scholarly journals White tea (Camellia sinensis) extract reduces oxidative stress and triacylglycerols in obese mice

2012 ◽  
Vol 32 (4) ◽  
pp. 733-741 ◽  
Author(s):  
Lílian Gonçalves Teixeira ◽  
Priscilla Ceci Lages ◽  
Tatianna Lemos Jascolka ◽  
Edenil Costa Aguilar ◽  
Fabíola Lacerda Pires Soares ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Body Weight ◽  
Adipose Tissue ◽  
Camellia Sinensis ◽  
Reduce Food Intake ◽  
Obese Mice ◽  
White Tea ◽  
Diet Induced Obesity ◽  
Tea Extract ◽  
The Relationship

White tea is an unfermented tea made from young shoots of Camellia sinensis protected from sunlight to avoid polyphenol degradation. Although its levels of catechins are higher than those of green tea (derived from the same plant), there are no studies addressing the relationship between this tea and obesity associated with oxidative stress.The objective of this study was to evaluate the effect of white tea on obesity and its complications using a diet induced obesity model. Forty male C57BL/6 mice were fed a high-fat diet to induce obesity (Obese group) or the same diet supplemented with 0.5% white tea extract (Obese + WTE) for 8 weeks. Adipose tissue, serum lipid profile, and oxidative stress were studied. White tea supplementation was not able to reduce food intake, body weight, or visceral adiposity. Similarly, there were no changes in cholesterol rich lipoprotein profile between the groups. A reduction in blood triacylglycerols associated with increased cecal lipids was observed in the group fed the diet supplemented with white tea. White tea supplementation also reduced oxidative stress in liver and adipose tissue. In conclusion, white tea extract supplementation (0.5%) does not influence body weight or adiposity in obese mice. Its benefits are restricted to the reduction in oxidative stress associated with obesity and improvement of hypertriacylglycerolemia.

scholarly journals Adipokines: mechanisms of metabolic and behavioral disorders

2018 ◽  
Vol 15 (3) ◽  
pp. 14-20
Author(s):  
Yassine Chahirou ◽  
Abdelhalim Mesfioui ◽  
Ali Ouichou ◽  
Aboubaker Hessni
Keyword(s):  
Oxidative Stress ◽  
Insulin Resistance ◽  
Adipose Tissue ◽  
Lipid Metabolism ◽  
Behavioral Disorders ◽  
Health Problems ◽  
Endocrine Tissue ◽  
Physiological Functions ◽  
Relationship Of ◽  
The Relationship

Current studies show that metabolic and behavioral disorders represent severe health problems. Several questions arise about the molecular relationship of metabolic and behavioral disorders. This review will discuss the relationship of lipid metabolism and fructose consumption accompanied by an increase in weight as well as associated disorders: hypertension, insulin-resistance, oxidative stress and depression. Adipose tissue is considered as an endocrine tissue with intense secretory activities (metabolic and inflammatory). These adipokines are responsible for an alteration of several physiological functions. In this review we will try to understand how lipogenesis that causes dyslipidemia can influence insulin resistance, hypertension, oxidative stress, depression and the relationship between these various disorders.

Abstract 17023: Adipose Tissue Specific Temporal Deletion of Ager Induces Weight Loss in Diet Induced Obese Mice and Improves Glucose Homeostasis

Circulation ◽  
2020 ◽  
Vol 142 (Suppl_3) ◽  
Author(s):  
Robin Wilson ◽  
Lakshmi Arivazhagan ◽  
Henry Ruiz ◽  
Jay Pendse ◽  
Laura Frye ◽  
...  
Keyword(s):  
Weight Loss ◽  
Body Weight ◽  
Adipose Tissue ◽  
Glucose Homeostasis ◽  
Fasting Glucose ◽  
Obese Mice ◽  
Gene Encoding ◽  
Low Fat Diet ◽  
Insulin Tolerance ◽  
Specific Deletion

Introduction: The incidence of obesity and its comorbidities is increasing at an alarming rate in US and around the globe. Our previous studies showed that the receptor for advanced glycation end products (RAGE) and its ligands contribute to the pathogenesis of obesity and insulin resistance (IR), as global Ager (gene encoding RAGE) and adipocyte-specific Ager- deleted mice fed a high fat diet (HFD) showed protection from weight gain and IR. However, the role of Ager deletion in mice with established obesity, switched to low fat diet has not been tested. We hypothesize that temporal adipocyte-specific deletion of Ager in obese mice could enhance weight loss and improves glucose homeostasis. Methods: Mice with conditional adipocyte-specific Ager deletion were generated by breeding Ager flox/flox mice with AdipoQ ERT2 Cre recombinase mice resulting in Ager flox/flox / AdipoQ ERT2 Cre (+) and Cre (-) animals. Mice were fed HFD (60% kcal/fat) for 20 weeks starting at 8 weeks of age to establish obesity and were then treated with tamoxifen (TAM) (75 mg/kg per day x 3 alternative days) to induce deletion of Ager . After 4 weeks of TAM treatment, mice were switched to standard chow for 7 weeks and body weight was monitored regularly. Fasting glucose, insulin and glucose tolerance was measured. Results: After 7 weeks of switching to standard chow following TAM, Cre (+) lost significantly more body weight whereas Cre (-) mice showed no significant weight loss over 7 weeks. Furthermore, Cre (+) mice exhibited significantly higher food intake, lower fasting glucose, lower epididymal and inguinal white adipose tissue weights, and improved glucose and insulin tolerance compared to Cre (-) mice. Conclusions: Temporal adipocyte-specific deletion of Ager in mice with established obesity promotes weight loss and improves glucose homeostasis. RAGE may act as a novel therapeutic target in obesity.

White tea drink (Camellia sinensis) improves endurance and body weight maintenance of rats

2020 ◽  
Vol ahead-of-print (ahead-of-print) ◽  
Author(s):  
Mahmud Aditya Rifqi ◽  
Stefania Widya Setyaningtyas ◽  
Qonita Rachmah
Keyword(s):  
Body Weight ◽  
Weight Gain ◽  
Beneficial Effect ◽  
Camellia Sinensis ◽  
Intervention Research ◽  
The Body ◽  
Human Intervention ◽  
Content Type ◽  
White Tea ◽  
Significant Difference

PurposeWhite tea is an unfermented tea made from young shoots of Camellia sinensis protected from sunlight to avoid polyphenol degradation. White tea contains a high level of polyphenolic compounds known as catechins. Several types of evidence have suggested that tea consumption has benefits in body weight and endurance maintenance. This study was designed to evaluate the effect of white tea on body weight and endurance of animal models.Design/methodology/approachThis research was an intervention design using 20 Wistar white rats (Rattus Norvegicus) in body weight between 150 and 200 g. The rats were randomized into four groups, three groups receiving white tea drink (WTD) with different doses and the other group receiving plain water in equal volume as a control group for four weeks. The forced swim test (FST) was done to measure their struggling capacity, and digital bodyweight to measure the weight.FindingsIntervention (WTD Groups and Control) caused weight gain among except G3 with the highest doses of white tea. The result showed that WTD intake in G3 had a significant difference (p < 0.05) on body weight gain compared to control. The authors found that WTD in a specific dose (G3: 0.22 mg) tends to maintain the body weight of animals (219.2 ± 41.96; 212.6 ± 46.90, respectively), while other doses caused weight gain. WTD also significantly increased the swimming and struggling capacity of rats that represented improvements the endurance along with the test. There was a statistically significant difference in endurance among all groups (p < 0.05).Research limitations/implicationsThe results of this study can be followed as human intervention research as an input for nutritionists and sports scientists to explore the beneficial effect of white tea.Practical implicationsThe results of this study can be followed as human intervention research as an input for nutritionists and sports scientists to explore the beneficial effect of white tea.Originality/valueThis study adds more evidence and information about the advantages of white tea as potential beverages in future healthy lifestyles.

Genistein inhibits high fat diet-induced obesity through miR-222 by targeting BTG2 and adipor1

2020 ◽  
Vol 11 (3) ◽  
pp. 2418-2426 ◽  
Author(s):  
Mailin Gan ◽  
Linyuan Shen ◽  
Shujie Wang ◽  
Zhixian Guo ◽  
Ting Zheng ◽  
...  
Keyword(s):  
Adipose Tissue ◽  
Lipid Metabolism ◽  
High Fat Diet ◽  
Target Genes ◽  
Obese Mice ◽  
High Fat ◽  
Diet Induced Obesity ◽  
Regulate Lipid Metabolism

Genistein may regulate lipid metabolism in adipose tissue of obese mice by regulating the expression of miR-222 and its target genes, BTG2 and adipor1.

Effect of adrenalectomy on glucose tolerance and lipid metabolism in gold-thioglucose obese mice

1994 ◽  
Vol 266 (6) ◽  
pp. E993-E1000 ◽  
Author(s):  
S. C. Blair ◽  
I. D. Caterson ◽  
G. J. Cooney
Keyword(s):  
Body Weight ◽  
Adipose Tissue ◽  
Glucose Tolerance ◽  
Fatty Acid Content ◽  
Fasting Blood Glucose ◽  
Lipid Synthesis ◽  
Obese Mice ◽  
Interscapular Brown Adipose Tissue ◽  
Gold Thioglucose ◽  
Brown Adipose

The effect of adrenalectomy (ADX) on body weight, lipogenesis, and glucose tolerance was investigated in mice made obese by a single intraperitoneal injection of gold-thioglucose (GTG). Five weeks after ADX the weight of GTG-obese mice was significantly decreased (GTG-obese+sham-ADX: 39.8 +/- 0.8 g; GTG-obese+ADX: 27.6 +/- 1.1 g; P < 0.05). ADX also reduced serum glucose (GTG-obese+sham-ADX: 16.5 +/- 0.6 mmol/l; GTG-obese+ADX: 10.8 +/- 0.5 mmol/l; P < 0.05) and serum insulin concentrations (GTG-obese+sham-ADX: 197 +/- 36 microU/ml; GTG-obese+ADX: 38 +/- 7 microU/ml; P < 0.05) of fed GTG-obese mice and greatly improved glucose tolerance. ADX lowered liver glycogen content and reduced the fatty acid content of liver, epididymal white adipose tissue (WAT), and interscapular brown adipose tissue (BAT) of fed GTG-obese mice. Lipid synthesis in liver and WAT of GTG-obese mice was decreased by ADX, but lipogenesis in BAT was increased, possibly to provide substrate for increased thermogenesis in this tissue. Effects of ADX on metabolism were not confined to GTG-injected mice, as ADX also reduced body weight and altered the glucose tolerance of age-matched control mice. ADX increased lipid synthesis in liver, WAT, and BAT of fed control mice without an increase in lipid deposition, indicating that there was increased lipid turnover in these lipogenic tissues of ADX mice. ADX reduced the fasting blood glucose concentration of both control and GTG-obese mice to a level below that of sham-ADX control mice (sham-ADX control: 6.0 +/- 0.4 mM; ADX control: 2.9 +/- 0.5 mM; ADX GTG-obese: 3.3 +/- 0.2 mM).(ABSTRACT TRUNCATED AT 250 WORDS)

scholarly journals Cashew apple extract inhibition of fat storage and insulin resistance in the diet-induced obesity mouse model

2015 ◽  
Vol 4 ◽  
Author(s):  
Vickram Beejmohun ◽  
Cyril Mignon ◽  
Aude Mazollier ◽  
Marie Peytavy-Izard ◽  
Dominique Pallet ◽  
...  
Keyword(s):  
Insulin Resistance ◽  
Body Weight ◽  
Adipose Tissue ◽  
Mouse Model ◽  
Experimental Designs ◽  
Epididymal Adipose Tissue ◽  
Alcoholic Extract ◽  
Fat Storage ◽  
Diet Induced Obesity ◽  
Cashew Apple

AbstractThe cashew apple is an unvalued by-product from the cashew nut industry, of which millions of tonnes are simply discarded globally. Interestingly, however, cashew apple nutrients may have beneficial effects for health even if these are still poorly described. The present study was designed to evaluate the effect of a hydro-alcoholic extract of cashew apple (cashew apple extract; CAE; Cashewin™) on obesity and diabetes, in two experimental designs using the diet-induced obesity (DIO) mouse model. First, in the preventive design, mice were treated orally with the CAE at the dose of 200 mg/kg body weight from the first day under a high-fat diet (HFD) and during 8 weeks thereafter. Second, in the curative design, the animals were first maintained under the HFD for 4 weeks and then treated with the CAE for a further 4 weeks under the same regimen. For both experimental designs, body weight, peri-epididymal adipose tissue, liver weight, food consumption, glycaemia, insulinaemia and insulin resistance were assessed. In both designs, the CAE significantly reduced body-weight gain and fat storage in both the peri-epididymal adipose tissue and the liver for mice under the HFD. This was achieved without modifying their energy consumption. Furthermore, glycaemia, insulinaemia and insulin resistance (homeostasis model assessment-insulin resistance) of the DIO mice were significantly lowered compared with the control group. Thus, a well-designed hydro-alcoholic extract of cashew apple could provide an attractive nutritional food ingredient to help support the management of body weight and associated metabolic parameters such as blood glucose and insulin levels.

scholarly journals Effect of VPAC1 Blockade on Adipose Tissue Formation and Composition in Mouse Models of Nutritionally Induced Obesity

2010 ◽  
Vol 2010 ◽  
pp. 1-5 ◽  
Author(s):  
H. Roger Lijnen ◽  
Kathleen Freson ◽  
Marc F. Hoylaerts
Keyword(s):  
Body Weight ◽  
Adipose Tissue ◽  
Mouse Models ◽  
Tissue Formation ◽  
Tissue Mass ◽  
Diet Induced Obesity ◽  
Pituitary Adenylate Cyclase ◽  
Adipose Tissue Mass ◽  
Adipocyte Hypertrophy ◽  
G Protein Coupled

Background. The pituitary adenylate cyclase activating polypeptide (PACAP) may affect adipogenesis and adipose tissue formation through interaction with its G-protein-coupled receptor VPAC1.Methods. We have used a monoclonal antibody (MAb 23A11) blocking VPAC1 in mouse models of nutritionally induced obesity.Results. Administration of MAb 23A11 (25 mg/kg body weight i.p. twice weekly) to 5-week old male C57Bl/6 mice kept on a high-fat diet for 15 weeks had no significant effect on weight gain, nor on subcutaneous (SC) or gonadal (GON) adipose tissue mass, as compared to the control MAb 1C8. However, adipocyte hypertrophy was observed in SC adipose tissue of MAb 23A11 treated mice. In a second study, 24 weeks old obese mice were treated for 5 weeks with MAb 23A11, without effect on body weight or fat mass, as compared to treatment with MAb 1C8. In addition, MAb 23A11 had no significant effect on glucose tolerance or insulin resistance in lean or obese C57Bl/6 mice.Conclusion. Blocking VPAC1 does not significantly affect adipose tissue formation in mouse models of diet-induced obesity, although it may be associated with mild adipocyte hypertrophy.

scholarly journals Deficiency of lymphotoxin-α does not exacerbate high-fat diet-induced obesity but does enhance inflammation in mice

2012 ◽  
Vol 302 (8) ◽  
pp. E961-E971 ◽  
Author(s):  
Nathalie Pamir ◽  
Timothy S. McMillen ◽  
Kimberly A. Edgel ◽  
Francis Kim ◽  
Renée C. LeBoeuf
Keyword(s):  
Body Weight ◽  
Adipose Tissue ◽  
Glucose Tolerance ◽  
Tissue Level ◽  
Specific Gene ◽  
High Fat ◽  
Tissue Macrophage ◽  
Diet Induced Obesity ◽  
Inflammatory Status ◽  
Lymphotoxin Α

Lymphotoxin-α (LTα) is secreted by lymphocytes and acts through tumor necrosis factor-α receptors and the LTβ receptor. Our goals were to determine whether LT has a role in obesity and investigate whether LT contributes to the link between obesity and adipose tissue lymphocyte accumulation. LT deficient (LT−/−) and wild-type (WT) mice were fed standard pelleted rodent chow or a high-fat/high-sucrose diet (HFHS) for 13 wk. Body weight, body composition, and food intake were measured. Glucose tolerance was assessed. Systemic and adipose tissue inflammatory statuses were evaluated by quantifying plasma adipokine levels and tissue macrophage and T cell-specific gene expression in abdominal fat. LT−/− mice were smaller (20%) and leaner (25%) than WT controls after 13 wk of HFHS diet feeding. LT−/− mice showed improved glucose tolerance, suggesting that, in WT mice, LT may impair glucose metabolism. Surprisingly, adipose tissue from rodent chow- and HFHS-fed LT−/− mice exhibited increased T lymphocyte and macrophage infiltration compared with WT mice. Despite the fact that LT−/− mice exhibited an enhanced inflammatory status at the systemic and tissue level even when fed rodent chow, they were protected from enhanced diet-induced obesity and insulin resistance. Thus, LT contributes to body weight and adiposity and is required to modulate the accumulation of immune cells in adipose tissue.

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