scholarly journals The lysyl oxidase inhibitor  -aminopropionitrile reduces body weight gain and improves the metabolic profile in diet-induced obesity in rats

2015 ◽  
Vol 8 (6) ◽  
pp. 543-551 ◽  
Author(s):  
M. Miana ◽  
M. Galan ◽  
E. Martinez-Martinez ◽  
S. Varona ◽  
R. Jurado-Lopez ◽  
...  
Keyword(s):  
Body Weight ◽  
Weight Gain ◽  
Metabolic Profile ◽  
Lysyl Oxidase ◽  
Body Weight Gain ◽  
Oxidase Inhibitor ◽  
Diet Induced Obesity

Extract of Irish potatoes (Solanum tuberosumL.) decreases body weight gain and adiposity and improves glucose control in the mouse model of diet-induced obesity

2014 ◽  
Vol 58 (11) ◽  
pp. 2235-2238 ◽  
Author(s):  
Stan Kubow ◽  
Luc Hobson ◽  
Michèle M. Iskandar ◽  
Kebba Sabally ◽  
Danielle J. Donnelly ◽  
...  
Keyword(s):  
Body Weight ◽  
Weight Gain ◽  
Mouse Model ◽  
Glucose Control ◽  
Body Weight Gain ◽  
Diet Induced Obesity

scholarly journals Bauhiniastatin-1 alleviates diet induced obesity and lipid accumulation through modulating PPAR-γ/AMPK expressions: In-vitro, in-vivo and in-silico studies.

2021 ◽  
Author(s):  
Karunakaran Reddy Sankaran ◽  
Lokanatha Oruganti ◽  
Muni Swamy Ganjayi ◽  
Venkataramaiah Chintha ◽  
Muni Kesavulu Muppuru ◽  
...  
Keyword(s):  
Body Weight ◽  
Weight Gain ◽  
Western Blot ◽  
Blot Analysis ◽  
Body Weight Gain ◽  
Liver Lipid ◽  
Ppar Γ ◽  
Diet Induced Obesity

Abstract Background: Consumption of energy dense foods and sedentary lifestyles have led to high prevalence of obesity and associated disorders. Intensive research efforts have focussed to develop effective alternative therapeutics from plant sources. Bauhiniastatins have been reported to possess antineoplastic activity. In the present study, Bauhiniastatin-1 (BSTN1) was isolated and purified from Bauhinia purpurea and evaluated for its therapeutic efficacy against adipogenesis and obesity using high fat diet (HFD)-induced obese rodent model and 3T3-L1 cells.Methods: We performed in-vitro experiments like MTT assay, Oil Red O (ORO) stain, cellular lipid content, glycerol release and RT-PCR analysis in 3T3-L1 cells. In-vivo parameters like body weight gain, body composition, plasma adipokines, serum & liver lipid profiles, liver marker enzymes, western blot analysis and histopathological examination were conducted in rat model. In addition, molecular docking studies were also performed to understand interaction of BSTN1 with peroxisome proliferator-activated gamma receptor (PPAR-γ) and AMP-activated protein kinase (AMPK) which supported our experimental results.Results: BSTN1 at 20 μM significantly (p<0.001) inhibited cell differentiation and lipid accumulation of 3T3-L1 adipocytes. Mechanistic studies showed that mRNA expression of key adipogenic markers, PPAR-γ, fatty acid synthase (FAS) and sterol-regulatory element-binding protein-1 (SREBP1) were down-regulated while AMPK was up-regulated by BSTN1. Oral administration of BSTN1 (5 mg/kg. b.wt.) to HFD-induced obese rats substantially decreased body weight gain, fat mass, serum and liver lipid levels and promoted integrity of hepatic and adipose tissue architecture compared to HFD-control rats. In BSTN1 administered groups, decreased serum aspartate transaminase (AST) and alanine aminotransferase (ALT) levels, decreased plasma leptin but increased adiponectin levels were noted. Western blot analysis of adipose and hepatic tissues collected from BSTN1 treated rats showed decreased expression level of PPAR-γ but increase in AMPK expression relative to the untreated group. In-silico studies showed strong binding interactions of BSTN1 against PPAR-γ and AMPK, the key molecules of adipogenesis and obesity.Conclusions: Taken together, the results suggest that BSTN1 could be promising molecule for the treatment of diet-induced obesity and non-alcoholic fatty liver disease (NAFLD).

Abstract 295: Microsomal Prostaglandin E Synthase 1 Deficiency Attenuates Diet-Induced Obesity and Promotes the Formation of Brite Adipose Tissue

2012 ◽  
Vol 32 (suppl_1) ◽  
Author(s):  
Natalie J Moretz ◽  
Nicholas Hatch ◽  
Sarah Srodulski ◽  
Victoria L King
Keyword(s):  
Body Weight ◽  
Adipose Tissue ◽  
Weight Gain ◽  
Marked Reduction ◽  
Body Weight Gain ◽  
Prostaglandin E ◽  
Low Grade ◽  
Prostaglandin E Synthase ◽  
Diet Induced Obesity ◽  
Microsomal Prostaglandin E Synthase

Mice deficient in adipocyte specific phospholipases A2 have a marked reduction in prostaglandin E2 (PGE2) levels and are resistant to the development of diet-induced obesity. Clinical data suggest that obesity is a chronic low grade inflammatory disease, characterized by the influx of inflammatory cells into the adipose tissue. During a chronic inflammatory state, microsomal prostaglandin E synthase-1 (mPGES-1) is the primary source of PGE2. We have previously demonstrated that mice deficient in mPGES-1 (KO) have a marked reduction in body weight gain and adiposity compared to littermate controls (WT) fed a high fat (HF) diet with a concomitant reduction in urinary PGE2 concentrations and an increase in urinary PGI2 concentrations. The reduction in weight gain is not for accounted by alterations in food intake or locomotor activity. However, resting metabolic rate, measured by indirect calorimetry, was increased in KO mice compared to WT fed a HF diet. Moreover, body temperature was also increased in KO mice compared to WT mice (37.0 ± 0.2 vs 35.8 ± 0.2; P < 0.05) fed a HF diet. Taken together these data suggest that mPGES-1 deficiency increases energy expenditure in response to feeding a HF diet. Analysis of white adipose tissue (WAT) depots demonstrated an increase in number of smaller adipocytes per unit area in the KO mice compared to WT mice. The WAT from KO mice also had a marked decrease in triglyceride content, F4/80 staining and CD86 staining with a concomitant increase in CD206 staining suggesting an attenuation in macrophage recruitment into the WAT as well as an M2 phenotype. Additionally, COX-2 and UCP-1 and PPAR-γ expression were increased in WAT depots with a concomitant localization of multi-locular adipocytes in WAT depots, demonstrating the presence of brown adipocytes in WAT depots in KO mice fed a HF diet. These data suggest that the reduction in body weight gain in the KO mice may be due an increase in thermogenesis mediated by the formation of brite adipose tissue in WAT depots.

scholarly journals Melatonin Reduces Body Weight Gain in Sprague Dawley Rats with Diet-Induced Obesity

Endocrinology ◽  
2003 ◽  
Vol 144 (12) ◽  
pp. 5347-5352 ◽  
Author(s):  
Bénédicte Prunet-Marcassus ◽  
Mathieu Desbazeille ◽  
Arnaud Bros ◽  
Katie Louche ◽  
Philippe Delagrange ◽  
...  
Keyword(s):  
Body Weight ◽  
Weight Gain ◽  
Body Weight Gain ◽  
Sprague Dawley ◽  
Diet Induced Obesity ◽  
Sprague Dawley Rats

scholarly journals Aliskiren reduces body-weight gain, adiposity and plasma leptin during diet-induced obesity

2009 ◽  
Vol 158 (3) ◽  
pp. 771-778 ◽  
Author(s):  
Paula Stucchi ◽  
Victoria Cano ◽  
Mariano Ruiz-Gayo ◽  
María S Fernández-Alfonso
Keyword(s):  
Body Weight ◽  
Weight Gain ◽  
Body Weight Gain ◽  
Diet Induced Obesity ◽  
Plasma Leptin

Metabolic features of diet-induced obesity without hyperphagia in young rats

1986 ◽  
Vol 251 (3) ◽  
pp. R433-R440 ◽  
Author(s):  
B. E. Levin ◽  
J. Triscari ◽  
A. C. Sullivan
Keyword(s):  
Body Weight ◽  
Weight Gain ◽  
Food Intake ◽  
Body Weight Gain ◽  
Brown Adipocyte ◽  
Metabolic Efficiency ◽  
Interscapular Brown Adipose Tissue ◽  
Diet Induced Obesity ◽  
Brown Adipose

Diet-induced obesity (DIO) developed in 1-mo-old male Sprague-Dawley rats over an 8-wk period on a relatively high-fat (16%) high-calorie (4.6 kcal/g) diet (DIO diet). Percent carcass lipid (56%) and body weight gain (15%) were greater, whereas food intake was decreased over the first 3-5 wk in DIO diet-compared with chow-fed controls. Overall, 8-wk body weight gain (15%), percent carcass lipid (26%), and feed efficiency (15%) were greater, but food intake was not increased. Norepinephrine (NE) turnover rate, indicative of organ sympathetic activity, increased in interscapular brown adipose tissue (IBAT; 57-218%), heart (21-44%), and pancreas (25%) during the first 3 wk and remained elevated for the entire 8 wk. IBAT weight (51%) and in vitro lipolytic capacity (68%) increased by 1 wk and brown adipocyte size (43%) by 3 wk; IBAT thermogenic capacity (maximal NE-stimulated in vitro O2 consumption) increased by 5 wk (39%). Plasma insulin levels were similar in both diet groups over the entire 8-wk period. Why DIO diet-fed rats had increased metabolic efficiency is unknown, but activation of IBAT metabolism and thermogenesis failed to prevent the development of DIO.

Differential sensitivity of chronic high-fat-diet-induced obesity in Sprague-Dawley rats

2018 ◽  
Vol 29 (5) ◽  
pp. 553-563 ◽  
Author(s):  
Shakthi R.K. Devan ◽  
Surendar Arumugam ◽  
Ganesh Shankar ◽  
Suresh Poosala
Keyword(s):  
Body Weight ◽  
Weight Gain ◽  
High Fat Diet ◽  
Body Weight Gain ◽  
Differential Sensitivity ◽  
Sprague Dawley ◽  
High Fat ◽  
Diet Induced Obesity ◽  
High Fat Diets ◽  
Fat Diets

AbstractBackgroundThe prevalence of obesity is reported to be increasing owing to the high intake of dietary fat and is a predisposing risk factor with associated complex metabolic syndromes in the human population. Preclinical rodent models play a pivotal role in understanding the pathogenesis of obesity and development of new treatment strategies for humans. High-fat-diet (HFD)-induced rodents are used for chronic obesity models owing to their quick adaptation to high-fat diets and rapid body weight gain and different rats (Wistar Sprague-Dawley and Lewis) have been used by various researchers. However, the selection of appropriate stock contributes to the translation of clinically linked disease phenotypes to preclinical animal models.MethodsThe study was conducted using two commonly used rat stocks Hsd:Sprague-Dawley (SD) and Crl:Charles River (CD) to develop a chronic high-fat-diet-induced obesity model (DIO) to explore the underlying mechanisms of obesity and its utilization in drug discovery and development during preclinical stages. In addition two high-fat diets of different composition were evaluated (D12327; 40% kcal fat and D12492; 60% kcal fat) for their potential to induce obesity using these two stocks.ResultsA differential sensitivity to HFD was observed in body weight gain fat mass composition and obesity-linked symptoms such as impaired glucose tolerance insulin and leptin levels. The comparative research findings of Hsd:SD and Crl:CD rat stocks suggested that Crl:CD rats are more prone to diet-induced obesity and its associated complications.ConclusionsCrl:CD rats were found to be a suitable model for obesity over Hsd:SD when considering the important hallmarks of metabolic disorders that may be utilized for obesity-related research.

scholarly journals Gastric inhibitory polypeptide receptor antagonist, SKL-14959, suppressed body weight gain on diet-induced obesity mice

2018 ◽  
Vol 4 (2) ◽  
pp. 194-203 ◽  
Author(s):  
T. Nakamura ◽  
H. Tanimoto ◽  
Y. Mizuno ◽  
M. Okamoto ◽  
M. Takeuchi ◽  
...  
Keyword(s):  
Body Weight ◽  
Weight Gain ◽  
Receptor Antagonist ◽  
Body Weight Gain ◽  
Gastric Inhibitory Polypeptide ◽  
Diet Induced Obesity

Low doses of cocoa extract supplementation ameliorate diet-induced obesity and insulin resistance in rats

2019 ◽  
Vol 10 (8) ◽  
pp. 4811-4822 ◽  
Author(s):  
Paula Aranaz ◽  
Ana Romo-Hualde ◽  
David Navarro-Herrera ◽  
María Zabala ◽  
Miguel López-Yoldi ◽  
...  
Keyword(s):  
Insulin Resistance ◽  
Metabolic Syndrome ◽  
Body Weight ◽  
Weight Gain ◽  
Insulin Sensitivity ◽  
Glucose Tolerance ◽  
Body Weight Gain ◽  
Liver Steatosis ◽  
Low Doses ◽  
Diet Induced Obesity

Supplementation with low doses of a cocoa extract induces metabolic benefits in the prevention of metabolic syndrome in rats, reducing body-weight gain, visceral adiposity and liver steatosis and improving insulin sensitivity and glucose tolerance.

scholarly journals Time-Restricted Feeding Improves Body Weight Gain, Lipid Profiles, and Atherogenic Indices in Cafeteria-Diet-Fed Rats: Role of Browning of Inguinal White Adipose Tissue

Nutrients ◽  
2020 ◽  
Vol 12 (8) ◽  
pp. 2185
Author(s):  
Samira Aouichat ◽  
Meriem Chayah ◽  
Souhila Bouguerra-Aouichat ◽  
Ahmad Agil
Keyword(s):  
Body Weight ◽  
Adipose Tissue ◽  
Weight Gain ◽  
White Adipose Tissue ◽  
Body Weight Gain ◽  
Density Lipoprotein ◽  
Cafeteria Diet ◽  
Restricted Feeding ◽  
Diet Induced Obesity ◽  
Atherogenic Indices

Time-restricted feeding (TRF) showed a potent effect in preventing obesity and improving metabolicoutcomes in several animal models of obesity. However, there is, as of yet, scarce evidence concerning its effectiveness against obesogenic challenges that more accurately mimic human Western diets, such as the cafeteria diet. Moreover, the mechanism for its efficacy is poorly understood. White adipose browning has been linked to body weight loss. Herein, we tested whether TRF has the potential to induce browning of inguinal white adipose tissue (iWAT) and to attenuate obesity and associated dyslipidemia in a cafeteria-diet-induced obesity model. Male Wistar rats were fed normal laboratory chow (NC) or cafeteria diet (CAF) for 16 weeks and were subdivided into two groups that were subjected to either ad libitum (ad lib, A) or TRF (R) for 8 h per day. Rats under the TRF regimen had a lower body weight gain and adiposity than the diet-matchedad lib rats, despite equivalent levels of food intake and locomotor activity. In addition, TRF improved the deranged lipid profile (total cholesterol (TC), triglycerides (TG), high-density lipoprotein (HDL-c), low-density lipoprotein (LDL-c)) and atherogenic indices (atherogenic index of plasma (AIP), atherogenic coefficient (AC), coronary risk index (CRI) in CAF-fed rats. Remarkably, TRF resulted in decreased size of adipocytes and induced emergence of multilocular brown-like adipocytes in iWAT of NC- and CAF-fed rats. Protein expression of browning markers, such as uncoupling protein-1 (UCP1) and peroxisome proliferator-activated receptor gamma coactivator 1-alpha (PGC1α), were also up-regulated in the iWAToftime-restricted NC- or CAF-fed rats. These findings suggest that a TRF regimen is an effective strategy to improve CAF diet-induced obesity, probably via a mechanismthe involving WAT browning process.

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