ◽  
Chung Eun Hwang ◽  
Kye Man Cho ◽  
Sang Won Park ◽  
...  
Keyword(s):  
Insulin Resistance ◽  
Lipid Accumulation ◽  
High Fat Diet ◽  
High Fat ◽  
Polygonum Multiflorum ◽  
Metabolic Complications ◽  
In Vivo Models ◽  
Hepatic Lipid ◽  
Hepatic Lipid Accumulation ◽  
Glut4 Expression

Non-alcoholic steatosis and insulin resistance are critical health problems and cause metabolic complications worldwide. In this study, we investigated the molecular mechanism of Polygonum multiflorum Thunb. (PM) against hepatic lipid accumulation and insulin resistance by using in vitro and in vivo models. PM extract significantly attenuated the accumulation of lipid droplets and hepatic triglyceride in free fatty acid (FFA)-exposed HepG2 cells. PM extract increased the AMPK and ACC phosphorylation and GLUT4 expression, whose levels were downregulated in FFA-exposed cells. PM extract also decreased precursor and mature forms of SREBP-1 in FFA-exposed cells. C57BL/6 mice fed with normal diet (ND) or high-fat diet (HFD) were administered PM extract (100 mg/kg) or vehicle orally for 16 weeks. PM extract attenuated the increases of the epididymal and perirenal fats on HFD feeding. PM extract markedly reduced hepatic lipid accumulation and fasting glucose levels, and improved glucose and insulin sensitivity in HFD-fed mice. HFD-fed mice decreased the AMPK and ACC phosphorylation and GLUT4 expression, and increased precursor and mature forms of SREBP-1; these changes were significantly restored by PM extract. In conclusion, PM extract alleviates non-alcoholic steatosis and insulin resistance through modulating the expression of proteins on lipid metabolism and glucose transport in the liver.

Asiatic Acid Ameliorates Hepatic Lipid Accumulation and Insulin Resistance in Mice Consuming a High-Fat Diet

2014 ◽  
Vol 62 (20) ◽  
pp. 4625-4631 ◽  
Author(s):  
Sheng-Lei Yan ◽  
Hui-Ting Yang ◽  
Yi-Ju Lee ◽  
Chun-Che Lin ◽  
Ming-Hui Chang ◽  
...  
Keyword(s):  
Insulin Resistance ◽  
Lipid Accumulation ◽  
High Fat Diet ◽  
Asiatic Acid ◽  
High Fat ◽  
Hepatic Lipid ◽  
Hepatic Lipid Accumulation

Supplementation with Vitis vinifera L. skin extract improves insulin resistance and prevents hepatic lipid accumulation and steatosis in high-fat diet–fed mice

2017 ◽  
Vol 43 ◽  
pp. 69-81 ◽  
Author(s):  
Izabelle Barcellos Santos ◽  
Graziele Freitas de Bem ◽  
Viviane Silva Cristino Cordeiro ◽  
Cristiane Aguiar da Costa ◽  
Lenize Costa Reis Marins de Carvalho ◽  
...  
Keyword(s):  
Insulin Resistance ◽  
Vitis Vinifera ◽  
Lipid Accumulation ◽  
High Fat Diet ◽  
Vitis Vinifera L ◽  
Skin Extract ◽  
High Fat ◽  
Hepatic Lipid ◽  
Hepatic Lipid Accumulation

scholarly journals Sasa quelpaertensis Leaf Extract Ameliorates Dyslipidemia, Insulin Resistance, and Hepatic Lipid Accumulation in High-Fructose-Diet-Fed Rats

Nutrients ◽  
2020 ◽  
Vol 12 (12) ◽  
pp. 3762
Author(s):  
Jeong Yong Park ◽  
Mi Gyeong Jang ◽  
Jung Min Oh ◽  
Hee Chul Ko ◽  
Sung-Pyo Hur ◽  
...  
Keyword(s):  
Insulin Resistance ◽  
Signaling Pathway ◽  
Lipid Accumulation ◽  
Leaf Extract ◽  
Metabolic Disorders ◽  
Metabolic Dysfunction ◽  
Hepatic Lipid ◽  
High Fructose Diet ◽  
Hepatic Lipid Accumulation ◽  
High Fructose

Background: Increased dietary fructose consumption is closely associated with lipid and glucose metabolic disorders. Sasa quelpaertensis Nakai possesses various health-promoting properties, but there has been no research on its protective effect against fructose-induced metabolic dysfunction. In this study, we investigated the effects of S. quelpaertensis leaf extract (SQE) on metabolic dysfunction in high-fructose-diet-fed rats. Methods: Animals were fed a 46% carbohydrate diet, a 60% high-fructose diet, or a 60% high-fructose diet with SQE (500 mg/kg of body weight (BW)/day) in drinking water for 16 weeks. Serum biochemical parameters were measured and the effects of SQE on hepatic histology, protein expression, and transcriptome profiles were investigated. Results: SQE improved dyslipidemia and insulin resistance induced in high-fructose-diet-fed rats. SQE ameliorated the lipid accumulation and inflammatory response in liver tissues by modulating the expressions of key proteins related to lipid metabolism and antioxidant response. SQE significantly enriched the genes related to the metabolic pathway, namely, the tumor necrosis factor (TNF) signaling pathway and the PI3K-Akt signaling pathway. Conclusions: SQE could effectively prevent dyslipidemia, insulin resistance, and hepatic lipid accumulation by regulation of metabolism-related gene expressions, suggesting its role as a functional ingredient to prevent lifestyle-related metabolic disorders.

scholarly journals Prevention and Reversal of Lipotoxicity-Induced Hepatic Insulin Resistance and Steatohepatitis in Mice by an Antioxidant Carotenoid, β-Cryptoxanthin

Endocrinology ◽  
2015 ◽  
Vol 156 (3) ◽  
pp. 987-999 ◽  
Author(s):  
Yinhua Ni ◽  
Mayumi Nagashimada ◽  
Lili Zhan ◽  
Naoto Nagata ◽  
Masuko Kobori ◽  
...  
Keyword(s):  
Insulin Resistance ◽  
Mrna Expression ◽  
Kupffer Cells ◽  
Lipid Accumulation ◽  
Hepatic Insulin Resistance ◽  
Therapeutic Effects ◽  
Dependent Manner ◽  
High Fat ◽  
Hepatic Lipid ◽  
Hepatic Lipid Accumulation

Abstract Excessive hepatic lipid accumulation promotes macrophages/Kupffer cells activation, resulting in exacerbation of insulin resistance and progression of nonalcoholic steatohepatitis (NASH). However, few promising treatment modalities target lipotoxicity-mediated hepatic activation/polarization of macrophages for NASH. Recent epidemiological surveys showed that serum β-cryptoxanthin, an antioxidant carotenoid, was inversely associated with the risks of insulin resistance and liver dysfunction. In the present study, we first showed that β-cryptoxanthin administration ameliorated hepatic steatosis in high-fat diet-induced obese mice. Next, we investigated the preventative and therapeutic effects of β-cryptoxanthin using a lipotoxic model of NASH: mice fed a high-cholesterol and high-fat (CL) diet. After 12 weeks of CL diet feeding, β-cryptoxanthin administration attenuated insulin resistance and excessive hepatic lipid accumulation and peroxidation, with increases in M1-type macrophages/Kupffer cells and activated stellate cells, and fibrosis in CL diet-induced NASH. Comprehensive gene expression analysis showed that β-cryptoxanthin down-regulated macrophage activation signal-related genes significantly without affecting most lipid metabolism-related genes in the liver. Importantly, flow cytometry analysis revealed that, on a CL diet, β-cryptoxanthin caused a predominance of M2 over M1 macrophage populations, in addition to reducing total hepatic macrophage and T-cell contents. In parallel, β-cryptoxanthin decreased lipopolysaccharide-induced M1 marker mRNA expression in peritoneal macrophages, whereas it augmented IL-4-induced M2 marker mRNA expression, in a dose-dependent manner. Moreover, β-cryptoxanthin reversed steatosis, inflammation, and fibrosis progression in preexisting NASH in mice. In conclusion, β-cryptoxanthin prevents and reverses insulin resistance and steatohepatitis, at least in part, through an M2-dominant shift in macrophages/Kupffer cells in a lipotoxic model of NASH.

Black garlic melanoidins prevent obesity, reduce serum LPS levels and modulate the gut microbiota composition in high-fat diet-induced obese C57BL/6J mice

2020 ◽  
Vol 11 (11) ◽  
pp. 9585-9598
Author(s):  
Jianfu Wu ◽  
Yanan Liu ◽  
Zishan Dou ◽  
Tao Wu ◽  
Rui Liu ◽  
...  
Keyword(s):  
Insulin Resistance ◽  
Gut Microbiota ◽  
Lipid Accumulation ◽  
High Fat Diet ◽  
Microbiota Composition ◽  
High Fat ◽  
Hepatic Lipid ◽  
Hepatic Lipid Accumulation ◽  
Gut Microbiota Composition

Black garlic MLDs fermented in the colon, produced SCFAs and modulated gut microbiota composition, thereby protected against hepatic lipid accumulation, insulin resistance, and inflammation partly.

Uridine attenuates obesity, ameliorates hepatic lipid accumulation and modifies the gut microbiota composition in mice fed with a high-fat diet

2021 ◽  
Author(s):  
Yilin Liu ◽  
Chunyan Xie ◽  
Zhenya Zhai ◽  
Ze-yuan Deng ◽  
Hugo R. De Jonge ◽  
...  
Keyword(s):  
Gut Microbiota ◽  
Lipid Accumulation ◽  
High Fat Diet ◽  
Microbiota Composition ◽  
High Fat ◽  
Fat Accumulation ◽  
Hepatic Lipid ◽  
Hepatic Lipid Accumulation ◽  
Gut Microbiota Composition

This study aimed to investigate the effect of uridine on obesity, fat accumulation in liver, and gut microbiota composition in high-fat diet-fed mice.

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