Activation of peroxisome proliferator-activated receptor gamma/small heterodimer partner pathway prevents high fat diet-induced obesity and hepatic steatosis in Sprague–Dawley rats fed soybean meal

Obesity has adverse effects on male fertility and usually is diagnosed with a prevalence of vitamin D deficiency (VD-). Discussion on the impact of obesity/VD- on sperm function has been limited. This study analyzed the effects of diet-induced obesity/VD- on viability and plasma membrane integrity (PMI), superoxide anion (O2-) level, and DNA fragmentation (DNAfrag) in sperm Sprague-Dawley rats. The males were randomized into four groups and fed for a period of 12 weeks: G1: control diet with vitamin D (C/VD+), G2: control diet without vitamin D (C/VD-), G3: high-fat diet with vitamin D (HF/VD+), and G4: high-fat diet without vitamin D (HF/VD-). Sperm function parameters were analyzed by flow cytometry. PMI percentages and O2- levels were not affected by any of the diets. DNA fragmentation was increasing significantly (p<0.05) in the spermatozoa of animals with diets vitamin D deficient (G2) and diet-induced obesity (G4). Our results allow us to point out that diet-induced obesity and VD- produce greater damage in DNA sperm of rats. The use of nutraceuticals containing vitamin D could be reducing the risk of fragmentation of DNA in spermatozoa.

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The chloroform extract of Cyclocarya paliurus attenuates high-fat diet induced non-alcoholic hepatic steatosis in Sprague Dawley rats

Phytomedicine ◽

10.1016/j.phymed.2016.08.003 ◽

2016 ◽

Vol 23 (12) ◽

pp. 1475-1483 ◽

Cited By ~ 16

Author(s):

Zi Lin ◽

Zheng-Feng Wu ◽

Cui-Hua Jiang ◽

Qing-Wen Zhang ◽

Sheng Ouyang ◽

...

Keyword(s):

Hepatic Steatosis ◽

High Fat Diet ◽

Chloroform Extract ◽

Sprague Dawley ◽

High Fat ◽

Cyclocarya Paliurus ◽

Sprague Dawley Rats

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Atypical cannabinoid ligands O-1602 and O-1918 administered chronically in diet-induced obesity

Endocrine Connections ◽

10.1530/ec-18-0535 ◽

2019 ◽

Vol 8 (3) ◽

pp. 203-216 ◽

Cited By ~ 3

Author(s):

Anna C Simcocks ◽

Kayte A Jenkin ◽

Lannie O’Keefe ◽

Chrishan S Samuel ◽

Michael L Mathai ◽

...

Keyword(s):

Body Weight ◽

G Protein ◽

High Fat Diet ◽

Chow Diet ◽

Sprague Dawley ◽

High Fat ◽

G Protein Coupled Receptor ◽

Diet Induced Obesity ◽

Sprague Dawley Rats ◽

G Protein Coupled

Atypical cannabinoid compounds O-1602 and O-1918 are ligands for the putative cannabinoid receptors G protein-coupled receptor 55 and G protein-coupled receptor 18. The role of O-1602 and O-1918 in attenuating obesity and obesity-related pathologies is unknown. Therefore, we aimed to determine the role that either compound had on body weight and body composition, renal and hepatic function in diet-induced obesity. Male Sprague–Dawley rats were fed a high-fat diet (40% digestible energy from lipids) or a standard chow diet for 10 weeks. In a separate cohort, male Sprague–Dawley rats were fed a high-fat diet for 9 weeks and then injected daily with 5 mg/kg O-1602, 1 mg/kg O-1918 or vehicle (0.9% saline/0.75% Tween 80) for a further 6 weeks. Our data demonstrated that high-fat feeding upregulates whole kidney G protein receptor 55 expression. In diet-induced obesity, we also demonstrated O-1602 reduces body weight, body fat and improves albuminuria. Despite this, treatment with O-1602 resulted in gross morphological changes in the liver and kidney. Treatment with O-1918 improved albuminuria, but did not alter body weight or fat composition. In addition, treatment with O-1918 also upregulated circulation of pro-inflammatory cytokines including IL-1α, IL-2, IL-17α, IL-18 and RANTES as well as plasma AST. Thus O-1602 and O-1918 appear not to be suitable treatments for obesity and related comorbidities, due to their effects on organ morphology and pro-inflammatory signaling in obesity.

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A Novel Peroxisome Proliferator-activated Receptor (PPAR)α Agonist and PPARγ Antagonist, Z-551, Ameliorates High-fat Diet-induced Obesity and Metabolic Disorders in Mice

Journal of Biological Chemistry ◽

10.1074/jbc.m114.622191 ◽

2015 ◽

Vol 290 (23) ◽

pp. 14567-14581 ◽

Cited By ~ 26

Author(s):

Yoshihiro Shiomi ◽

Toshimasa Yamauchi ◽

Masato Iwabu ◽

Miki Okada-Iwabu ◽

Ryo Nakayama ◽

...

Keyword(s):

High Fat Diet ◽

Metabolic Disorders ◽

Peroxisome Proliferator ◽

High Fat ◽

Peroxisome Proliferator Activated Receptor ◽

Diet Induced Obesity

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Tetrahydroxanthohumol, a xanthohumol derivative, attenuates high-fat diet-induced hepatic steatosis by antagonizing PPARγ

eLife ◽

10.7554/elife.66398 ◽

2021 ◽

Vol 10 ◽

Author(s):

Yang Zhang ◽

Gerd Bobe ◽

Cristobal L Miranda ◽

Malcolm B Lowry ◽

Victor L Hsu ◽

...

Keyword(s):

Hepatic Steatosis ◽

High Fat Diet ◽

Caloric Intake ◽

Peroxisome Proliferator ◽

High Fat ◽

Peroxisome Proliferator Activated Receptor ◽

Competitive Binding Assay ◽

Docking Simulations ◽

Synthetic Derivative

We previously reported xanthohumol (XN), and its synthetic derivative tetrahydro-XN (TXN), attenuates high-fat diet (HFD)-induced obesity and metabolic syndrome in C57Bl/6J mice. The objective of the current study was to determine the effect of XN and TXN on lipid accumulation in the liver. Non-supplemented mice were unable to adapt their caloric intake to 60% HFD, resulting in obesity and hepatic steatosis; however, TXN reduced weight gain and decreased hepatic steatosis. Liver transcriptomics indicated that TXN might antagonize lipogenic PPARγ actions in vivo. XN and TXN inhibited rosiglitazone-induced 3T3-L1 cell differentiation concomitant with decreased expression of lipogenesis-related genes. A peroxisome proliferator activated receptor gamma (PPARγ) competitive binding assay showed that XN and TXN bind to PPARγ with an IC50 similar to pioglitazone and 8–10 times stronger than oleate. Molecular docking simulations demonstrated that XN and TXN bind in the PPARγ ligand-binding domain pocket. Our findings are consistent with XN and TXN acting as antagonists of PPARγ.

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The influence of high fat diet on plasma incretins and insulin concentrations in Sprague-Dawley rats with diet-induced obesity and glucose intolerance undergoing ileal transposition

Peptides ◽

10.1016/j.peptides.2019.04.001 ◽

2019 ◽

Vol 115 ◽

pp. 75-84

Author(s):

Tomasz Sawczyn ◽

Dominika Stygar ◽

Katarzyna Nabrdalik ◽

Michał Kukla ◽

Bronisława Skrzep-Poloczek ◽

...

Keyword(s):

Glucose Intolerance ◽

High Fat Diet ◽

Ileal Transposition ◽

Sprague Dawley ◽

High Fat ◽

Diet Induced Obesity ◽

Sprague Dawley Rats

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Effect of Treatment of Sprague Dawley Rats with AVE7688, Enalapril, or Candoxatril on Diet-Induced Obesity

Journal of Obesity ◽

10.1155/2011/686952 ◽

2011 ◽

Vol 2011 ◽

pp. 1-9 ◽

Cited By ~ 16

Author(s):

Eric P. Davidson ◽

Lawrence J. Coppey ◽

Brian Dake ◽

Mark A. Yorek

Keyword(s):

Glucose Tolerance ◽

Impaired Glucose Tolerance ◽

High Fat Diet ◽

Sensory Nerve ◽

Sensory Neuropathy ◽

Neutral Endopeptidase ◽

Sprague Dawley ◽

High Fat ◽

Diet Induced Obesity ◽

Sprague Dawley Rats

The objective of this study was to determine the effect of AVE7688, a drug that inhibits both angiotensin converting enzyme (ACE) and neutral endopeptidase (NEP) activity, on neural and vascular defects caused by diet induced obesity (DIO). Rats at 12 weeks of age were fed a standard or high fat diet with or without AVE7688 for 24 weeks. DIO rats had impaired glucose tolerance and developed sensory neuropathy. Vascular relaxation to acetylcholine and calcitonin gene-related peptide was decreased in epineurial arterioles of DIO rats. Rats fed a high fat diet containing AVE7688 did not become obese and vascular and sensory nerve dysfunction and impaired glucose tolerance were improved. DIO is associated with increased expression of NEP in epineurial arterioles. NEP degrades vasoactive peptides which may explain the decrease in neurovascular function in DIO.

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