Effect of selenium-enriched kiwifruit on body fat reduction and liver protection in hyperlipidaemic mice

2021 ◽  
Vol 12 (5) ◽  
pp. 2044-2057
Author(s):  
Xiaoni Zhang ◽  
Haidong Xia ◽  
Jie Wang ◽  
Ruyue Leng ◽  
Xiaojing Zhou ◽  
...  

This study aimed to investigate the effects and mechanism of selenium-enriched kiwifruit (Se-Kiwi) on lipid-lowering and liver protection in hyperlipidaemic mice induced by consuming a long-term high-fat diet.

2006 ◽  
Vol 290 (2) ◽  
pp. E258-E267 ◽  
Author(s):  
S. F. Leibowitz ◽  
G.-Q. Chang ◽  
J. T. Dourmashkin ◽  
R. Yun ◽  
C. Julien ◽  
...  

The objective of this study was to investigate meal-related endocrine changes that permit one to identify Sprague-Dawley rats at normal weight that are prone (OP) vs. resistant (OR) to obesity. In blood collected via chronic cardiac catheters, a 2-h high-fat meal (HFM, 50% fat, 40 kcal) at dark onset caused a significant increase in leptin, insulin, and triglycerides compared with premeal levels. Similar to patterns in already obese compared with lean rats on a high-fat diet, these meal-induced endocrine changes in normal-weight rats on lab chow were almost twofold larger in OP rats that, compared with OR rats, subsequently accumulated 100% more fat mass on a chronic high-fat diet. These exaggerated endocrine changes were similarly observed in blood collected using a simpler tail vein puncture procedure. In three separate experiments, the HFM-induced rise in leptin was found to be the strongest, positive correlate ( r = +0.58, +0.62 and +0.64) of long-term body fat accrual. The lowest (2–5 ng/ml) vs. highest (6–9 ng/ml) scores for this post-HFM leptin measurement identified distinct OR and OP subgroups, respectively, when they were similar in body weight (340–350 g), premeal leptin (2.6–3.4 ng/ml), and meal size (40 kcal). Subsequent tests in these normal-weight OP rats revealed a distinct characteristic compared with OR rats, namely, exaggerated HFM-induced rise in expression of the orexigenic peptide galanin in the paraventricular nucleus. Thus, with this HFM-induced leptin measurement, OP rats can be identified while still at normal weight and then investigated for mechanisms that contribute to their excessive body fat accrual on a high-fat diet.


2016 ◽  
Vol 26 (1) ◽  
pp. 13-31 ◽  
Author(s):  
Ha-Il Lee ◽  
Jong-Ha Lee ◽  
Young-Mi Kwon ◽  
Yung-Sun Song

2021 ◽  
Vol 16 (3) ◽  
pp. 1934578X2110012
Author(s):  
Enas M. Moustafa ◽  
Engy R. Rashed ◽  
Rasha R. Rashed

Repeated exposure to ionizing radiation has been reported to increase the risk of chronic metabolic disorders such as systemic hyperlipidemia and intracellular lipid accumulation that might lead to diabetes-induced heart disease. The purpose of this study was to investigate the effect of pterostilbene on high-fat diet rats suffering from ionizing radiation-induced hyperlipidemia. High-fat diet rats showed an increase in body weight and body fat compared with rats fed with normal chow. Pterostilbene and Orlistat treatments resulted in lower body weight and body fat gain, insulin resistance, reduced lipid peroxidation with attenuated liver enzyme levels, and regulated lipogenesis-related genes in the HFD + IR rat group. Regulation of Peroxisome proliferator-activated receptor-γ (PPAR-γ) mRNA enhanced paraoxonase-1 (PON-1) and arylesterase (AE) activities and inhibited that of 3-hydroxy-3-methylglutaryl coenzyme A reductase (HMG-CoA). It also increased the activities of plasma lecithin-cholesterol acyltransferase (LCAT) and lipoprotein lipase (LPL). Pterostilbene and Orlistat also corrected the alterations of serum leptin and adiponectin levels in lipidemic rats. Such findings provide evidence that Pterostilbene and Orlistat can act as normolipidemic agents that possess lipid-lowering effects and potential as a radioprotector.


2021 ◽  
Author(s):  
Qi Guan ◽  
Xinwen Ding ◽  
Lingyue Zhong ◽  
Chuang Zhu ◽  
Pan Nie ◽  
...  

Long term high-fat diet (HF) can cause metabolic disorders, which might induce fatty liver. Fermented whole cereal food exhibit healthy potential due to their unique phytochemical composition and probiotics. In...


2021 ◽  
Vol 22 (4) ◽  
pp. 1647
Author(s):  
Brandi Miller ◽  
Rabina Mainali ◽  
Ravinder Nagpal ◽  
Hariom Yadav

The prevalence of type 2 diabetes mellitus (T2D) is increasing worldwide, and there are no long-term preventive strategies to stop this growth. Emerging research shows that perturbations in the gut microbiome significantly contribute to the development of T2D, while microbiome modulators may be beneficial for T2D prevention. However, microbiome modulators that are effective, safe, affordable, and able to be administered daily are not yet available. Based on our previous pro- and prebiotic studies, we developed a novel synbiotic yogurt comprised of human-origin probiotics and plant-based prebiotics and investigated its impact on diet- and streptozotocin-induced T2D in mice. We compared the effects of our synbiotic yogurt to those of a commercially available yogurt (control yogurt). Interestingly, we found that the feeding of the synbiotic yogurt significantly reduced the development of hyperglycemia (diabetes) in response to high-fat diet feeding and streptozotocin compared to milk-fed controls. Surprisingly, the control yogurt exacerbated diabetes progression. Synbiotic yogurt beneficially modulated the gut microbiota composition compared to milk, while the control yogurt negatively modulated it by significantly increasing the abundance of detrimental bacteria such as Proteobacteria and Enterobacteriaceae. In addition, the synbiotic yogurt protected pancreatic islet morphology compared to the milk control, while the control yogurt demonstrated worse effects on islets. These results suggest that our newly developed synbiotic yogurt protects against diabetes in mice and can be used as a therapeutic to prevent diabetes progression.


2011 ◽  
Vol 108 (6) ◽  
pp. 1025-1033 ◽  
Author(s):  
Sumithra Urs ◽  
Terry Henderson ◽  
Phuong Le ◽  
Clifford J. Rosen ◽  
Lucy Liaw

We recently characterised Sprouty1 (Spry1), a growth factor signalling inhibitor as a regulator of marrow progenitor cells promoting osteoblast differentiation at the expense of adipocytes. Adipose tissue-specific Spry1 expression in mice resulted in increased bone mass and reduced body fat, while conditional knockout of Spry1 had the opposite effect with decreased bone mass and increased body fat. Because Spry1 suppresses normal fat development, we tested the hypothesis that Spry1 expression prevents high-fat diet-induced obesity, bone loss and associated lipid abnormalities, and demonstrate that Spry1 has a long-term protective effect on mice fed a high-energy diet. We studied diet-induced obesity in mice with fatty acid binding promoter-driven expression or conditional knockout of Spry1 in adipocytes. Phenotyping was performed by whole-body dual-energy X-ray absorptiometry, microCT, histology and blood analysis. In conditional Spry1-null mice, a high-fat diet increased body fat by 40 %, impaired glucose regulation and led to liver steatosis. However, overexpression of Spry1 led to 35 % (P < 0·05) lower body fat, reduced bone loss and normal metabolic function compared with single transgenics. This protective phenotype was associated with decreased circulating insulin (70 %) and leptin (54 %; P < 0·005) compared with controls on a high-fat diet. Additionally, Spry1 expression decreased adipose tissue inflammation by 45 %. We show that conditional Spry1 expression in adipose tissue protects against high-fat diet-induced obesity and associated bone loss.


Fitoterapia ◽  
2010 ◽  
Vol 81 (8) ◽  
pp. 1129-1133 ◽  
Author(s):  
Rahul Birari ◽  
Vishal Javia ◽  
Kamlesh Kumar Bhutani

2021 ◽  
pp. 113470
Author(s):  
Everett Altherr ◽  
Aundrea Rainwater ◽  
Darian Kaviani ◽  
Qijun Tang ◽  
Ali D. Güler

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