scholarly journals Time course of the development of non-alcoholic hepatic steatosis in response to high-fat diet-induced obesity in rats

2006 ◽  
Vol 95 (2) ◽  
pp. 273-281 ◽  
Author(s):  
Marie-Soleil Gauthier ◽  
Roland Favier ◽  
Jean-Marc Lavoie
Keyword(s):  
Body Weight ◽  
Hepatic Steatosis ◽  
Body Fat ◽  
Lipid Content ◽  
Time Course ◽  
Liver Lipid ◽  
High Fat ◽  
Liver Lipid Content ◽  
Sd Rats ◽  
Fat Accretion

The aim of the study was to characterize the time course of the development of high-fat diet-induced hepatic steatosis and its relation to body fat accretion and changes in plasma lipid profile. Female Sprague–Dawley rats were high-fat fed (HF; 42%, kJ) for 1, 2, 4, 6, 12 and 16 weeks and compared to standard fed rats (SD). Data obtained from HF rats were further analysed by classifying the animals into obesity-prone and obesity-resistant. In HF rats, liver lipid content increased rapidly by approximately 200% during the first 2 weeks, decreased almost to baseline levels between weeks 2 and 6, and re-increased by 17% between weeks 6 and 16 (P<0·05). Body weight, body fat accretion, plasma leptin, NEFA and glycerol concentrations were higher in HF than in SD rats (P<0·05). These higher values were established in 2 weeks and the differences between the groups did not further enlarge from weeks 2 to 16. Obesity-prone rats depicted higher body weight and body fat accretion than obesity-resistant and SD rats. Surprisingly, however, liver lipid content was the same in obesity-prone as in obesity-resistant rats as they were both higher than in SD rats (weeks 2 and 16; P<0·05). Our data support the hypothesis that the liver acts as a systemic buffer, largely increasing its lipid content in the early stage of high-fat feeding. Our results also suggest that the development of non-alcoholic hepatic steatosis is more linked to dietary fat ingestion than to body weight gain.

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.

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 Prenatal hyperandrogenism induces alterations that affect liver lipid metabolism

2016 ◽  
Vol 230 (1) ◽  
pp. 67-79 ◽  
Author(s):  
Giselle Adriana Abruzzese ◽  
Maria Florencia Heber ◽  
Silvana Rocio Ferreira ◽  
Leandro Martin Velez ◽  
Roxana Reynoso ◽  
...  
Keyword(s):  
Metabolic Syndrome ◽  
Lipid Metabolism ◽  
Glucose Tolerance ◽  
Fatty Liver ◽  
Lipid Content ◽  
Liver Lipid ◽  
Acid Oxidation ◽  
Liver Lipid Content ◽  
Increased Risk ◽  
Liver Lipid Metabolism

Prenatal hyperandrogenism is hypothesized as one of the main factors contributing to the development of polycystic ovary syndrome (PCOS). PCOS patients have high risk of developing fatty liver and steatosis. This study aimed to evaluate the role of prenatal hyperandrogenism in liver lipid metabolism and fatty liver development. Pregnant rats were hyperandrogenized with testosterone. At pubertal age, the prenatally hyperandrogenized (PH) female offspring displayed both ovulatory (PHov) and anovulatory (PHanov) phenotypes that mimic human PCOS features. We evaluated hepatic transferases, liver lipid content, the balance between lipogenesis and fatty acid oxidation pathway, oxidant/antioxidant balance and proinflammatory status. We also evaluated the general metabolic status through growth rate curve, basal glucose and insulin levels, glucose tolerance test, HOMA-IR index and serum lipid profile. Although neither PH group showed signs of liver lipid content, the lipogenesis and fatty oxidation pathways were altered. The PH groups also showed impaired oxidant/antioxidant balance, a decrease in the proinflammatory pathway (measured by prostaglandin E2 and cyclooxygenase-2 levels), decreased glucose tolerance, imbalance of circulating lipids and increased risk of metabolic syndrome. We conclude that prenatal hyperandrogenism generates both PHov and PHanov phenotypes with signs of liver alterations, imbalance in lipid metabolism and increased risk of developing metabolic syndrome. The anovulatory phenotype showed more alterations in liver lipogenesis and a more impaired balance of insulin and glucose metabolism, being more susceptible to the development of steatosis.

Pharmacological characterization of a small molecule inhibitor of c-Jun kinase

2008 ◽  
Vol 295 (5) ◽  
pp. E1142-E1151 ◽  
Author(s):  
Helen Cho ◽  
Shawn C. Black ◽  
David Looper ◽  
Manli Shi ◽  
Dawn Kelly-Sullivan ◽  
...  
Keyword(s):  
Body Weight ◽  
Adipose Tissue ◽  
Body Fat ◽  
Small Molecule ◽  
Glycogen Synthase ◽  
High Fat ◽  
Pharmacological Characterization ◽  
Compound A ◽  
Weight Decrease

c-Jun NH2-terminal kinase (JNK) plays an important role in insulin resistance; however, identification of pharmacologically potent and selective small molecule JNK inhibitors has been limited. Compound A has a cell IC50 of 102 nM and is at least 100-fold selective against related kinases and 27-fold selective against glycogen synthase kinase-3β and cyclin-dependent kinase-2. In C57BL/6 mice, compound A reduced LPS-mediated increases in both plasma cytokine levels and phosphorylated c-Jun in adipose tissue. Treatment of mice fed a high-fat diet with compound A for 3 wk resulted in a 13.1 ± 1% decrease in body weight and a 9.3 ± 1.5% decrease in body fat, compared with a 6.6 ± 2.1% increase in body weight and a 6.7 ± 2.1% increase in body fat in vehicle-treated mice. Mice pair fed to those that received compound A exhibited a body weight decrease of 7 ± 1% and a decrease in body fat of 1.6 ± 1.3%, suggesting that reductions in food intake could not account solely for the reductions in adiposity observed. Compound A dosed at 30 mg/kg for 13 days in high-fat fed mice resulted in a significant decrease in phosphorylated c-Jun in adipose tissue accompanied by a decrease in weight and reductions in glucose and triglycerides and increases in insulin sensitivity to levels comparable with those in lean control mice. The ability of compound A to reduce the insulin-stimulated phosphorylation of insulin receptor substrate-1 (IRS-1) von Ser307 and partially reverse the free fatty acid inhibition of glucose uptake in 3T3L1 adipocytes, suggests that enhancement of insulin signaling in addition to weight loss may contribute to the effects of compound A on insulin sensitization in vivo. Pharmacological inhibition of JNK using compound A may therefore offer an effective therapy for type 2 diabetes mediated at least in part via weight reduction.

scholarly journals Evaluation of Anti-Obesity Activity, Acute Toxicity, and Subacute Toxicity of Probiotic Dark Tea

Biomolecules ◽  
2018 ◽  
Vol 8 (4) ◽  
pp. 99 ◽  
Author(s):  
Wang Ling ◽  
Shungeng Li ◽  
Xingcai Zhang ◽  
Yongquan Xu ◽  
Ying Gao ◽  
...  
Keyword(s):  
Body Weight ◽  
High Fat Diet ◽  
Metabolic Disorders ◽  
The Body ◽  
High Fat ◽  
Water Group ◽  
Subacute Toxicity ◽  
Infusion Group ◽  
Sd Rats ◽  
Group Ii

: Probiotic dark tea (PDT) is a novel kind of dark tea produced by fresh albino tea leaves and fermented with specific probiotics. Our study demonstrates that PDT can ameliorate high-fat diet-induced overweight and lipid metabolic disorders and shows no acute or subacute toxicity in Sprague-Dawley (SD) rats. Daily intragastric administration of 5% PDT infusion for 14 days caused no obvious effect on general physiological features and behaviors of rats. Oral administration of 1%, 2%, and 3% of PDT infusion for six weeks had no influence on the biochemistry and histopathology of rats’ organs and blood, as well as the body weight and ratios of organ/body weight. To investigate its anti-obesity activity, SD rats were randomly divided into four groups, treated with normal diet + water (Group I), high-fat diet + water (Group II), high-fat diet + 3% traditional dark tea infusion (Group III), high-fat diet + 3% PDT infusion (Group IV). After six weeks, the body weight, serum total triacylglycerol (TG) and serum total cholesterol (TC) levels of rats in Group II were significantly increased and the high-density lipoprotein cholesterol (HDL) levels were significantly decreased compared with those in the other three groups. Both traditional dark tea and PDT treatment effectively counteracted the adverse effect of a high-fat diet in SD rats. These results suggest that PDT could be applied for the prevention of obesity, which ameliorates overweight and lipid metabolic disorders and which shows no acute or subacute toxicity.

Effect of Methionine on Liver Lipid Content and Lipid Metabolism of Rats Fed a Protein-free Diet

1973 ◽  
Vol 103 (1) ◽  
pp. 54-60 ◽  
Author(s):  
Yoritaka Aoyama ◽  
Masashi Nakanishi ◽  
Kiyoshi Ashida
Keyword(s):  
Lipid Metabolism ◽  
Lipid Content ◽  
Liver Lipid ◽  
Liver Lipid Content ◽  
Protein Free Diet

scholarly journals Apolipoprotein CIII Overexpression-Induced Hypertriglyceridemia Increases Nonalcoholic Fatty Liver Disease in Association with Inflammation and Cell Death

2017 ◽  
Vol 2017 ◽  
pp. 1-18 ◽  
Author(s):  
Adriene A. Paiva ◽  
Helena F. Raposo ◽  
Amarylis C. B. A. Wanschel ◽  
Tarlliza R. Nardelli ◽  
Helena C. F. Oliveira
Keyword(s):  
Cell Death ◽  
Liver Disease ◽  
Fatty Liver ◽  
Nonalcoholic Fatty Liver Disease ◽  
Lipid Content ◽  
Fatty Liver Disease ◽  
Liver Lipid ◽  
Hepatic Insulin Resistance ◽  
Nonalcoholic Fatty Liver ◽  
Liver Lipid Content

Nonalcoholic fatty liver disease (NAFLD) is the principal manifestation of liver disease in obesity and metabolic syndrome. By comparing hypertriglyceridemic transgenic mice expressing apolipoprotein (apo) CIII with control nontransgenic (NTg) littermates, we demonstrated that overexpression of apoCIII, independent of a high-fat diet (HFD), produces NAFLD-like features, including increased liver lipid content; decreased antioxidant power; increased expression of TNFα, TNFα receptor, cleaved caspase-1, and interleukin-1β; decreased expression of adiponectin receptor-2; and increased cell death. This phenotype is aggravated and additional NAFLD features are differentially induced in apoCIII mice fed a HFD. HFD induced glucose intolerance together with increased gluconeogenesis, indicating hepatic insulin resistance. Additionally, the HFD led to marked increases in plasma TNFα (8-fold) and IL-6 (60%) in apoCIII mice. Cell death signaling (Bax/Bcl2), effector (caspase-3), and apoptosis were augmented in apoCIII mice regardless of whether a HFD or a low-fat diet was provided. Fenofibrate treatment reversed several of the effects associated with diet and apoCIII expression but did not normalize inflammatory traits even when liver lipid content was fully corrected. These results indicate that apoCIII and/or hypertriglyceridemia plays a major role in liver inflammation and cell death, which in turn increases susceptibility to and the severity of diet-induced NAFLD.

INFLUENCE OF DIET COMPOSITION AND CALORIC INTAKE ON BODY WEIGHT OF WARM- AND COLD-ACCLIMATED RATS

1963 ◽  
Vol 41 (1) ◽  
pp. 2225-2235
Author(s):  
A. DesMarais ◽  
P. A. Lachance
Keyword(s):  
Body Weight ◽  
Body Fat ◽  
Total Body Weight ◽  
Lean Body Weight ◽  
High Fat ◽  
High Carbohydrate ◽  
Exposure To Cold ◽  
Total Body Fat ◽  
Ad Libitum ◽  
Total Body

The well known reduction in growth rate of cold-acclimated rats has been shown to depend on a decreased gain in total body fat, without change in the gain in lean body weight. This has been observed in rats fed Lab Chow or a high-fat diet ad libitum. In those groups fed a high-carbohydrate diet ad libitum or calorie-restricted high-fat or high-carbohydrate diets, exposure to cold had no effect on the gain in neither total body weight nor lean body weight, which were already reduced by the diet; in those animals, the significant decrease in the gain in total body fat upon exposure to cold was compensated by a slight but unsignificant increase in the gain in lean body weight, so that differences in gain in total body weight were not significant.

Diminished satiation in rats exposed to elevated levels of endogenous or exogenous cholecystokinin

2001 ◽  
Vol 280 (2) ◽  
pp. R331-R337 ◽  
Author(s):  
Mihai Covasa ◽  
Jeremy K. Marcuson ◽  
Robert C. Ritter
Keyword(s):  
Body Weight ◽  
Food Intake ◽  
Body Fat ◽  
Peritoneal Cavity ◽  
Dietary Protein ◽  
High Protein ◽  
High Fat ◽  
Low Fat ◽  
Osmotic Minipumps ◽  
Fat Composition

Rats maintained on a high-fat (HF) diet exhibit reduced sensitivity to the satiation-producing effect of exogenous CCK. Because more CCK is released in response to HF meals than low-fat (LF) meals, we hypothesized that increased circulating CCK associated with ingestion of HF diets contributes to the development of decreased CCK sensitivity. To test this hypothesis, we implanted osmotic minipumps filled with either NaCl or CCK octapeptide into the peritoneal cavity. Subsequently, we examined the effect of intraperitoneal NaCl or CCK (0.5 μg/kg) injection on 30-min food intake. CCK significantly reduced 30-min food intake less in rats implanted with CCK-releasing minipumps compared with those with NaCl-releasing minipumps. Because dietary protein is a potent releaser of endogenous CCK, we hypothesized that rats adapted to a high-protein (HP) diet might also exhibit reduced sensitivity to exogenous CCK. Therefore, in a second experiment, we examined CCK-induced reduction of food intake in rats maintained on LF and rats maintained on HF or HP. Ingestion of LF stimulates very little endogenous CCK secretion, whereas both HF and HP markedly increase plasma CCK concentrations. Both doses of CCK reduced food intake significantly less in HF and HP rats compared with LF rats. There were no differences in 24-h food intake, body weight, or body fat composition among LF-, HF-, and HP-fed rats. These results are consistent with the hypothesis that sustained elevation of CCK either by infusion of exogenous CCK or by dietary-induced elevation of plasma CCK contributes to the development of reduced sensitivity to exogenous CCK.

Sign in / Sign up

Export Citation Format

Share Document