scholarly journals Heat‐killed Lactobacillus brevis KB290 attenuates visceral fat accumulation induced by high‐fat diet in mice

Author(s):  
Jun Watanabe ◽  
Naoto Hashimoto ◽  
Tingyu Yin ◽  
Bayanjargal Sandagdorj ◽  
Chinatsu Arakawa ◽  
...  
Obesity ◽  
2008 ◽  
Vol 16 (6) ◽  
pp. 1261-1269 ◽  
Author(s):  
C.S. Kim ◽  
S.C. Lee ◽  
Y.M. Kim ◽  
B.S. Kim ◽  
H.S. Choi ◽  
...  

2020 ◽  
pp. 1-14
Author(s):  
T. Yin ◽  
S. Bayanjargal ◽  
B. Fang ◽  
C. Inaba ◽  
M. Mutoh ◽  
...  

Lactobacillus plantarum Shinshu N-07 (N07) and Lactobacillus curvatus #4G2 (#4G2) were isolated from fermented Brassica rapa L. and selected as promising probiotics with anti-adiposity activities based on in vitro assays. The anti-adiposity effects of these two strains were investigated using a diet-induced obesity animal model. Epididymal adipose tissue weight and adipocyte area were significantly lower and serum triglycerides and glucose tended to be lower in mice fed the high-fat diet supplemented with N07 compared with those fed the unsupplemented high-fat diet. Strain N07 suppressed hepatic steatosis, with accompanying downregulation of lipogenic genes in the liver. Expression of inflammatory cytokines and macrophage infiltration markers tended to be suppressed by N07 supplementation. Upregulation of uncoupling protein-1 in epididymal adipose tissue by N07 suggested that the transformation of white adipose tissue to brown might have been induced. Intestinal microbiota analysis revealed that a decrease in abundance of family S24-7 (phylum Bacteroidetes) following ingestion of the high-fat diet was partly recovered by supplementation with N07. Changes in those parameters were not observed in mice fed the high-fat diet supplemented with strain #4G2, suggesting strain specificities. Thus, N07 is a potential probiotic strain that could be used to develop functional foods that attenuate visceral fat accumulation after an appropriate human intervention trial.


2015 ◽  
Vol 64 (12) ◽  
pp. 1243-1250 ◽  
Author(s):  
Azusa Takahashi ◽  
Hisae Shimizu ◽  
Yukako Okazaki ◽  
Hirohide Sakaguchi ◽  
Toshio Taira ◽  
...  

2000 ◽  
Vol 279 (6) ◽  
pp. R2057-R2065 ◽  
Author(s):  
Jong-Yeon Kim ◽  
Lorraine A. Nolte ◽  
Polly A. Hansen ◽  
Dong-Ho Han ◽  
Kevin Ferguson ◽  
...  

It has been variously hypothesized that the insulin resistance induced in rodents by a high-fat diet is due to increased visceral fat accumulation, to an increase in muscle triglyceride (TG) content, or to an effect of diet composition. In this study we used a number of interventions: fish oil, leptin, caloric restriction, and shorter duration of fat feeding, to try to disassociate an increase in visceral fat from muscle insulin resistance. Substituting fish oil (18% of calories) for corn oil in the high-fat diet partially protected against both the increase in visceral fat and muscle insulin resistance without affecting muscle TG content. Injections of leptin during the last 4 days of a 4-wk period on the high-fat diet partially reversed the increase in visceral fat and the muscle insulin resistance, while completely normalizing muscle TG. Restricting intake of the high-fat diet to 75% of ad libitum completely prevented the increase in visceral fat and muscle insulin resistance. Maximally insulin-stimulated glucose transport was negatively correlated with visceral fat mass ( P < 0.001) in both the soleus and epitrochlearis muscles and with muscle TG concentration in the soleus ( P < 0.05) but not in the epitrochlearis. Thus we were unable to dissociate the increase in visceral fat from muscle insulin resistance using a variety of approaches. These results support the hypothesis that an increase in visceral fat is associated with development of muscle insulin resistance.


Nutrients ◽  
2021 ◽  
Vol 13 (5) ◽  
pp. 1462
Author(s):  
Kristýna Junková ◽  
Lukáš F. Mirchi ◽  
Blanka Chylíková ◽  
Michaela Janků ◽  
Jan Šilhavý ◽  
...  

Metabolic syndrome (MetS) is an important cause of worldwide morbidity and mortality. Its complex pathogenesis includes, on the one hand, sedentary lifestyle and high caloric intake, and, on the other hand, there is a clear genetic predisposition. PD (Polydactylous rat) is an animal model of hypertriglyceridemia, insulin resistance, and obesity. To unravel the genetic and pathophysiologic background of this phenotype, we compared morphometric and metabolic parameters as well as liver transcriptomes among PD, spontaneously hypertensive rat, and Brown Norway (BN) strains fed a high-fat diet (HFD). After 4 weeks of HFD, PD rats displayed marked hypertriglyceridemia but without the expected hepatic steatosis. Moreover, the PD strain showed significant weight gain, including increased weight of retroperitoneal and epididymal fat pads, and impaired glucose tolerance. In the liver transcriptome, we found 5480 differentially expressed genes, which were enriched for pathways involved in fatty acid beta and omega oxidation, glucocorticoid metabolism, oxidative stress, complement activation, triacylglycerol and lipid droplets synthesis, focal adhesion, prostaglandin synthesis, interferon signaling, and tricarboxylic acid cycle pathways. Interestingly, the PD strain, contrary to SHR and BN rats, did not express the Acsm3 (acyl-CoA synthetase medium-chain family member 3) gene in the liver. Together, these results suggest disturbances in fatty acid utilization as a molecular mechanism predisposing PD rats to hypertriglyceridemia and fat accumulation.


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