Improvement in High-Fat Diet-Induced Obesity and Body Fat Accumulation by aNelumbo nuciferaLeaf Flavonoid-Rich Extract in Mice

2010 ◽  
Vol 58 (11) ◽  
pp. 7075-7081 ◽  
Author(s):  
Cheng-Hsun Wu ◽  
Mon-Yuan Yang ◽  
Kuei-Chuan Chan ◽  
Pei-Jun Chung ◽  
Ting-Tsz Ou ◽  
...  
Keyword(s):  
Body Fat ◽  
High Fat Diet ◽  
High Fat ◽  
Fat Accumulation ◽  
Diet Induced Obesity

scholarly journals Loss of Selenoprotein V Predisposes Mice to Body Fat Accumulation (OR11-02-19)

2019 ◽  
Vol 3 (Supplement_1) ◽  
Author(s):  
Lingli Chen ◽  
Jiaqiang Huang ◽  
Yuanyuan Wu ◽  
Fazheng Ren ◽  
Xin Gen Lei
Keyword(s):  
Gene Expression ◽  
Body Fat ◽  
High Fat Diet ◽  
The Body ◽  
High Fat ◽  
Fat Accumulation ◽  
Diet Induced Obesity ◽  
Body Weights ◽  
Its Gene ◽  
Selenoprotein V

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.

scholarly journals Tissue-specific expression of Sprouty1 in mice protects against high-fat diet-induced fat accumulation, bone loss and metabolic dysfunction

2011 ◽  
Vol 108 (6) ◽  
pp. 1025-1033 ◽  
Author(s):  
Sumithra Urs ◽  
Terry Henderson ◽  
Phuong Le ◽  
Clifford J. Rosen ◽  
Lucy Liaw
Keyword(s):  
Adipose Tissue ◽  
Bone Loss ◽  
Bone Mass ◽  
Body Fat ◽  
High Fat Diet ◽  
Conditional Knockout ◽  
Whole Body ◽  
High Fat ◽  
Tissue Specific ◽  
Diet Induced Obesity

We recently characterised Sprouty1 (Spry1), a growth factor signalling inhibitor as a regulator of marrow progenitor cells promoting osteoblast differentiation at the expense of adipocytes. Adipose tissue-specific Spry1 expression in mice resulted in increased bone mass and reduced body fat, while conditional knockout of Spry1 had the opposite effect with decreased bone mass and increased body fat. Because Spry1 suppresses normal fat development, we tested the hypothesis that Spry1 expression prevents high-fat diet-induced obesity, bone loss and associated lipid abnormalities, and demonstrate that Spry1 has a long-term protective effect on mice fed a high-energy diet. We studied diet-induced obesity in mice with fatty acid binding promoter-driven expression or conditional knockout of Spry1 in adipocytes. Phenotyping was performed by whole-body dual-energy X-ray absorptiometry, microCT, histology and blood analysis. In conditional Spry1-null mice, a high-fat diet increased body fat by 40 %, impaired glucose regulation and led to liver steatosis. However, overexpression of Spry1 led to 35 % (P < 0·05) lower body fat, reduced bone loss and normal metabolic function compared with single transgenics. This protective phenotype was associated with decreased circulating insulin (70 %) and leptin (54 %; P < 0·005) compared with controls on a high-fat diet. Additionally, Spry1 expression decreased adipose tissue inflammation by 45 %. We show that conditional Spry1 expression in adipose tissue protects against high-fat diet-induced obesity and associated bone loss.

scholarly journals Dietary Isoliquiritigenin at a Low Dose Ameliorates Insulin Resistance and NAFLD in Diet-Induced Obesity in C57BL/6J Mice

2018 ◽  
Vol 19 (10) ◽  
pp. 3281 ◽  
Author(s):  
Youngmi Lee ◽  
Eun-Young Kwon ◽  
Myung-Sook Choi
Keyword(s):  
Insulin Resistance ◽  
Energy Expenditure ◽  
Body Fat ◽  
Fat Mass ◽  
High Fat Diet ◽  
Plasma Cholesterol ◽  
Cellular Respiration ◽  
Body Fat Mass ◽  
High Fat ◽  
Diet Induced Obesity

Isoliquiritigenin (ILG) is a flavonoid constituent of Glycyrrhizae plants. The current study investigated the effects of ILG on diet-induced obesity and metabolic diseases. C57BL/6J mice were fed a normal diet (AIN-76 purified diet), high-fat diet (40 kcal% fat), and high-fat diet +0.02% (w/w) ILG for 16 weeks. Supplementation of ILG resulted in decreased body fat mass and plasma cholesterol level. ILG ameliorated hepatic steatosis by suppressing the expression of hepatic lipogenesis genes and hepatic triglyceride and fatty acid contents, while enhancing β-oxidation in the liver. ILG improved insulin resistance by lowering plasma glucose and insulin levels. This was also demonstrated by the intraperitoneal glucose tolerance test (IPGTT). Additionally, ILG upregulated the expression of insulin signaling-related genes in the liver and muscle. Interestingly, ILG elevated energy expenditure by increasing the expression of thermogenesis genes, which is linked to stimulated mitochondrial biogenesis and uncoupled cellular respiration in brown adipose tissue. ILG also suppressed proinflammatory cytokine levels in the plasma. These results suggest that ILG supplemented at 0.02% in the diet can ameliorate body fat mass, plasma cholesterol, non-alcoholic fatty liver disease, and insulin resistance; these effects were partly mediated by increasing energy expenditure in high-fat fed mice.

Effect of High-fat Diet Feeding over Generations on Body Fat Accumulation

2015 ◽  
pp. 181-190 ◽  
Author(s):  
Kiwon Lim ◽  
Yoshiharu Shimomura ◽  
Masashige Suzuki
Keyword(s):  
Body Fat ◽  
High Fat Diet ◽  
High Fat ◽  
Fat Accumulation

scholarly journals Urtica dioica Whole Vegetable as a Functional Food Targeting Fat Accumulation and Insulin Resistance-a Preliminary Study in a Mouse Pre-Diabetic Model

Nutrients ◽  
2020 ◽  
Vol 12 (4) ◽  
pp. 1059
Author(s):  
Si Fan ◽  
Samnhita Raychaudhuri ◽  
Olivia Kraus ◽  
Md Shahinozzaman ◽  
Leila Lofti ◽  
...  
Keyword(s):  
Insulin Resistance ◽  
Skeletal Muscle ◽  
Adipose Tissue ◽  
Glucose Metabolism ◽  
High Fat Diet ◽  
Urtica Dioica ◽  
Whole Body ◽  
High Fat ◽  
Fat Accumulation ◽  
Diet Induced Obesity

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.

scholarly journals MEK6 Overexpression Exacerbates Fat Accumulation and Inflammatory Cytokines in High-Fat Diet-Induced Obesity

2021 ◽  
Vol 22 (24) ◽  
pp. 13559
Author(s):  
Suyeon Lee ◽  
Myoungsook Lee
Keyword(s):  
Adipose Tissue ◽  
Inflammatory Cytokines ◽  
High Fat Diet ◽  
Liver Lipid ◽  
Mapk Signaling ◽  
Chow Diet ◽  
High Fat ◽  
Fat Accumulation ◽  
Diet Induced Obesity ◽  
Lipid Formation

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.

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
Keyword(s):  
High Fat Diet ◽  
High Fat ◽  
Fat Accumulation ◽  
Diet Induced Obesity

Coffee polyphenols suppress diet-induced body fat accumulation by downregulating SREBP-1c and related molecules in C57BL/6J mice

2011 ◽  
Vol 300 (1) ◽  
pp. E122-E133 ◽  
Author(s):  
Takatoshi Murase ◽  
Koichi Misawa ◽  
Yoshihiko Minegishi ◽  
Masafumi Aoki ◽  
Hideo Ominami ◽  
...  
Keyword(s):  
Body Fat ◽  
High Fat Diet ◽  
Active Form ◽  
Pyruvate Dehydrogenase Kinase ◽  
Liver Fat ◽  
Mrna Levels ◽  
Acetyl Coa Carboxylase ◽  
High Fat ◽  
Acetyl Coa ◽  
Fat Accumulation

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.

Sign in / Sign up

Export Citation Format

Share Document