Effects of ingesting a high-fat diet upon exercise-training cessation on fat accretion in the liver and adipose tissue of rats

2006 ◽  
Vol 31 (4) ◽  
pp. 367-375 ◽  
Author(s):  
Siham Yasari ◽  
Amélie Paquette ◽  
Alexandre Charbonneau ◽  
Marie-Soleil Gauthier ◽  
Roland Savard ◽  
...  
Keyword(s):  
Body Fat ◽  
High Fat Diet ◽  
Liver Lipid ◽  
Female Rats ◽  
Cell Diameter ◽  
Standard Diet ◽  
High Fat ◽  
Fat Cell ◽  
Fat Accumulation ◽  
Fat Accretion

The purpose of the present study was to determine if exercise trained rats might benefit from protection against fat accumulation in response to an obesity stimulus initiated upon training cessation. Two groups of female rats were either treadmill trained for 8 weeks (DTr) or remained sedentary (Sed). They were then submitted either to a high-fat diet (HF; 42 E%) or kept on a standard diet (SD; 12.5 E% lipids) for another 6 weeks while remaining sedentary. Fat accumulation in liver and adipocytes along with fat-cell diameter and plasma free fatty acid (FFA) levels were measured 0, 2, and 6 weeks after training cessation. Immediately after the training period (t = 0), DTr rats exhibited similar body mass and higher dietary intake but smaller body fat content (4 fat pads) compared with Sed rats. DTr rats, under both diets, exhibited higher gains in body fat than Sed rats (DTr vs. Sed, 71% vs. 8% and 132% vs. 55% for SD and HF, respectively), such that fat mass in all 4 depots was similar to Sed rats 6 weeks after training cessation. Despite higher adipocyte fat accretion, liver lipid infiltration was not increased in DTr animals and plasma FFA levels were lower throughout the detraining period. In addition, plasma leptin levels remained lower in DTr animals throughout the detraining period under the HF diet condition. The present results indicate that previously exercise trained rats are not protected against adipocyte fat accumulation whether they ingest a standard or a high-fat diet.

scholarly journals Time course of changes in in vitro lipolysis of intra-abdominal fat depots in relation to high-fat diet-induced hepatic steatosis in rats

2006 ◽  
Vol 96 (2) ◽  
pp. 268-275 ◽  
Author(s):  
Pascal Collin ◽  
Natalie Chapados ◽  
Elise Dufresne ◽  
Pierre Corriveau ◽  
Pascal Imbeault ◽  
...  
Keyword(s):  
Hepatic Steatosis ◽  
High Fat Diet ◽  
Time Course ◽  
Liver Lipid ◽  
Abdominal Fat ◽  
Standard Diet ◽  
High Fat ◽  
Fat Depots ◽  
Fat Accretion

The purpose of the present study was to determine the time course of changes in in vitro lipolysis and in perilipin content (Western blot) in the mesenteric and/or the retroperitoneal fat depots in relation to the development of hepatic steatosis in high-fat diet-fed rats. Female Sprague-Dawley rats were submitted to a high-fat diet (HF diet; 42% as kJ) or a standard diet (SD diet) for 1, 2, 3 or 8 weeks. Fat accretion in the mesenteric and retroperitoneal tissues was higher (P<0·01) in HF diet-fed than in SD diet-fed rats as soon as 1 week after the beginning of the diet. Liver triacylglycerol concentrations were significantly (P<0·01) higher in HF diet-fed than in SD diet-fed rats throughout the experiment, the highest values being reached at week 2 of the diet. Basal and stimulated lipolysis (10−4 to 10−7m-isoproterienol) in the mesenteric and retroperitoneal fat depots was not changed during the first 3 weeks, regardless of the diet. Lipolysis in the mesenteric adipose tissue in the basal and stimulated states was, however, higher (P<0·01) in HF diet-fed than in SD diet-fed rats after 8 weeks of the diets. There were no significant (P>0·05) effects of diet and time on perilipin content of mesenteric tissue. In spite of a rapid fat accretion, the present results do not provide any evidence of a rapid (3 weeks) increase in in vitro lipolysis in intra-abdominal fat depots upon the undertaking of an HF diet at a time where liver lipid infiltration is the most significant.

Acute effect of high-intensity interval training exercise on redox status in the ovaries of rats fed a high-fat diet

2021 ◽  
Vol 33 (12) ◽  
pp. 713
Author(s):  
Rodrigo L. Furtado ◽  
Jonathan Elias R. Martins ◽  
Maria Alice F. Oliveira ◽  
Denise D. Guerreiro ◽  
Naiza A. R. de Sá ◽  
...  
Keyword(s):  
High Intensity ◽  
High Fat Diet ◽  
Interval Training ◽  
Redox Status ◽  
Female Rats ◽  
Standard Diet ◽  
High Intensity Interval Training ◽  
High Fat ◽  
Antral Follicles ◽  
High Intensity Interval

This study demonstrates the effect of a single high-intensity interval training (HIIT) session on the redox status of rat ovaries with excess adiposity. Forty Wistar female rats (mean (±s.e.m.) weight 94.40 ± 13.40 g) were divided into two groups and fed either a standard diet (SD) or a high-fat diet (HFD) for 62 days. At the end of this period, the rats were subjected to a single HIIT session and were killed 24 h after exercise. Both groups subjected to exercise (SDex and HFDex) generated a significantly higher antioxidant environment by presenting a higher thiol content, which represents a lower oxidation rate of GSH than their respective controls (SD and HFD). The percentage of morphologically normal primary follicles decreased, whereas that of antral follicles increased, in the SDex group. In addition, the HFD group had a higher percentage of degenerated antral follicles than the SD and SDex groups. Cells immunoreactive for α-smooth muscle actin were seen in the cortical stroma and thecal layer enclosing late secondary and tertiary follicles in all groups. Moreover, heme oxygenase and cytochrome P450 family 19 subfamily A member 1 (Cyp19A1) labelling was seen in all antral follicles. Progesterone concentrations were significantly higher in the HFDex than SDex group. In conclusion, this study indicates that a single session of HIIT may result in an improvement in ovary redox status because of metabolic muscle activity by inducing physiological adaptation after exercise in a paracrine manner.

Effect of High-fat Diet Feeding over Generations on Body Fat Accumulation

2015 ◽  
pp. 181-190 ◽  
Author(s):  
Kiwon Lim ◽  
Yoshiharu Shimomura ◽  
Masashige Suzuki
Keyword(s):  
Body Fat ◽  
High Fat Diet ◽  
High Fat ◽  
Fat Accumulation

Effect of the detraining status on high-fat diet induced fat accumulation in the adipose tissue and liver in female rats

2007 ◽  
Vol 91 (2-3) ◽  
pp. 281-289 ◽  
Author(s):  
Siham Yasari ◽  
Elise Dufresne ◽  
Denis Prud'homme ◽  
Jean-Marc Lavoie
Keyword(s):  
Adipose Tissue ◽  
High Fat Diet ◽  
Female Rats ◽  
High Fat ◽  
Fat Accumulation

Effects of a Long-Term High-Fat Diet and Switching from a High-Fat to Low-Fat, Standard Diet on Hepatic Fat Accumulation in Sprague-Dawley Rats

2008 ◽  
Vol 53 (12) ◽  
pp. 3206-3212 ◽  
Author(s):  
Katsuhisa Omagari ◽  
Shigeko Kato ◽  
Koichi Tsuneyama ◽  
Chisato Inohara ◽  
Yu Kuroda ◽  
...  
Keyword(s):  
High Fat Diet ◽  
Standard Diet ◽  
Sprague Dawley ◽  
High Fat ◽  
Low Fat ◽  
Fat Accumulation ◽  
Sprague Dawley Rats ◽  
Hepatic Fat

scholarly journals SUN-239 Effects of High-Fat Diet-Induced Obesity on Pulsatile LH Secretion and Hypothalamic KISS1 Expression in Female Rats

2020 ◽  
Vol 4 (Supplement_1) ◽  
Author(s):  
Shiori Minabe ◽  
Kinuyo Iwata ◽  
Youki Watanabe ◽  
Hitoshi Ozawa
Keyword(s):  
Body Weight ◽  
High Fat Diet ◽  
Pulse Frequency ◽  
Female Rats ◽  
Standard Diet ◽  
High Fat ◽  
Estrous Cycles ◽  
Menstrual Dysfunction ◽  
Estrous Cyclicity ◽  
Lh Secretion

Abstract Female obesity is associated with menstrual dysfunction leading to anovulation and infertility. It has recently been reported obesity-induced infertility is involved in the dysfunction of a kisspeptin neuron, a key player in reproduction via direct stimulation of gonadotropin releasing hormone (GnRH) and subsequent gonadotropin release in mammalian species. Previous studies reported that obesity due to high-fat diet (HFD) for 8 months induced a disruption in estrous cyclicity, caused by a decrease in Kiss1 (coding kisspeptin) expression in the hypothalamic arcuate nucleus (ARC) in female rodents. Here we showed the effects of shorter-term (4 months) HFD on pulsatile LH secretion and hypothalamic Kiss1 expression to show pathogenic mechanism underlying obesity-induced infertility. Female Wistar-Imamichi strain rats (7 weeks old) fed on either a standard diet (10% calories from fat) or a high-fat diet (45% calories from fat) for 4 months. Estrous cyclicity and body weight were monitored regularly. All animals were implanted with a jugular catheter and collected blood samples to analyze pulsatile LH secretion, after a week of the ovariectomy with low-dose replacement estradiol to negate influence of changes in ovarian steroid levels and mimic diestrous levels of plasma estrogen. On the next day of the blood sampling, rats were perfused with 0.05 M PBS followed by 4% paraformaldehyde and their brains were collected for in situ hybridization of Kiss1 and Gnrh1. The HFD-fed rats showed progressive increases in body weight, along with hyperphagia and adipose tissue accumulation, compared with control animals. Fifty-eight percent of the HFD-fed rats exhibited irregular estrous cycles, whereas remaining HFD-fed rats showed regular cycles. Two out of 7 rats showing HFD-induced irregular estrous cycles exhibited profound suppression of the LH pulse frequency and the number of Kiss1-expressing cells in the ARC, whereas remaining HFD-fed rats showed normal LH pulses and ARC Kiss1 expressions. The number of Kiss1-expressing cells in the ARC had close positive correlation with LH pulse frequency (R2=0.6872, P&lt;0.001) in both groups. Additionally, the number of Kiss1- or Gnrh1-expressing cells in the anteroventral periventricular nucleus or the preoptic area, were comparable between groups. Taken together, our finding reveals the possibility that irregular menstruation was also induced by changes in the kisspeptin-GnRH independent pathway during the incipient stage of obese infertility.

scholarly journals MEK6 Overexpression Exacerbates Fat Accumulation and Inflammatory Cytokines in High-Fat Diet-Induced Obesity

2021 ◽  
Vol 22 (24) ◽  
pp. 13559
Author(s):  
Suyeon Lee ◽  
Myoungsook Lee
Keyword(s):  
Adipose Tissue ◽  
Inflammatory Cytokines ◽  
High Fat Diet ◽  
Liver Lipid ◽  
Mapk Signaling ◽  
Chow Diet ◽  
High Fat ◽  
Fat Accumulation ◽  
Diet Induced Obesity ◽  
Lipid Formation

Obesity is a state of abnormal fat accumulation caused by an energy imbalance potentially caused by changes in multiple factors. MEK6 engages in cell growth, such as inflammation and apoptosis, as one of the MAPK signaling pathways. The MEK6 gene was found to be related to RMR, a gene associated with obesity. Because only a few studies have investigated the correlation between MEK6 and obesity or the relevant mechanisms, we conducted an experiment using a TgMEK6 model with MEK6 overexpression with non-Tg and chow diet as the control to determine changes in lipid metabolism in plasma, liver, and adipose tissue after a 15-week high-fat diet (HFD). MEK6 overexpression in the TgMEK6 model significantly increased body weight and plasma triglyceride and total cholesterol levels. p38 activity declined in the liver and adipose tissues and lowered lipolysis, oxidation, and thermogenesis levels, contributing to decreased energy consumption. In the liver, lipid formation and accumulation increased, and in adipose, adipogenesis and hypertrophy increased. The adiponectin/leptin ratio significantly declined in plasma and adipose tissue of the TgMEK6 group following MEK6 expression and the HFD, indicating the role of MEK6 expression in adipokine regulation. Plasma and bone-marrow-derived macrophages (BMDM) of the TgMEK6 group increased MEK6 expression-dependent secretion of pro-inflammatory cytokines but decreased levels of anti-inflammatory cytokines, further exacerbating the results exhibited by the diet-induced obesity group. In conclusion, this study demonstrated the synergistic effect of MEK6 with HFD in fat accumulation by significantly inhibiting the mechanisms of lipolysis in the adipose and M2 associated cytokines secretion in the BMDM.

A high-fat diet increases risk of ventricular arrhythmia in female rats: enhanced arrhythmic risk in the absence of obesity or hyperlipidemia

2010 ◽  
Vol 108 (4) ◽  
pp. 933-940 ◽  
Author(s):  
Marie-Claude Aubin ◽  
Sophie Cardin ◽  
Philippe Comtois ◽  
Robert Clément ◽  
Hugues Gosselin ◽  
...  
Keyword(s):  
Wound Healing ◽  
Ventricular Arrhythmia ◽  
Protein Expression ◽  
Cardiac Arrhythmias ◽  
High Fat Diet ◽  
Connexin 43 ◽  
Ischemia Reperfusion ◽  
Female Rats ◽  
Standard Diet ◽  
High Fat

Obesity increases the incidence of cardiac arrhythmias and impairs wound healing. However, it is presently unknown whether a high-fat diet affects arrhythmic risk or wound healing before the onset of overt obesity or hyperlipidemia. After 8 wk of feeding a high-fat diet to adult female rats, a nonsignificant increase in body weight was observed and associated with a normal plasma lipid profile. Following ischemia/reperfusion injury, scar length (standard diet 0.29 ± 0.09 vs. high-fat 0.32 ± 0.13 cm), thickness (standard diet 0.047 ± 0.02 vs. high-fat 0.059 ± 0.01 cm), and collagen α1 type 1 content (standard diet 0.21 ± 0.04 vs. high-fat 0.20 ± 0.04 arbitrary units/mm2) of infarcted hearts were not altered by the high-fat diet. However, the mortality rate was greatly increased 24 h postinfarction (from 5% to 46%, P < 0.01 for ischemia/reperfusion rats; from 20% to 89%, P < 0.0001, in complete-occlusion rats) in high-fat fed rats, in association with a higher prevalence of ventricular arrhythmias. Ventricular arrhythmia inducibility was also significantly increased in noninfarcted rats fed a high-fat diet. In the hearts of rats fed a high-fat diet, connexin-40 expression was absent, connexin-43 was hypophosphorylated and lateralized, and neurofilament-M immunoreactive fiber density (standard diet 2,020 ± 260 vs. high-fat diet 2,830 ± 250 μm2/mm2) and tyrosine hydroxylase protein expression were increased ( P < 0.05). Thus, in the absence of overt obesity and hyperlipidemia, sympathetic hyperinnervation and an aberrant pattern of gap junctional protein expression and regulation in the heart of female rats fed a high-fat diet may have contributed in part to the higher incidence of inducible cardiac arrhythmias.

scholarly journals Loss of Selenoprotein V Predisposes Mice to Body Fat Accumulation (OR11-02-19)

2019 ◽  
Vol 3 (Supplement_1) ◽  
Author(s):  
Lingli Chen ◽  
Jiaqiang Huang ◽  
Yuanyuan Wu ◽  
Fazheng Ren ◽  
Xin Gen Lei
Keyword(s):  
Gene Expression ◽  
Body Fat ◽  
High Fat Diet ◽  
The Body ◽  
High Fat ◽  
Fat Accumulation ◽  
Diet Induced Obesity ◽  
Body Weights ◽  
Its Gene ◽  
Selenoprotein V

Abstract Objectives Metabolic function of selenoprotein V (SELENOV) remains unknown, although we previously showed a strong correlation of its gene expression with the high-fat diet-induced obesity in pigs. This study was conducted to explore the role and mechanism of SELENOV in body fat metabolism. Methods We applied the CRISPR/Cas9 gene-targeting deletion to generate Selenovknockout (KO) mice (C57BL/6 J background). Male KO and their wild-type (WT) (8 weeks old, n = 10 per genotype by treatment group) were fed a normal diet (NF, 10% calories coming from fat) or a high-fat diet (HF, 60% calories coming from fat) for 27 weeks. At the end, body weights and composition of mice were recorded, and tissues were collected to assay for gene expression and protein production related to lipid metabolism. Results Body weights of the KO mice fed the NF or HF diet were 16–19% higher (P < 0.05) than those of the WT mice. Total fat mass of the KO mice was 54% higher (P < 0.05) than the WT mice fed either diet, whereas total lean mass of the KO mice was 5 and 35% lower (P < 0.05) than that of WT mice fed the NF and HF diets, respectively. Gene expression of key enzymes (Fasn, Acaca, Dgat1, and Lpl) involved in lipogenesis was elevated (P < 0.05) in the white adipose tissue of the KO mice compared with the WT mice. In contrast, differences in gene expression of enzymes related to lipolysis and fatty acid oxidation (Atgl, Hsl, Ces1d, and Cpt1a) between the two genotypes were exactly the opposite (P < 0.05). Consistently, levels of proteins related to lipid accumulation (pACC, ACC, FAS, and LPL) were upregulated (P < 0.05) and proteins related to lipolysis (ATGL, HSL, and pHSL) were down-regulated (P < 0.05) in the KO mice compared with the WT mice. Conclusions Knockout of Selenov predisposed the male mice to elevated lipogenesis and attenuated lipolyis, leading to the body fat accumulation. This illustrated role and mechanism of SELENOV helps explain our previously-reported correlation between its gene expression and the high-fat diet-induced obesity in pigs. Funding Sources This research was supported in part by a NSFC grant #31,320,103,920.

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