scholarly journals Salvianolic acid B plays an anti-obesity role in high fat diet-induced obese mice by regulating the expression of mRNA, circRNA, and lncRNA

PeerJ ◽  
2019 ◽  
Vol 7 ◽  
pp. e6506 ◽  
Author(s):  
Tian An ◽  
Jing Zhang ◽  
Bohan Lv ◽  
Yufei Liu ◽  
Jiangpinghao Huang ◽  
...  
Keyword(s):  
Adipose Tissue ◽  
White Adipose Tissue ◽  
High Fat Diet ◽  
Metabolic Diseases ◽  
Water Soluble ◽  
Salvianolic Acid B ◽  
Obese Mice ◽  
High Fat ◽  
Salvianolic Acid ◽  
Resistance Pathway

Background Adipose tissue plays a central role in obesity-related metabolic diseases such as type 2 diabetes. Salvianolic acid B (Sal B), a water-soluble ingredient derived from Salvia miltiorrhiza, has been shown to reduce obesity and obesity-related metabolic diseases by suppressing adipogenesis. However, the role of Sal B in white adipose tissue (WAT) is not yet clear. Methods Illumina Hiseq 4000 was used to study the effects of Sal B on the expression of long non-coding RNA (lncRNA) and circular RNA (circRNA) in epididymal white adipose tissue induced by a high fat diet in obese mice. Results RNA-Seq data showed that 234 lncRNAs, 19 circRNAs, and 132 mRNAs were differentially expressed in WAT under Sal B treatment. The up-regulated protein-coding genes in WAT of the Sal B-treated group were involved in the insulin resistance pathway, while the down-regulated genes mainly participated in the IL-17 signaling pathway. Other pathways may play an important role in the formation and differentiation of adipose tissue, such as B cell receptor signaling. Analysis of the lncRNA–mRNA network provides potential targets for lncRNAs in energy metabolism. We speculate that Sal B may serve as a potential therapeutic approach for obesity.

scholarly journals Activation of AMP-Activated Protein Kinase-Sirtuin 1 Pathway Contributes to Salvianolic Acid A-Induced Browning of White Adipose Tissue in High-Fat Diet Fed Male Mice

2021 ◽  
Vol 12 ◽  
Author(s):  
Jianfei Lai ◽  
Qianyu Qian ◽  
Qinchao Ding ◽  
Li Zhou ◽  
Ai Fu ◽  
...  
Keyword(s):  
Adipose Tissue ◽  
Protein Kinase ◽  
White Adipose Tissue ◽  
High Fat Diet ◽  
Sirtuin 1 ◽  
Male Mice ◽  
High Fat ◽  
Sirt1 Expression ◽  
Salvianolic Acid ◽  
Amp Activated Protein Kinase

Background: Salvianolic acid A (Sal A), a natural polyphenolic compound extracted from Radix Salvia miltiorrhiza (Danshen), exhibits exceptional pharmacological activities against cardiovascular diseases. While a few studies have reported anti-obesity properties of Sal A, the underlying mechanisms are largely unknown. Given the prevalence of obesity and promising potential of browning of white adipose tissue to combat obesity, recent research has focused on herbal ingredients that may promote browning and increase energy expenditure.Purpose: The present study was designed to investigate the protective antiobesity mechanisms of Sal A, in part through white adipose browning.Methods: Both high-fat diet (HFD)-induced obese (DIO) male mice model and fully differentiated C3H10T1/2 adipocytes from mouse embryo fibroblasts were employed in this study. Sal A (20 and 40 mg/kg) was administrated to DIO mice by intraperitoneal injection for 13-weeks. Molecular mechanisms mediating effects of Sal A were evaluated.Resluts: Sal A treatment significantly attenuated HFD-induced weight gain and lipid accumulation in epididymal fat pad. Uncoupling protein 1 (UCP-1), a specialized thermogenic protein and marker for white adipocyte browning, was significantly induced by Sal A treatment in both white adipose tissues and cultured adipocytes. Further mechanistic investigations revealed that Sal A robustly reversed HFD-decreased AMP-activated protein kinase (AMPK) phosphorylation and sirtuin 1 (SIRT1) expression in mice. Genetically silencing either AMPK or SIRT1 using siRNA abolished UCP-1 upregulation by Sal A. AMPK silencing significantly blocked Sal A-increased SIRT1 expression, while SIRT1 silencing did not affect Sal A-upregulated phosphorylated-AMPK. These findings indicate that AMPK was involved in Sal A-increased SIRT1.Conclusion: Sal A increases white adipose tissue browning in HFD-fed male mice and in cultured adipocytes. Thus, Sal is a potential natural therapeutic compound for treating and/or preventing obesity.

scholarly journals Oxyresveratrol Increases Energy Expenditure through Foxo3a-Mediated Ucp1 Induction in High-Fat-Diet-Induced Obese Mice

2018 ◽  
Vol 20 (1) ◽  
pp. 26 ◽  
Author(s):  
Jin Choi ◽  
No-Joon Song ◽  
A Lee ◽  
Dong Lee ◽  
Min-Ju Seo ◽  
...  
Keyword(s):  
Adipose Tissue ◽  
Energy Expenditure ◽  
High Fat Diet ◽  
Adipocyte Differentiation ◽  
Metabolic Diseases ◽  
Biological Activities ◽  
Obese Mice ◽  
High Fat ◽  
White Adipocyte

The phytochemical oxyresveratrol has been shown to exert diverse biological activities including prevention of obesity. However, the exact reason underlying the anti-obese effects of oxyresveratrol is not fully understood. Here, we investigated the effects and mechanism of oxyresveratrol in adipocytes and high-fat diet (HFD)-fed obese mice. Oxyresveratrol suppressed lipid accumulation and expression of adipocyte markers during the adipocyte differentiation of 3T3-L1 and C3H10T1/2 cells. Administration of oxyresveratrol in HFD-fed obese mice prevented body-weight gains, lowered adipose tissue weights, improved lipid profiles, and increased glucose tolerance. The anti-obese effects were linked to increases in energy expenditure and higher rectal temperatures without affecting food intake, fecal lipid content, and physical activity. The increased energy expenditure by oxyresveratrol was concordant with the induction of thermogenic genes including Ucp1, and the reduction of white adipocyte selective genes in adipose tissue. Furthermore, Foxo3a was identified as an oxyresveratrol-induced gene and it mimicked the effects of oxyresveratrol for induction of thermogenic genes and suppression of white adipocyte selective genes, suggesting the role of Foxo3a in oxyresveratrol-mediated anti-obese effects. Taken together, these data show that oxyresveratrol increases energy expenditure through the induction of thermogenic genes in adipose tissue and further implicates oxyresveratrol as an ingredient and Foxo3a as a molecular target for the development of functional foods in obesity and metabolic diseases.

scholarly journals Proteomic white adipose tissue analysis of obese mice fed with a high-fat diet and treated with oral angiotensin-(1–7)

Peptides ◽  
2014 ◽  
Vol 60 ◽  
pp. 56-62 ◽  
Author(s):  
João Marcus Oliveira Andrade ◽  
Fernanda de Oliveira Lemos ◽  
Simone da Fonseca Pires ◽  
Ruben Dario Sinisterra Millán ◽  
Frederico Barros de Sousa ◽  
...  
Keyword(s):  
Adipose Tissue ◽  
White Adipose Tissue ◽  
High Fat Diet ◽  
Tissue Analysis ◽  
Obese Mice ◽  
High Fat

scholarly journals Lyophilized Maqui (Aristotelia chilensis) Berry Induces Browning in the Subcutaneous White Adipose Tissue and Ameliorates the Insulin Resistance in High Fat Diet-Induced Obese Mice

Antioxidants ◽  
2019 ◽  
Vol 8 (9) ◽  
pp. 360 ◽  
Author(s):  
Viviana Sandoval ◽  
Antoni Femenias ◽  
Úrsula Martínez-Garza ◽  
Hèctor Sanz-Lamora ◽  
Juan Castagnini ◽  
...  
Keyword(s):  
Insulin Resistance ◽  
Adipose Tissue ◽  
White Adipose Tissue ◽  
High Fat Diet ◽  
Binding Protein ◽  
Fibroblast Growth Factor 21 ◽  
Obese Mice ◽  
High Fat ◽  
Subcutaneous White Adipose Tissue ◽  
Aristotelia Chilensis

Maqui (Aristotelia Chilensis) berry features a unique profile of anthocyanidins that includes high amounts of delphinidin-3-O-sambubioside-5-O-glucoside and delphinidin-3-O-sambubioside and has shown positive effects on fasting glucose and insulin levels in humans and murine models of type 2 diabetes and obesity. The molecular mechanisms underlying the impact of maqui on the onset and development of the obese phenotype and insulin resistance was investigated in high fat diet-induced obese mice supplemented with a lyophilized maqui berry. Maqui-dietary supplemented animals showed better insulin response and decreased weight gain but also a differential expression of genes involved in de novo lipogenesis, fatty acid oxidation, multilocular lipid droplet formation and thermogenesis in subcutaneous white adipose tissue (scWAT). These changes correlated with an increased expression of the carbohydrate response element binding protein b (Chrebpb), the sterol regulatory binding protein 1c (Srebp1c) and Cellular repressor of adenovirus early region 1A–stimulated genes 1 (Creg1) and an improvement in the fibroblast growth factor 21 (FGF21) signaling. Our evidence suggests that maqui dietary supplementation activates the induction of fuel storage and thermogenesis characteristic of a brown-like phenotype in scWAT and counteracts the unhealthy metabolic impact of an HFD. This induction constitutes a putative strategy to prevent/treat diet-induced obesity and its associated comorbidities.

scholarly journals Anti-Obesity Effects of Sargassum thunbergii via Downregulation of Adipogenesis Gene and Upregulation of Thermogenic Genes in High-Fat Diet-Induced Obese Mice

Nutrients ◽  
2020 ◽  
Vol 12 (11) ◽  
pp. 3325
Author(s):  
Min-Cheol Kang ◽  
Hyo-Geun Lee ◽  
Hyun-Soo Kim ◽  
Kyung-Mo Song ◽  
Yong-Gi Chun ◽  
...  
Keyword(s):  
Type 2 Diabetes ◽  
Cardiovascular Disease ◽  
Adipose Tissue ◽  
White Adipose Tissue ◽  
High Fat Diet ◽  
Obese Mice ◽  
High Fat ◽  
Sargassum Thunbergii ◽  
Fat Accumulation

Obesity is a metabolic disease characterized by an increased risk of type 2 diabetes, hypertension, and cardiovascular disease. We have previously reported that compounds isolated from brown alga, Sargassum thunbergii (ST; Sargassum thunbergii (Mertens ex Roth) Kuntze), inhibit adipogenesis in 3T3-L1 cells. However, the in vivo anti-obesity effects of these compounds have not been previously reported. Therefore, the objective of this study was to determine the effects of ST on weight loss, fat accumulation, as well as risk factors for type 2 diabetes and cardiovascular disease in high-fat diet (HFD)-induced obese mice. ST treatment significantly decreased body weight and fat accumulation in HFD-induced obese mice, while reducing insulin and factors related to cardiovascular diseases (triglyceride and total cholesterol) in serum. ST-induced downregulation of PPARγ in white adipose tissue, and upregulation of the thermogenic genes, UCP-1 and UCP-3, in brown adipose tissue was also observed. In addition, oral administration of ST reduced the occurrence of fatty liver, as well as the amount of white adipose tissue in HFD mice. Cumulatively, these results suggest that ST exerts anti-obesity effects and may serve as a potential anti-obesity therapeutic agent.

scholarly journals Effect of Exercise Training On Autophagic Process in White Adipose Tissue of High Fat Diet-Induced Obese Mice

2021 ◽  
Author(s):  
Saeed Daneshyar ◽  
Gholamreza Tavoosidana ◽  
Fatemeh Jalali-Moghim ◽  
Sadegh Amani-Shalamzari
Keyword(s):  
Adipose Tissue ◽  
Exercise Training ◽  
Training Program ◽  
White Adipose Tissue ◽  
High Fat Diet ◽  
Intermediate Step ◽  
Obese Mice ◽  
High Fat ◽  
Protein Levels ◽  
Autophagic Process

Abstract Background. Some studies have established a relationship between obesity and the autophagic process in adipose tissue. This study aimed to investigate the effect of exercise training on the autophagic process in white adipose tissue (WAT) of high fat diet-induced obese mice.Methods and Results. C57BL/6 mice were assigned into three groups included: 1) Control 2), High-Fat Diet-induced Obesity (HFD-Ob), and 3) High-Fat Diet with Exercise Training (HFD-Ex). The subjects of HFD-Ob were fed a high-fat diet for 14 weeks. The mice of HFD-Ex had eight weeks of endurance training on a treadmill in addition to having the HFD. The Real-Time–PCR and western blot methods were used to measure the mRNA and protein levels of markers of the autophagic process. HFD caused an upregulation in the factors of the autophagosome formation, including ATG5 and ATG7, LC3, and the exercise training could augment the upregulation. Further, the training program prevented the change in LAMP2 expression (a marker of autophagolysosome), which being reduced by HFD. The lysosomal clearance factors (CTSB and CTSL) were raised in HFD-Ob and differently changed in HFD-Ex.Conclusion. HFD-induced obesity promoted the early and last steps of autophagy whereas defected the intermediate-step of it. Interestingly, the exercise training enhanced the early phase of autophagy, which being increased by HFD. Further, the training program could modify the rising effect of HFD on the last step of autophagy. It seems that a part of the protective effect of exercise training on obesity-related complications may be mediated by modulating the autophagic process in white adipose tissue.

scholarly journals Allium hookeri Root Extract Inhibits Adipogenesis by Promoting Lipolysis in High Fat Diet-Induced Obese Mice

Nutrients ◽  
2019 ◽  
Vol 11 (10) ◽  
pp. 2262 ◽  
Author(s):  
Kim ◽  
Jang ◽  
Lee
Keyword(s):  
Gene Expression ◽  
Adipose Tissue ◽  
Fatty Acid ◽  
White Adipose Tissue ◽  
High Fat Diet ◽  
Obese Mice ◽  
High Fat ◽  
Tissue Weight ◽  
Adipose Tissue Weight ◽  
Allium Hookeri

: Allium hookeri (AH) is widely consumed as a herbal medicine. It possesses biological activity against metabolic diseases. The objective of this study was to investigate effects of AH root water extract (AHR) on adipogenesis in 3T3-L1 cells and in high-fat diet (HFD)-induced obese mice. AHR inhibited lipid accumulation during adipocyte differentiation by downregulation of gene expression, such as hormone sensitive lipase (HSL), lipoprotein lipase (LPL) and an adipogenic gene, CCAAT/enhancer binding protein-α in 3T3-L1 preadipocytes. Oral administration of AHR significantly suppressed body weight gain, adipose tissue weight, serum leptin levels, and adipocyte cell size in HFD-induced obese mice. Moreover, AHR significantly decreased hepatic mRNA expression levels of cholesterol synthesis genes, such as 3-hydroxy-3-methylglutaryl CoA reductase, sterol regulatory element-binding transcription factor (SREBP)-2, and low-density lipoprotein receptor, as well as fatty acid synthesis genes, such as SREBP-1c and fatty acid synthase. Serum triglyceride levels were also lowered by AHR, likely as a result of the upregulating gene involved in fatty acid β-oxidation, carnitine palmitoyltransferase 1a, in the liver. AHR treatment activated gene expression of peroxisome proliferator-activated receptor-γ, which might have promoted HSL and LPL-medicated lipolysis, thereby reducing white adipose tissue weight. In conclusion, AHR treatment can improve metabolic alterations induced by HFD in mice by modifying expression levels of genes involved in adipogenesis, lipogenesis, and lipolysis in the white adipose tissue and liver.

Chia oil induces browning of white adipose tissue in high-fat diet-induced obese mice

2020 ◽  
Vol 507 ◽  
pp. 110772
Author(s):  
Thamiris de Souza ◽  
Simone Vargas da Silva ◽  
Thaís Fonte-Faria ◽  
Vany Nascimento-Silva ◽  
Christina Barja-Fidalgo ◽  
...  
Keyword(s):  
Adipose Tissue ◽  
White Adipose Tissue ◽  
High Fat Diet ◽  
Obese Mice ◽  
High Fat ◽  
Chia Oil
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