scholarly journals Body Fat Accumulation in the Male Offspring of Rats Fed High-Fat Diet.

1998 ◽  
Vol 25 (2) ◽  
pp. 71-79 ◽  
Author(s):  
Qing WU ◽  
Yasuhiro MIZUSHIMA ◽  
Masahiko KOMIYA ◽  
Tatsuhiro MATSUO ◽  
Masashige SUZUKI
2015 ◽  
pp. 181-190 ◽  
Author(s):  
Kiwon Lim ◽  
Yoshiharu Shimomura ◽  
Masashige Suzuki

2019 ◽  
Vol 3 (Supplement_1) ◽  
Author(s):  
Lingli Chen ◽  
Jiaqiang Huang ◽  
Yuanyuan Wu ◽  
Fazheng Ren ◽  
Xin Gen Lei

Abstract Objectives Metabolic function of selenoprotein V (SELENOV) remains unknown, although we previously showed a strong correlation of its gene expression with the high-fat diet-induced obesity in pigs. This study was conducted to explore the role and mechanism of SELENOV in body fat metabolism. Methods We applied the CRISPR/Cas9 gene-targeting deletion to generate Selenovknockout (KO) mice (C57BL/6 J background). Male KO and their wild-type (WT) (8 weeks old, n = 10 per genotype by treatment group) were fed a normal diet (NF, 10% calories coming from fat) or a high-fat diet (HF, 60% calories coming from fat) for 27 weeks. At the end, body weights and composition of mice were recorded, and tissues were collected to assay for gene expression and protein production related to lipid metabolism. Results Body weights of the KO mice fed the NF or HF diet were 16–19% higher (P < 0.05) than those of the WT mice. Total fat mass of the KO mice was 54% higher (P < 0.05) than the WT mice fed either diet, whereas total lean mass of the KO mice was 5 and 35% lower (P < 0.05) than that of WT mice fed the NF and HF diets, respectively. Gene expression of key enzymes (Fasn, Acaca, Dgat1, and Lpl) involved in lipogenesis was elevated (P < 0.05) in the white adipose tissue of the KO mice compared with the WT mice. In contrast, differences in gene expression of enzymes related to lipolysis and fatty acid oxidation (Atgl, Hsl, Ces1d, and Cpt1a) between the two genotypes were exactly the opposite (P < 0.05). Consistently, levels of proteins related to lipid accumulation (pACC, ACC, FAS, and LPL) were upregulated (P < 0.05) and proteins related to lipolysis (ATGL, HSL, and pHSL) were down-regulated (P < 0.05) in the KO mice compared with the WT mice. Conclusions Knockout of Selenov predisposed the male mice to elevated lipogenesis and attenuated lipolyis, leading to the body fat accumulation. This illustrated role and mechanism of SELENOV helps explain our previously-reported correlation between its gene expression and the high-fat diet-induced obesity in pigs. Funding Sources This research was supported in part by a NSFC grant #31,320,103,920.


2011 ◽  
Vol 300 (1) ◽  
pp. E122-E133 ◽  
Author(s):  
Takatoshi Murase ◽  
Koichi Misawa ◽  
Yoshihiko Minegishi ◽  
Masafumi Aoki ◽  
Hideo Ominami ◽  
...  

The prevalence of obesity is increasing globally, and obesity is a major risk factor for type 2 diabetes and cardiovascular disease. We investigated the effects of coffee polyphenols (CPP), which are abundant in coffee and consumed worldwide, on diet-induced body fat accumulation. C57BL/6J mice were fed either a control diet, a high-fat diet, or a high-fat diet supplemented with 0.5 to 1.0% CPP for 2–15 wk. Supplementation with CPP significantly reduced body weight gain, abdominal and liver fat accumulation, and infiltration of macrophages into adipose tissues. Energy expenditure evaluated by indirect calorimetry was significantly increased in CPP-fed mice. The mRNA levels of sterol regulatory element-binding protein (SREBP)-1c, acetyl-CoA carboxylase-1 and -2, stearoyl-CoA desaturase-1, and pyruvate dehydrogenase kinase-4 in the liver were significantly lower in CPP-fed mice than in high-fat control mice. Similarly, CPP suppressed the expression of these molecules in Hepa 1–6 cells, concomitant with an increase in microRNA-122. Structure-activity relationship studies of nine quinic acid derivatives isolated from CPP in Hepa 1–6 cells suggested that mono- or di-caffeoyl quinic acids (CQA) are active substances in the beneficial effects of CPP. Furthermore, CPP and 5-CQA decreased the nuclear active form of SREBP-1, acetyl-CoA carboxylase activity, and cellular malonyl-CoA levels. These findings indicate that CPP enhances energy metabolism and reduces lipogenesis by downregulating SREBP-1c and related molecules, which leads to the suppression of body fat accumulation.


2019 ◽  
Vol 9 (13) ◽  
pp. 2750 ◽  
Author(s):  
Ga Young Do ◽  
Eun-Young Kwon ◽  
Yun Jin Kim ◽  
Youngji Han ◽  
Seong-Bo Kim ◽  
...  

D-allulose, which has 70% of the sweet taste of sucrose but nearly no calories, has been reported to inhibit the absorption of lipids and suppress body weight gain in obese mice. Fats in non-dairy creamer consist of highly saturated fatty acids, which can cause various lipid disorders when consumed over a long period. We investigated whether D-allulose supplementation alleviates the effects of a non-dairy creamer-enriched high-fat diet on lipid metabolism. High-fat diets enriched with non-dairy creamer were administered to C57BL/6J mice with or without D-allulose supplementation for eight weeks by the pair-feeding design. Lipid metabolic markers were compared between the non-dairy creamer control group (NDC) and non-dairy creamer allulose group (NDCA). Body, adipose tissue, and liver weights, and fasting blood glucose levels, were significantly lower in the NDCA group than in the NDC group. Fecal fatty acid and triglyceride levels were significantly higher in the NDCA group than in the NDC group. Supplementing a non-dairy creamer-enriched high-fat diet with D-allulose improved overall lipid metabolism, including the plasma and hepatic lipid profiles, hepatic and adipose tissue morphology, and plasma inflammatory adipokine levels in mice. These results suggest that D-allulose can be used as a functional food component for preventing body fat accumulation from a high-fat diet that includes hydrogenated plant fats.


2013 ◽  
Vol 77 (11) ◽  
pp. 2294-2297 ◽  
Author(s):  
Su-Jung YEON ◽  
Soo-Ki KIM ◽  
Jong Moon KIM ◽  
Si-Kyung LEE ◽  
Chi-Ho LEE

2010 ◽  
Vol 58 (11) ◽  
pp. 7075-7081 ◽  
Author(s):  
Cheng-Hsun Wu ◽  
Mon-Yuan Yang ◽  
Kuei-Chuan Chan ◽  
Pei-Jun Chung ◽  
Ting-Tsz Ou ◽  
...  

2006 ◽  
Vol 31 (4) ◽  
pp. 367-375 ◽  
Author(s):  
Siham Yasari ◽  
Amélie Paquette ◽  
Alexandre Charbonneau ◽  
Marie-Soleil Gauthier ◽  
Roland Savard ◽  
...  

The purpose of the present study was to determine if exercise trained rats might benefit from protection against fat accumulation in response to an obesity stimulus initiated upon training cessation. Two groups of female rats were either treadmill trained for 8 weeks (DTr) or remained sedentary (Sed). They were then submitted either to a high-fat diet (HF; 42 E%) or kept on a standard diet (SD; 12.5 E% lipids) for another 6 weeks while remaining sedentary. Fat accumulation in liver and adipocytes along with fat-cell diameter and plasma free fatty acid (FFA) levels were measured 0, 2, and 6 weeks after training cessation. Immediately after the training period (t = 0), DTr rats exhibited similar body mass and higher dietary intake but smaller body fat content (4 fat pads) compared with Sed rats. DTr rats, under both diets, exhibited higher gains in body fat than Sed rats (DTr vs. Sed, 71% vs. 8% and 132% vs. 55% for SD and HF, respectively), such that fat mass in all 4 depots was similar to Sed rats 6 weeks after training cessation. Despite higher adipocyte fat accretion, liver lipid infiltration was not increased in DTr animals and plasma FFA levels were lower throughout the detraining period. In addition, plasma leptin levels remained lower in DTr animals throughout the detraining period under the HF diet condition. The present results indicate that previously exercise trained rats are not protected against adipocyte fat accumulation whether they ingest a standard or a high-fat diet.


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