scholarly journals Metabolic Syndrome Is Reduced in C57BL/6J Mice Fed High-Fat Diets Supplemented with Oak Tannins

2020 ◽  
Vol 4 (4) ◽  
Author(s):  
Ting Luo ◽  
Tedd Goldfinger ◽  
Neil Shay
Keyword(s):  
Metabolic Syndrome ◽  
Body Weight ◽  
Weight Gain ◽  
Lipid Accumulation ◽  
Body Weight Gain ◽  
Mrna Levels ◽  
High Fat ◽  
Glutathione S Transferase ◽  
Hepatic Lipid ◽  
Hepatic Lipid Accumulation

ABSTRACT Background Wine aged in oak barrels will incorporate polyphenols inherent in the staves, suggesting that wine stored in these wooden containers will introduce oak compounds into the human body after consumption. Objective The purpose of the present study is to test whether consumption of these oak compounds could favorably influence metabolism in mice fed an obesogenic diet. Methods C57BL/6  male mice (n = 8) were fed diets for 10 wk as follows: low-fat (LF), high-fat (HF), and HF containing 0.17% of oak tannin (HF+OT). A second 10-wk study was completed; mice were provided LF, HF, and HF diets supplemented with 7.0% of concentrates made from oaked wine (HF+OWC) or unoaked wine (HF+UWC). Physiological parameters were measured during the feeding trial and serum markers and hepatic gene expression measured from samples obtained at necropsy. Results Intake of HF+OT significantly reduced body-weight gain (18.4 ± 1.2 g in HF vs. 13.2 ± 1.4 g in HF+OT, P < 0.05). Serum resistin concentrations were lower in HF+OT mice compared with HF mice (301 ± 10.1 pg/mL in HF+OT vs. 374 ± 10.9 pg/mL in HF; P < 0.05). Hepatic lipid accumulation and expression of glutathione-S-transferase-m2 (Gstm2) and NAD(P)H:quinone oxidoreductase (Nqo1) mRNAs were significantly decreased in HF+OT compared with HF mice (P < 0.05). When compared with HF-fed mice, intake of both OWC and UWC decreased body-weight gain (P < 0.05), with no significant impact on food consumption. Fasting glucose concentrations, serum insulin, and hepatic lipid accumulation were reduced in HF+OWC-fed mice compared with HF+UWC-fed mice (P < 0.05). Furthermore, hepatic glutathione-S-transferase-a1 (Gsta1) mRNA levels were significantly reduced in OWC-supplemented (0.25 ± 0.08) compared with UWC-supplemented (1.71 ± 0.24) mice (P < 0.05). Conclusions In this mouse model of metabolic disease, intake of OTs and a concentrate made from an oaked wine had a potent impact on alleviating HF-induced metabolic syndrome. Thus, intake of OTs, provided passively in oaked wine or as a dietary supplement, may act as an agent to attenuate the markers of metabolic syndrome.

Consumption of the edible sea urchin Mesocentrotus nudus attenuates body weight gain and hepatic lipid accumulation in mice

2018 ◽  
Vol 47 ◽  
pp. 40-47 ◽  
Author(s):  
Ryoko Yamamoto ◽  
Hisanori Minami ◽  
Hiromi Matsusaki ◽  
Mami Sakashita ◽  
Naoki Morita ◽  
...  
Keyword(s):  
Body Weight ◽  
Weight Gain ◽  
Sea Urchin ◽  
Lipid Accumulation ◽  
Body Weight Gain ◽  
Hepatic Lipid ◽  
Hepatic Lipid Accumulation ◽  
Mesocentrotus Nudus

scholarly journals Neoagarooligosaccharides modulate gut microbiota and alleviate body weight gain and metabolic syndrome in high-fat diet-induced obese rats

2022 ◽  
Vol 88 ◽  
pp. 104869
Author(s):  
Ju Kyoung Oh ◽  
Robie Vasquez ◽  
Sang Hoon Kim ◽  
Je Hyeon Lee ◽  
Eun Joo Kim ◽  
...  
Keyword(s):  
Metabolic Syndrome ◽  
Body Weight ◽  
Weight Gain ◽  
Gut Microbiota ◽  
High Fat Diet ◽  
Body Weight Gain ◽  
High Fat ◽  
Obese Rats

scholarly journals Lactobacillus Brevis OPK-3 from Kimchi Prevents Obesity and Modulates the Expression of Adipogenic and Pro-Inflammatory Genes in Adipose Tissue of Diet-Induced Obese Mice

Nutrients ◽  
2020 ◽  
Vol 12 (3) ◽  
pp. 604 ◽  
Author(s):  
Jung Eun Park ◽  
Suk-Heung Oh ◽  
Youn-Soo Cha
Keyword(s):  
Body Weight ◽  
Adipose Tissue ◽  
Weight Gain ◽  
High Fat Diet ◽  
Body Weight Gain ◽  
Epididymal Adipose Tissue ◽  
Pcr Analysis ◽  
Distilled Water ◽  
Mrna Levels ◽  
High Fat

Our previous study reported that lactic acid bacteria (L. brevis OPK-3) isolated from kimchi ameliorated intracellular lipid accumulation in 3T3-L1 adipocyte. The current study explored potential roles of L. brevis OPK-3 (KLAB) on preventing body weight gain and its effect on the inflammatory response of adipose tissue. Male C57BL/6 mice (n = 10) were divided into four groups: normal diet with distilled water (NDC), high-fat diet with distilled water (HDC), high-fat diet with L-ornithine (OTC) or high-fat diet with KLAB. The KLAB supplement resulted in significantly lower body weight, lower epididymal fat tissue mass, and lower serum and hepatic TG levels than the HDC. KLAB supplementation improved serum cytokines, and real-time polymerase chain reaction (PCR) analysis showed significantly lower inflammatory cytokine mRNA levels in epididymal adipose tissue. These results suggest that the administration of KLAB inhibits the induction of inflammation in adipose tissue along with the inhibition of weight gain. Therefore, this study demonstrates the therapeutic and beneficial value of this strain produced during the fermentation of kimchi.

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.

Eisenia bicyclis Inhibits Body Weight Gain and Fat Accumulation Induced by High-Fat Diets in Mice

2010 ◽  
Vol 15 (4) ◽  
pp. 262-266 ◽  
Author(s):  
Won-Hee Choi ◽  
Ji-Yun Ahn ◽  
Sun-A Kim ◽  
Tae-Wan Kim ◽  
Tae-Youl Ha
Keyword(s):  
Body Weight ◽  
Weight Gain ◽  
Body Weight Gain ◽  
High Fat ◽  
Eisenia Bicyclis ◽  
Fat Accumulation ◽  
High Fat Diets ◽  
Fat Diets

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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