scholarly journals Hepatic Transcriptome Profiling Reveals Lack of Acsm3 Expression in Polydactylous Rats with High-Fat Diet-Induced Hypertriglyceridemia and Visceral Fat Accumulation

Nutrients ◽  
2021 ◽  
Vol 13 (5) ◽  
pp. 1462
Author(s):  
Kristýna Junková ◽  
Lukáš F. Mirchi ◽  
Blanka Chylíková ◽  
Michaela Janků ◽  
Jan Šilhavý ◽  
...  
Keyword(s):  
Fatty Acid ◽  
High Fat Diet ◽  
Spontaneously Hypertensive Rat ◽  
Tricarboxylic Acid Cycle ◽  
Caloric Intake ◽  
Transcriptome Profiling ◽  
Brown Norway ◽  
High Fat ◽  
Fat Accumulation ◽  
Visceral Fat Accumulation

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.

scholarly journals Visceral Fat Accumulation Induced by a High-fat Diet Causes the Atrophy of Mesenteric Lymph Nodes in Obese Mice

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 ◽  
...  
Keyword(s):  
Lymph Nodes ◽  
Visceral Fat ◽  
High Fat Diet ◽  
Obese Mice ◽  
High Fat ◽  
Mesenteric Lymph Nodes ◽  
Fat Accumulation ◽  
Visceral Fat Accumulation ◽  
Mesenteric Lymph

Detrimental metabolic effects of combining long-term cigarette smoke exposure and high-fat diet in mice

2007 ◽  
Vol 293 (6) ◽  
pp. E1564-E1571 ◽  
Author(s):  
Hui Chen ◽  
Michelle J. Hansen ◽  
Jessica E. Jones ◽  
Ross Vlahos ◽  
Gary P. Anderson ◽  
...  
Keyword(s):  
High Fat Diet ◽  
Caloric Intake ◽  
Fold Increase ◽  
Smoke Exposure ◽  
Metabolic Effects ◽  
Cigarette Smoke Exposure ◽  
High Fat ◽  
Fat Accumulation ◽  
Reduced Body ◽  
Plasma Leptin

Obesity and cigarette smoking are both important risk factors for insulin resistance, cardiovascular disease, and cancer. Smoking reduces appetite, which makes many people reluctant to quit. Few studies have documented the metabolic impact of combined smoke exposure (se) and high-fat-diet (HFD). Neuropeptide Y (NPY) is a powerful hypothalamic feeding stimulator that promotes obesity. We investigated how chronic se affects caloric intake, adiposity, plasma hormones, inflammatory mediators, and hypothalamic NPY peptide in animals fed a palatable HFD. Balb/c mice (5 wk old, male) were exposed to smoke (2 cigarettes, twice/day, 6 days/wk, for 7 wk) with or without HFD. Sham-exposed mice were handled similarly without se. Plasma leptin, hypothalamic NPY, and adipose triglyceride lipase (ATGL) mRNA were measured. HFD induced a 2.3-fold increase in caloric intake, increased adiposity, and glucose in both sham and se cohorts. Smoke exposure decreased caloric intake by 23%, with reduced body weight in both dietary groups. Fat mass and glucose were reduced only by se in the chow-fed animals. ATGL mRNA was reduced by HFD in se animals. Total hypothalamic NPY was reduced by HFD, but only in sham-exposed animals; se increased arcuate NPY. We conclude that although se ameliorated hyperphagia and reversed the weight gain associated with HFD, it failed to reverse fat accumulation and hyperglycemia. The reduced ATGL mRNA expression induced by combined HFD and se may contribute to fat retention. Our data support a powerful health message that smoking in the presence of an unhealthy Western diet increases metabolic disorders and fat accumulation.

Lactobacillus plantarum Shinshu N-07 isolated from fermented Brassica rapa L. attenuates visceral fat accumulation induced by high-fat diet in mice

2020 ◽  
pp. 1-14
Author(s):  
T. Yin ◽  
S. Bayanjargal ◽  
B. Fang ◽  
C. Inaba ◽  
M. Mutoh ◽  
...  
Keyword(s):  
Adipose Tissue ◽  
Lactobacillus Plantarum ◽  
Brassica Rapa ◽  
Visceral Fat ◽  
High Fat Diet ◽  
Uncoupling Protein ◽  
Epididymal Adipose Tissue ◽  
High Fat ◽  
Fat Accumulation ◽  
Visceral Fat Accumulation

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.

scholarly journals Anthocyanin-rich Phytochemicals from Aronia Fruits Inhibit Visceral Fat Accumulation and Hyperglycemia in High-fat Diet-induced Dietary Obese Rats

2015 ◽  
Vol 64 (12) ◽  
pp. 1243-1250 ◽  
Author(s):  
Azusa Takahashi ◽  
Hisae Shimizu ◽  
Yukako Okazaki ◽  
Hirohide Sakaguchi ◽  
Toshio Taira ◽  
...  
Keyword(s):  
Visceral Fat ◽  
High Fat Diet ◽  
High Fat ◽  
Fat Accumulation ◽  
Visceral Fat Accumulation ◽  
Obese Rats

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

2011 ◽  
Vol 300 (3) ◽  
pp. E543-E553 ◽  
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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