Fucoidan Prevents High-Fat Diet-Induced Obesity in Animals by Suppression of Fat Accumulation

2013 ◽  
Vol 28 (1) ◽  
pp. 137-143 ◽  
Author(s):  
Mi-Ja Kim ◽  
Joseph Jeon ◽  
Jin-Sil Lee
Nutrients ◽  
2020 ◽  
Vol 12 (4) ◽  
pp. 1059
Author(s):  
Si Fan ◽  
Samnhita Raychaudhuri ◽  
Olivia Kraus ◽  
Md Shahinozzaman ◽  
Leila Lofti ◽  
...  

The shoot of Urtica dioica is used in several cultures as a vegetable or herb. However, not much has been studied about the potential of this plant when consumed as a whole food/vegetable rather than an extract for dietary supplements. In a 12-week dietary intervention study, we tested the effect of U. dioica vegetable on high fat diet induced obesity and insulin resistance in C57BL/6J mice. Mice were fed ad libitum with isocaloric diets containing 10% fat or 45% fat with or without U. dioica. The diet supplemented with U. dioica attenuated high fat diet induced weight gain (p < 0.005; n = 9), fat accumulation in adipose tissue (p < 0.005; n = 9), and whole-body insulin resistance (HOMA-IR index) (p < 0.001; n = 9). Analysis of gene expression in skeletal muscle showed no effect on the constituents of the insulin signaling pathway (AKT, IRS proteins, PI3K, GLUT4, and insulin receptor). Notable genes that impact lipid or glucose metabolism and whose expression was changed by U. dioica include fasting induced adipocyte factor (FIAF) in adipose and skeletal muscle, peroxisome proliferator-activated receptor-α (Ppar-α) and forkhead box protein (FOXO1) in muscle and liver, and Carnitine palmitoyltransferase I (Cpt1) in liver (p < 0.01). We conclude that U. dioica vegetable protects against diet induced obesity through mechanisms involving lipid accumulation and glucose metabolism in skeletal muscle, liver, and adipose tissue.


2021 ◽  
Vol 22 (24) ◽  
pp. 13559
Author(s):  
Suyeon Lee ◽  
Myoungsook Lee

Obesity is a state of abnormal fat accumulation caused by an energy imbalance potentially caused by changes in multiple factors. MEK6 engages in cell growth, such as inflammation and apoptosis, as one of the MAPK signaling pathways. The MEK6 gene was found to be related to RMR, a gene associated with obesity. Because only a few studies have investigated the correlation between MEK6 and obesity or the relevant mechanisms, we conducted an experiment using a TgMEK6 model with MEK6 overexpression with non-Tg and chow diet as the control to determine changes in lipid metabolism in plasma, liver, and adipose tissue after a 15-week high-fat diet (HFD). MEK6 overexpression in the TgMEK6 model significantly increased body weight and plasma triglyceride and total cholesterol levels. p38 activity declined in the liver and adipose tissues and lowered lipolysis, oxidation, and thermogenesis levels, contributing to decreased energy consumption. In the liver, lipid formation and accumulation increased, and in adipose, adipogenesis and hypertrophy increased. The adiponectin/leptin ratio significantly declined in plasma and adipose tissue of the TgMEK6 group following MEK6 expression and the HFD, indicating the role of MEK6 expression in adipokine regulation. Plasma and bone-marrow-derived macrophages (BMDM) of the TgMEK6 group increased MEK6 expression-dependent secretion of pro-inflammatory cytokines but decreased levels of anti-inflammatory cytokines, further exacerbating the results exhibited by the diet-induced obesity group. In conclusion, this study demonstrated the synergistic effect of MEK6 with HFD in fat accumulation by significantly inhibiting the mechanisms of lipolysis in the adipose and M2 associated cytokines secretion in the BMDM.


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.


2021 ◽  
Vol 12 ◽  
Author(s):  
Zhuohui Luo ◽  
Jiawen Huang ◽  
Zhiping Li ◽  
Zhiwen Liu ◽  
Linchun Fu ◽  
...  

Cajanolactone A (CLA) is a stilbenoid isolated from Cajanus canjan (L.) Millsp with the potential to prevent postmenopausal obesity. In this study, the effect of CLA on high-fat diet (HFD)-induced obesity in female C57BL/6 mice was investigated. It was found that, treatment with CLA reduced the energy intake and effectively protected the mice from HFD-induced body weight gain, fat accumulation within the adipose tissues and liver, and impairment in energy metabolism. Further investigation revealed that CLA significantly down-regulated the expression of ORX, ORXR2, pMCH, and Gal in the hypothalamus and antagonized HFD-induced changes in the expression of UCP1, Pgc-1α, Tfam, and Mfn1 in the inguinal white adipose tissue (iWAT); Caveolin-1, MT and UCP3 in the perigonadal white adipose tissue (pWAT); and Pdhb, IRS2, Mttp, Hadhb, and Cpt1b in the liver. CLA also protected the pWAT and liver from HFD-induced mitochondrial damage. However, neither HFD nor CLA showed an effect on the mass of brown adipose tissue (BAT) or the expression of UCP1 in the BAT. In summary, our findings suggest that CLA is a potential drug candidate for preventing diet-induced obesity, at least in females. CLA works most likely by suppressing the hypothalamic expression of orexigenic genes, which leads to reduced energy intake, and subsequently, reduced fat accumulation, thereby protecting the adipose tissues and the liver from lipid-induced mitochondrial dysfunction.


PLoS ONE ◽  
2015 ◽  
Vol 10 (12) ◽  
pp. e0142041 ◽  
Author(s):  
Ji-Hye Lee ◽  
Taesoo Kim ◽  
Jung-Jin Lee ◽  
Kwang Jin Lee ◽  
Hyun-Kyu Kim ◽  
...  

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

Metabolism ◽  
2017 ◽  
Vol 71 ◽  
pp. 1-6 ◽  
Author(s):  
Yukie Kusumoto ◽  
Junichiro Irie ◽  
Kaho Iwabu ◽  
Hirotsune Tagawa ◽  
Arata Itoh ◽  
...  

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