Weissella cibaria MG5285 and Lactobacillus reuteri MG5149 attenuated fat accumulation in adipose and hepatic steatosis in high-fat diet-induced C57BL/6J obese mice

Background: Excessive consumption of dietary fat is closely related to obesity, diabetes, insulin resistance, cardiovascular disease, hypertension, and non-alcoholic fatty liver disease. Recently, probiotics have been highly proposed as biotherapeutic to treat and prevent diseases. Previously, there are studies that demonstrated the beneficial effects of probiotics against metabolic disorders, including obesity and diabetes. Objective: We investigated the anti-obesity effect and mechanism of action of four human-derived lactic acid bacterial (LAB) strains (Lacticaseibacillus rhamnosus MG4502, Lactobacillus gasseri MG4524, Limosilactobacillus reuteri MG5149, and Weissella cibaria MG5285) in high-fat diet (HFD)-induced obese mice. Design: Obesity was induced in mice over 8 weeks, with a 60% HFD. The four human-derived LAB strains (2 × 108 CFU/mouse) were orally administered to male C57BL/6J mice once daily for 8 weeks. Body weight, liver and adipose tissue (AT) weights, glucose tolerance, and serum biochemistry profiles were determined. After collecting the tissues, histopathological and Western blot analyses were conducted. Results: Administration of these LAB strains resulted in decreased body weight, liver and AT weights, and glucose tolerance. Serum biochemistry profiles, including triglyceride (TG), total cholesterol, low-density lipoprotein cholesterol, and leptin, pro-inflammatory cytokines, improved. Hepatic steatosis and TG levels in liver tissue were significantly reduced. In addition, the size of adipocytes in epididymal tissue was significantly reduced. In epididymal tissues, Limosilactobacillus reuteri MG5149 and Weissella cibaria MG5285 groups showed a significantly reduced expression of lipogenic proteins, including peroxisome proliferator-activated receptor γ, CCAAT/enhancer-binding protein α, fatty acid synthase (FAS), and adipocyte-protein 2. In addition, sterol regulatory element-binding protein 1-c and its downstream protein FAS in the liver tissue were significantly decreased. These strains attenuated fat accumulation in the liver and AT by upregulating the phosphorylation of AMP-activated protein kinase and acetyl-CoA carboxylase in HFD-fed mice. Conclusion: We suggest that L. reuteri MG5149 and W. cibaria MG5285 could be used as potential probiotic candidates to prevent obesity.

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Polyphenol-Rich Fraction of Brown AlgaEcklonia cavaCollected from Gijang, Korea, Reduces Obesity and Glucose Levels in High-Fat Diet-Induced Obese Mice

Evidence-based Complementary and Alternative Medicine ◽

10.1155/2012/418912 ◽

2012 ◽

Vol 2012 ◽

pp. 1-11 ◽

Cited By ~ 15

Author(s):

Eun Young Park ◽

Eung Hwi Kim ◽

Mi Hwi Kim ◽

Young Wan Seo ◽

Jung Im Lee ◽

...

Keyword(s):

Type 2 Diabetes ◽

Body Weight ◽

Glucose Tolerance ◽

Mrna Expression ◽

Inflammatory Cytokines ◽

High Fat Diet ◽

Obese Mice ◽

High Fat ◽

Glucose Levels

Ecklonia cava (E. cava)is a brown alga that has beneficial effects in models of type 1 and type 2 diabetes. However, the effects ofE. cavaextracts on diet-induced obesity and type 2 diabetes have not been specifically examined. We investigated the effects ofE. cavaon body weight, fat content, and hyperglycemia in high-fat diet- (HFD) induced obese mice and sought the mechanisms involved. C57BL/6 male mice were fed a HFD (60% fat) diet or normal chow. After 3 weeks, the HFD diet group was given extracts (200 mg/kg) ofE. cavaharvested from Jeju (CA) or Gijang (G-CA), Korea or PBS by oral intubation for 8 weeks. Body weights were measured weekly. Blood glucose and glucose tolerance were measured at 7 weeks, and fat pad content and mRNA expression of adipogenic genes and inflammatory cytokines were measured after 8 weeks of treatment. G-CA was effective in reducing body weight gain, body fat, and hyperglycemia and improving glucose tolerance as compared with PBS-HFD mice. The mRNA expression of adipogenic genes was increased, and mRNA expression of inflammatory cytokines and macrophage marker gene was decreased in G-CA-treated obese mice. We suggest that G-CA reduces obesity and glucose levels by anti-inflammatory actions and improvement of lipid metabolism.

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Effect of Silybin on Body Weight and Glucose Tolerance in High-fat-diet Induced Obese Mice

KSBB Journal ◽

10.7841/ksbbj.2011.26.1.078 ◽

2011 ◽

Vol 26 (1) ◽

pp. 78-82 ◽

Cited By ~ 3

Author(s):

Haeng-Jeon Hur ◽

Jin-Taek Hwang

Keyword(s):

Body Weight ◽

Glucose Tolerance ◽

High Fat Diet ◽

Obese Mice ◽

High Fat

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COH-SR4 Reduces Body Weight, Improves Glycemic Control and Prevents Hepatic Steatosis in High Fat Diet-Induced Obese Mice

PLoS ONE ◽

10.1371/journal.pone.0083801 ◽

2013 ◽

Vol 8 (12) ◽

pp. e83801 ◽

Cited By ~ 15

Author(s):

James Lester Figarola ◽

Preeti Singhal ◽

Samuel Rahbar ◽

Bogdan Gabriel Gugiu ◽

Sanjay Awasthi ◽

...

Keyword(s):

Body Weight ◽

Glycemic Control ◽

Hepatic Steatosis ◽

High Fat Diet ◽

Obese Mice ◽

High Fat

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Ricekojireduced body weight gain, fat accumulation, and blood glucose level in high-fat diet-induced obese mice

PeerJ ◽

10.7717/peerj.540 ◽

2014 ◽

Vol 2 ◽

pp. e540 ◽

Cited By ~ 13

Author(s):

Yumiko Yoshizaki ◽

Chihiro Kawasaki ◽

Kai-Chun Cheng ◽

Miharu Ushikai ◽

Haruka Amitani ◽

...

Keyword(s):

Body Weight ◽

Weight Gain ◽

Blood Glucose ◽

Blood Glucose Level ◽

Glucose Level ◽

High Fat Diet ◽

Body Weight Gain ◽

Obese Mice ◽

High Fat ◽

Fat Accumulation

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Ginkgolide B lowers body weight and ameliorates hepatic steatosis in high-fat diet-induced obese mice correlated with pregnane X receptor activation

RSC Advances ◽

10.1039/c7ra05621d ◽

2017 ◽

Vol 7 (60) ◽

pp. 37858-37866 ◽

Cited By ~ 6

Author(s):

Lingling Luo ◽

Yin Li ◽

Dongshan Wang ◽

Yuanyuan Zhao ◽

Yahui Wang ◽

...

Keyword(s):

Body Weight ◽

Hepatic Steatosis ◽

High Fat Diet ◽

Pregnane X Receptor ◽

Receptor Activation ◽

Ginkgolide B ◽

Obese Mice ◽

High Fat

Ginkgolide B (GB) is a natural occurring terpene lactone and a selective agonistic ligand of hPXR.

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Follistatin-derived peptide expression in muscle decreases adipose tissue mass and prevents hepatic steatosis

AJP Endocrinology and Metabolism ◽

10.1152/ajpendo.00430.2010 ◽

2011 ◽

Vol 300 (3) ◽

pp. E543-E553 ◽

Cited By ~ 21

Author(s):

Masashi Nakatani ◽

Masahiro Kokubo ◽

Yutaka Ohsawa ◽

Yoshihide Sunada ◽

Kunihiro Tsuchida

Keyword(s):

Skeletal Muscle ◽

Fatty Acid ◽

Glucose Tolerance ◽

Hepatic Steatosis ◽

Muscle Mass ◽

High Fat Diet ◽

Skeletal Muscle Mass ◽

Related Gene ◽

High Fat ◽

Fat Accumulation

Myostatin, a member of the transforming growth factor (TGF)-β superfamily, plays a potent inhibitory role in regulating skeletal muscle mass. Inhibition of myostatin by gene disruption, transgenic (Tg) expression of myostatin propeptide, or injection of propeptide or myostatin antibodies causes a widespread increase in skeletal muscle mass. Several peptides, in addition to myostatin propeptide and myostatin antibodies, can bind directly to and neutralize the activity of myostatin. These include follistatin and follistatin-related gene. Overexpression of follistatin or follistatin-related gene in mice increased the muscle mass as in myostatin knockout mice. Follistatin binds to myostatin but also binds to and inhibits other members of the TGF-β superfamily, notably activins. Therefore, follistatin regulates both myostatin and activins in vivo. We previously reported the development and characterization of several follistatin-derived peptides, including FS I-I (Nakatani M, Takehara Y, Sugino H, Matsumoto M, Hashimoto O, Hasegawa Y, Murakami T, Uezumi A, Takeda S, Noji S, Sunada Y, Tsuchida K. FASEB J 22: 477–487, 2008). FS I-I retained myostatin-inhibitory activity without affecting the bioactivity of activins. Here, we found that inhibition of myostatin increases skeletal muscle mass and decreases fat accumulation in FS I-I Tg mice. FS I-I Tg mice also showed decreased fat accumulation even on a control diet. Interestingly, the adipocytes in FS I-I Tg mice were much smaller than those of wild-type mice. Furthermore, FS I-I Tg mice were resistant to high-fat diet-induced obesity and hepatic steatosis and had lower hepatic fatty acid levels and altered fatty acid composition compared with control mice. FS I-I Tg mice have improved glucose tolerance when placed on a high-fat diet. These data indicate that inhibiting myostatin with a follistatin-derived peptide provides a novel therapeutic option to decrease adipocyte size, prevent obesity and hepatic steatosis, and improve glucose tolerance.

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