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

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

Comparative effects of tamoxifen and angiotensin II type-1 receptor antagonist therapy on the hemodynamic profile of the ovariectomized female rat

2003 ◽  
Vol 81 (9) ◽  
pp. 915-919 ◽  
Author(s):  
My-Lan Pham-Dang ◽  
Robert Clement ◽  
Isabelle Mercier ◽  
Angelino Calderone
Keyword(s):  
Body Weight ◽  
Weight Gain ◽  
Angiotensin Ii ◽  
Receptor Antagonist ◽  
Body Weight Gain ◽  
Left Ventricular ◽  
Female Rat ◽  
Ovx Rats ◽  
Hemodynamic Profile

Hormonal replacement therapy (HRT) has failed to provide a cardioprotective action in postmenopausal women, and thus alternative pharmacological approaches are required. The present study examined the therapeutic potential of the partial estrogen receptor agonist tamoxifen and the angiotensin II type-1 receptor antagonist irbesartan on the hemodynamic profile of ovariectomized (OVX) female Sprague–Dawley rats (9–11 weeks). Three weeks following ovariectomy, uterine atrophy was evident and body weight was increased as compared with sham-operated animals. Left ventricular systolic pressure (LVSP), left ventricular end-diastolic pressure (LVEDP), and mean arterial pressure (MAP) were significantly increased in the OVX rats as compared with sham rats. One week following ovariectomy, rats were treated with either tamoxifen (10 mg kg–1 day–1) or irbesartan (40 mg kg–1 day–1) for a period of 2 weeks. The administration of tamoxifen to OVX rats partially reversed uterine atrophy and prevented body weight gain, albeit body weight remained significantly lower than in sham-operated animals. LVSP and LVEDP were normalized in the tamoxifen-treated OVX rats, whereas MAP remained elevated. Irbesartan partially reduced the body weight gain of the OVX rats and did not influence uterine atrophy. LVSP and MAP were normalized in irbesartan-treated OVX rats, whereas LVEDP remained elevated. These data demonstrate that irbesartan rather than tamoxifen was efficacious in normalizing MAP in the OVX rats without a secondary effect on the uterus.Key words: ovariectomy, hemodynamics, tamoxifen, AT1 receptor antagonists.

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).

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

Food intake inhibition and reduction in body weight gain in rats treated with GI264879A, a non-selective NPY-Y1 receptor antagonist

Peptides ◽  
2001 ◽  
Vol 22 (3) ◽  
pp. 483-491 ◽  
Author(s):  
A.J Danielsa ◽  
W.T Chance ◽  
M.K Grizzle ◽  
D Heyer ◽  
J.E Matthews
Keyword(s):  
Body Weight ◽  
Weight Gain ◽  
Food Intake ◽  
Receptor Antagonist ◽  
Body Weight Gain ◽  
Y1 Receptor

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
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