scholarly journals High Dietary Fat and Selenium Concentrations Exert Tissue- and Glutathione Peroxidase 1–Dependent Impacts on Lipid Metabolism of Young-Adult Mice

2020 ◽  
Vol 150 (7) ◽  
pp. 1738-1748
Author(s):  
Zeping Zhao ◽  
Jonggun Kim ◽  
Xin Gen Lei
Keyword(s):  
Body Weight ◽  
Adipose Tissue ◽  
Lipid Metabolism ◽  
Young Adult ◽  
Glutathione Peroxidase ◽  
Control Diet ◽  
High Fat ◽  
Metabolic Potential ◽  
Glutathione Peroxidase 1 ◽  
Adult Mice

ABSTRACT Background Excessive dietary selenium (Se; 3 mg/kg) or fat (>25%) intakes and overproduction of glutathione peroxidase 1 (GPX1) adversely affect body lipid metabolism. Objective The objective was to reveal impacts and mechanisms of a moderately high Se and a high fat intake on lipid metabolism in Gpx1 knockout (KO) and wild-type (WT) mice. Methods The KO and WT mice (males, 12-wk-old, body weight = 24.8 ± 0.703 g) were allotted to 4 groups each (n = 5) and fed a sucrose-torula yeast basal diet (5% corn oil) supplemented with 0.3 or 1.0 mg (+Se) Se/kg (as sodium selenite) and 0% or 25% [high-fat (HF)] lard for 6 wk. Multiple physiological and molecular biomarkers (68) related to lipid metabolism and selenogenome expression in plasma, liver, and/or adipose tissue were analyzed by 2-way (+Se by HF) ANOVA. Results Compared with the control diet, the +Se diet decreased (P < 0.05) body-weight gain and plasma and liver concentrations of lipids (22–66%) but elevated (≤1.5-fold, P < 0.05) adipose tissue concentrations of lipids in the WT mice. The +Se diet up- and downregulated (P < 0.05) mRNA and/or protein concentrations of factors related to lipogenesis, selenogenome, and transcription, stress, and cell cycle in the liver (26% to 176-fold) and adipose tissues (14% to 1-fold), respectively, compared with the control diet in the WT mice. Many of these +Se diet effects were different (P < 0.05) from those of the HF diet and were eliminated or altered (P < 0.05) by the KO. Conclusions The +Se and HF diets exerted tissue-specific and GPX1 expression–dependent impacts on lipid metabolism and related gene expression in the young-adult mice. Our findings will help reveal metabolic potential and underlying mechanisms of supplementing moderately high Se to subjects with HF intakes.

scholarly journals Eicosapentaenoic acid actions on adiposity and insulin resistance in control and high-fat-fed rats: role of apoptosis, adiponectin and tumour necrosis factor-α

2007 ◽  
Vol 97 (2) ◽  
pp. 389-398 ◽  
Author(s):  
Patricia Pérez-Matute ◽  
Nerea Pérez-Echarri ◽  
J. Alfredo Martínez ◽  
Amelia Marti ◽  
María J. Moreno-Aliaga
Keyword(s):  
Gene Expression ◽  
Insulin Resistance ◽  
Body Weight ◽  
Adipose Tissue ◽  
Weight Gain ◽  
Body Weight Gain ◽  
Control Diet ◽  
Cafeteria Diet ◽  
High Fat ◽  
Beneficial Effects

n-3 PUFA have shown potential anti-obesity and insulin-sensitising properties. However, the mechanisms involved are not clearly established. The aim of the present study was to assess the effects of EPA administration, one of the n-3 PUFA, on body-weight gain and adiposity in rats fed on a standard or a high-fat (cafeteria) diet. The actions on white adipose tissue lipolysis, apoptosis and on several genes related to obesity and insulin resistance were also studied. Control and cafeteria-induced overweight male Wistar rats were assigned into two subgroups, one of them daily received EPA ethyl ester (1 g/kg) for 5 weeks by oral administration. The high-fat diet induced a very significant increase in both body weight and fat mass. Rats fed with the cafeteria diet and orally treated with EPA showed a marginally lower body-weight gain (P = 0·09), a decrease in food intake (P < 0·01) and an increase in leptin production (P < 0·05). EPA administration reduced retroperitoneal adipose tissue weight (P < 0·05) which could be secondary to the inhibition of the adipogenic transcription factor PPARγ gene expression (P < 0·001), and also to the increase in apoptosis (P < 0·05) found in rats fed with a control diet. TNFα gene expression was significantly increased (P < 0·05) by the cafeteria diet, while EPA treatment was able to prevent (P < 0·01) the rise in this inflammatory cytokine. Adiposity-corrected adiponectin plasma levels were increased by EPA. These actions on both TNFα and adiponectin could explain the beneficial effects of EPA on insulin resistance induced by the cafeteria diet.

scholarly journals Polydatin Inhibits Adipose Tissue Inflammation and Ameliorates Lipid Metabolism in High-Fat-Fed Mice

2019 ◽  
Vol 2019 ◽  
pp. 1-10
Author(s):  
Li Zheng ◽  
Jiayuan Wu ◽  
Juanfen Mo ◽  
Li Guo ◽  
Xiaoyan Wu ◽  
...  
Keyword(s):  
Body Weight ◽  
Adipose Tissue ◽  
Lipid Metabolism ◽  
Density Lipoprotein ◽  
Chinese Herbs ◽  
Adipose Tissue Inflammation ◽  
High Fat ◽  
Tissue Inflammation ◽  
Protein Expressions ◽  
Anti Inflammation

Polydatin (PD), an active component of Chinese herbs, is reported to have many biological functions, such as cardioprotective actions, anti-inflammatory activities, and antitumor effects. In this study, we investigated the effects of PD on body weight control, glucose and lipid metabolic regulation, and anti-inflammation in a high-fat-diet- (HFD-) induced obese mice model. After treatment of PD (100 mg/kg/d for 4 weeks), HFD mice reduced body weight, retroperitoneal fat mass, and adipose cell sizes; significantly lowered serum total cholesterol triglyceride (TG) and low-density lipoprotein (LDL) levels; and increased high-density lipoprotein (HDL) levels compared with the HFD control mice. Further studies showed that PD downregulated the mRNA and protein expressions of peroxisome proliferator-activated receptor gamma (PPARγ), a transcription factor involving in the regulation of adipocyte differentiation, in the retroperitoneal fat of HFD mice. Additionally, PD significantly upregulated the mRNA and protein expressions of leptin, an adipocyte-derived anorexic hormone that regulates food intake and energy expenditure, in the adipose tissues of HFD mice. Moreover, PD reduced the expression levels of monocyte chemoattractant protein-1 (MCP-1) and tumor necrosis factor-alpha (TNF-α) in the retroperitoneal and epididymal tissues of HFD mice, suggesting that PD prevented adipose tissue inflammation. In conclusion, PD may serve as a pharmaceutic candidate for obesity-related lipid metabolism, anti-inflammation, and body weight loss.

Effects of Nannochloropsis Fed on Serum and Tissue Lipids Metabolism in Obese Offspring of Overfed Dams

2019 ◽  
Vol 15 (1) ◽  
pp. 72-86
Author(s):  
Soraya Bendimerad-Benmokhtar ◽  
Samira Bouanane ◽  
Hafida Merzouk ◽  
Fatima Zohra Baba Ahmed ◽  
Asme Bendaoud
Keyword(s):  
Body Weight ◽  
Adipose Tissue ◽  
Lipid Metabolism ◽  
Maternal Diet ◽  
Control Diet ◽  
Visceral Obesity ◽  
Female Offspring ◽  
The Body ◽  
Cafeteria Diet ◽  
Lipids Metabolism

Background: The present work aims at determining the effects of maternal-diet-induced obesity on offspring metabolism. The short-term of a marine microalgae diet and its effects on lipids metabolism was investigated. </P><P> Method: Before gestation, some rats are fed control diet and others cafeteria diet. Moreover, two groups of dams were fed standard and cafeteria diets, and two other groups were fed the same diets but containing 10% of microalgae. This feeding started at gestation, and continued throughout parturition, lactation until their offspring&#039;s weaning age. </P><P> Results: Cafeteria diet was shown to increase the body weight and visceral obesity, with aberration in lipid metabolism. The results obtained show that the microalgae diet supplement induces a significant decrease in the maternal body weight and relative adipose tissue weight, plasma glucose and lipid levels, liver-triglyceride (TG) and adipose tissue-TG at parturition and at the end of lactation. Also, the addition of the microalgae in both males and female offspring fed dams at birth and weaning showed significant decrease in body weight, liver-TG whereas significant increase in TG-HDL. </P><P> Conclusion: In the end, it was noted that the incorporation of 10% of microalgae has a beneficial effect on body weight and lipid metabolism.

scholarly journals AB-Kefir Reduced Body Weight and Ameliorated Inflammation in Adipose Tissue of Obese Mice Fed a High-Fat Diet, but Not a High-Sucrose Diet

Nutrients ◽  
2021 ◽  
Vol 13 (7) ◽  
pp. 2182
Author(s):  
Yung-Tsung Chen ◽  
Ai-Hua Hsu ◽  
Shiou-Yun Chiou ◽  
Yu-Chun Lin ◽  
Jin-Seng Lin
Keyword(s):  
Body Weight ◽  
Adipose Tissue ◽  
Gut Microbiota ◽  
High Fat Diet ◽  
Body Weight Gain ◽  
Control Diet ◽  
Liver Weight ◽  
High Fat ◽  
Reduced Body ◽  
Different Types

Consumption of different types of high-calorie foods leads to the development of various metabolic disorders. However, the effects of multi-strain probiotics on different types of diet-induced obesity and intestinal dysbiosis remain unclear. In this study, mice were fed a control diet, high-fat diet (HFD; 60% kcal fat and 20% kcal carbohydrate), or western diet (WD; 40% kcal fat and 43% kcal carbohydrate) and administered with multi-strain AB-Kefir containing six strains of lactic acid bacteria and a Bifidobacterium strain, at 109 CFU per mouse for 10 weeks. Results demonstrated that AB-Kefir reduced body weight gain, glucose intolerance, and hepatic steatosis with a minor influence on gut microbiota composition in HFD-fed mice, but not in WD-fed mice. In addition, AB-Kefir significantly reduced the weight and size of adipose tissues by regulating the expression of CD36, Igf1, and Pgc1 in HFD-fed mice. Although AB-Kefir did not reduce the volume of white adipose tissue, it markedly regulated CD36, Dgat1 and Mogat1 mRNA expression. Moreover, the abundance of Eubacterium_coprostanoligenes_group and Ruminiclostridium significantly correlated with changes in body weight, liver weight, and fasting glucose in test mice. Overall, this study provides important evidence to understand the interactions between probiotics, gut microbiota, and diet in obesity treatment.

scholarly journals GENETIC ANALYSIS OF BROWN ADIPOSE TISSUE, OBESITY AND GROWTH IN MICE

Genetics ◽  
1984 ◽  
Vol 106 (4) ◽  
pp. 705-718
Author(s):  
A M Saxton ◽  
E J Eisen
Keyword(s):  
Body Weight ◽  
Adipose Tissue ◽  
Body Size ◽  
Brown Adipose Tissue ◽  
Genetic Parameters ◽  
Control Diet ◽  
Correlated Response ◽  
High Fat ◽  
Brown Adipose ◽  
Selection For

ABSTRACT The hypothesis developed from single-gene mutant obese rodents that brown adipose tissue (BAT), through its thermogenic ability, is an important factor in the development of obesity, was tested in a randombred population of mice in which degree of adiposity is polygenically determined. Additive direct genetic parameters for measures of body size, lean, fatness and BAT at 6 wk of age were estimated under control and high-fat postweaning dietary regimens. Heritabilities were generally similar for the two diets. However, the lipid-free dry (LFD) component of BAT had a heritability estimate of 0.70 ± 0.26 on the control diet, but only 0.09 ± 0.20 on the high-fat diet. For all traits, genotype by diet interactions indicated that additive direct genetic rankings were not significantly different for the two diets. Based on estimates of genetic parameters in the control diet, selection for 6-wk body weight or 3- to 6-wk gain is expected to increase body size and adiposity. Selection for BAT weight is predicted to result in large, lean individuals. However, selection for the LFD content of BAT, generally believed to be a better indicator of thermogenic ability, is predicted to increase fatness as well as body size. Selection for LFD as a proportion of 6-wk body weight reduced the expected correlated response in fatness. It was concluded that BAT does not play a major role in determining the correlated response in obesity that is often found in populations selected for large body size.

Trans-palmitoleic Acid Reduces Adiposity via Increased Lipolysis in a Rodent Model of Diet-Induced Obesity

2021 ◽  
pp. 1-24
Author(s):  
L. Irasema Chávaro-Ortiz ◽  
Brenda D. Tapia-Vargas ◽  
Mariel Rico-Hidalgo ◽  
Ruth Gutiérrez-Aguilar ◽  
María E. Frigolet
Keyword(s):  
Adipose Tissue ◽  
Lipid Metabolism ◽  
Visceral Adipose Tissue ◽  
High Fat Diet ◽  
Palmitoleic Acid ◽  
Rodent Model ◽  
Adipocyte Size ◽  
High Fat ◽  
Diet Induced Obesity ◽  
Visceral Adipose

Abstract Obesity is defined as increased adiposity, which leads to metabolic disease. The growth of adipose tissue depends on its capacity to expand, through hyperplasia or hypertrophy, in order to buffer energy surplus. Also, during the establishment of obesity, adipose tissue expansion reflects adipose lipid metabolism (lipogenesis and/or lipolysis). It is well known that dietary factors can modify lipid metabolism promoting or preventing the development of metabolic abnormalities that concur with obesity. Trans-palmitoleic acid (TP), a biomarker of dairy consumption, has been associated with reduced adiposity in clinical studies. Thus, we aimed to evaluate the effect of TP over adiposity and lipid metabolism-related genes in a rodent model of diet-induced obesity (DIO). To fulfil this aim, we fed C57BL/6 mice with a Control or a High Fat diet, added with or without TP (3g/kg diet), during 11 weeks. Body weight and food intake were monitored, fat pads were weighted, histology of visceral adipose tissue was analysed, and lipid metabolism-related gene expression was explored by qPCR. Results show that TP consumption prevented weight gain induced by high fat diet, reduced visceral adipose tissue weight, and adipocyte size, while increasing the expression of lipolytic molecules. In conclusion, we show for the first time that TP influences adipose tissue metabolism, specifically lipolysis, resulting in decreased adiposity and reduced adipocyte size in a DIO mice model.

scholarly journals Flavonoids from Mulberry Leaves Alleviate Lipid Dysmetabolism in High Fat Diet-Fed Mice: Involvement of Gut Microbiota

2020 ◽  
Vol 8 (6) ◽  
pp. 860 ◽  
Author(s):  
Yinzhao Zhong ◽  
Bo Song ◽  
Changbing Zheng ◽  
Shiyu Zhang ◽  
Zhaoming Yan ◽  
...  
Keyword(s):  
Acetic Acid ◽  
Lipid Metabolism ◽  
Gut Microbiota ◽  
High Fat Diet ◽  
Control Diet ◽  
Liver Steatosis ◽  
High Fat ◽  
Acetic Acid Production ◽  
Mulberry Leaves ◽  
Brown Adipose

Here, we investigated the roles and mechanisms of flavonoids from mulberry leaves (FML) on lipid metabolism in high fat diet (HFD)-fed mice. ICR mice were fed either a control diet (Con) or HFD with or without FML (240 mg/kg/day) by oral gavage for six weeks. FML administration improved lipid accumulation, alleviated liver steatosis and the whitening of brown adipose tissue, and improved gut microbiota composition in HFD-fed mice. Microbiota transplantation from FML-treated mice alleviated HFD-induced lipid metabolic disorders. Moreover, FML administration restored the production of acetic acid in HFD-fed mice. Correlation analysis identified a significant correlation between the relative abundances of Bacteroidetes and the production of acetic acid, and between the production of acetic acid and the weight of selected adipose tissues. Overall, our results demonstrated that in HFD-fed mice, the lipid metabolism improvement induced by FML administration might be mediated by gut microbiota, especially Bacteroidetes-triggered acetic acid production.

scholarly journals Differential Effects of Short-term Ketogenic, High Fat and Fructose-enriched Diets on Metabolic Parameters in Mice (P08-042-19)

2019 ◽  
Vol 3 (Supplement_1) ◽  
Author(s):  
Natalia Cortez ◽  
John Solitro ◽  
Brian Hong ◽  
Emily Villarreal ◽  
Gerardo Mackenzie
Keyword(s):  
Body Composition ◽  
Body Weight ◽  
Grip Strength ◽  
Glucose Homeostasis ◽  
Control Diet ◽  
Oral Glucose ◽  
High Fat ◽  
Carbohydrate Source ◽  
Strength Performance ◽  
Glucose Levels

Abstract Objectives Dietary composition influences multiple facets of human health and is inextricably linked to chronic metabolic conditions such as obesity, type 2 diabetes, cardiovascular disease and cancer. Thus, the objective of this study was to evaluate the effects of a ketogenic (KD), a high fat (HF), and a fructose-enriched (FR) diets on glucose homeostasis, body composition and grip strength performance in mice. Methods Healthy C57BL/6 J mice (5–6 mice/group) were fed, either a control diet containing approximately 16% total calories from fat (CT), a diet containing 89% fat (KD), a diet with 50% total calories from fat (HF), or a diet with 32% fructose as carbohydrate source (FR). All diets contained 10% protein and all mice were fed ad libitum for 8 weeks. At baseline and 8 weeks, we evaluated body composition using NMR relaxometry, grip strength, non-fasting glucose levels, and ketone levels. In addition, oral glucose tolerance test (OGTT) was conducted by administering glucose by oral gavage (1 g/kg body weight) after 15 hour-fasting and blood glucose levels were measured at 0, 30, 60, 90, and 120 min after glucose administration. Results All mice, irrespectively of their experimental diet groups, increased their body weight, fat mass and adiposity without significant differences among them. After 4 weeks, the HF (P < 0.05) and FR (P < 0.01) groups had significantly higher glucose levels than control. At 8 weeks, the KD groups showed an improved glucose homeostasis compared to CT group, as determined by OGTT. Moreover, compared to the CT group, grip strength performance increased (although did not reached significance) in the KD group (P = 0.054), and decreased in the FR group (P < 0.05). Moreover, when compared to their respective baseline values, grip strength performance increased in KD-fed mice and decreased in FR-fed mice, but differences among them were not statistically significant (P = 0.07). Conclusions Our preliminary findings indicate that altering macronutrient composition can lead to metabolic and physiological changes. Among the three diets tested, the KD showed an improved glucose utilization and better grip strength performance in mice. Additional mechanistic studies are warranted to better understand these metabolic differences among the experimental diets. Funding Sources funds from the University of California, Davis.

scholarly journals Effect of selective expression of dominant-negative PPARγ in pro-opiomelanocortin neurons on the control of energy balance

2016 ◽  
Vol 48 (7) ◽  
pp. 491-501 ◽  
Author(s):  
Madeliene Stump ◽  
Deng-Fu Guo ◽  
Ko-Ting Lu ◽  
Masashi Mukohda ◽  
Xuebo Liu ◽  
...  
Keyword(s):  
Body Weight ◽  
Weight Gain ◽  
Energy Balance ◽  
High Fat Diet ◽  
Control Diet ◽  
Cre Recombinase ◽  
Dominant Negative ◽  
High Fat ◽  
Pparγ Agonist ◽  
The Brain

Peroxisome proliferator-activated receptor-γ (PPARγ), a master regulator of adipogenesis, was recently shown to affect energy homeostasis through its actions in the brain. Deletion of PPARγ in mouse brain, and specifically in the pro-opiomelanocortin (POMC) neurons, results in resistance to diet-induced obesity. To study the mechanisms by which PPARγ in POMC neurons controls energy balance, we constructed a Cre-recombinase-dependent conditionally activatable transgene expressing either wild-type (WT) or dominant-negative (P467L) PPARγ and the tdTomato reporter. Inducible expression of both forms of PPARγ was validated in cells in culture, in liver of mice infected with an adenovirus expressing Cre-recombinase (AdCre), and in the brain of mice expressing Cre-recombinase either in all neurons (NESCre/PPARγ-P467L) or selectively in POMC neurons (POMCCre/PPARγ-P467L). Whereas POMCCre/PPARγ-P467L mice exhibited a normal pattern of weight gain when fed 60% high-fat diet, they exhibited increased weight gain and fat mass accumulation in response to a 10% fat isocaloric-matched control diet. POMCCre/PPARγ-P467L mice were leptin sensitive on control diet but became leptin resistant when fed 60% high-fat diet. There was no difference in body weight between POMCCre/PPARγ-WT mice and controls in response to 60% high-fat diet. However, POMCCre/PPARγ-WT, but not POMCCre/PPARγ-P467L, mice increased body weight in response to rosiglitazone, a PPARγ agonist. These observations support the concept that alterations in PPARγ-driven mechanisms in POMC neurons can play a role in the regulation of metabolic homeostasis under certain dietary conditions.

Abstract 6260: Up-Regulated Expression of MicroRNA-143 in Association with Obesity in the Adipose Tissue of Mice Fed High Fat Diet

Circulation ◽  
2008 ◽  
Vol 118 (suppl_18) ◽  
Author(s):  
Rieko Takanabe ◽  
Koh Ono ◽  
Tomohide Takaya ◽  
Takahiro Horie ◽  
Hiromichi Wada ◽  
...  
Keyword(s):  
Gene Expression ◽  
Insulin Resistance ◽  
Body Weight ◽  
Adipose Tissue ◽  
High Fat Diet ◽  
Control Cell ◽  
High Fat ◽  
Expression Levels ◽  
Mesenteric Fat ◽  
Regulated Expression

Obesity is the result of an expansion and increase in the number of individual adipocytes. Since changes in gene expression during adipocyte differentiation and hypertrophy are closely associated with insulin resistance and cardiovascular diseases, further insight into the molecular basis of obesity is needed to better understand obesity-associated diseases. MicroRNAs (miRNAs) are approximately 17–24nt single stranded RNA, that post-transcriptionally regulate gene expression. MiRNAs control cell growth, differentiation and metabolism, and may be also involved in pathogenesis and pathophysiology of diseases. It has been proposed that miR-143 plays a role in the differentiation of preadipocytes into mature adipocytes in culture. However, regulated expression of miR-143 in the adult adipose tissue during the development of obesity in vivo is unknown. To solve this problem, C57BL/6 mice were fed with either high-fat diet (HFD) or normal chow (NC). Eight weeks later, severe insulin resistance was observed in mice on HFD. Body weight increased by 35% and the mesenteric fat weight increased by 3.3-fold in HFD mice compared with NC mice. We measured expression levels of miR-143 in the mesenteric fat tissue by real-time PCR and normalized with those of 5S ribosomal RNA. Expression of miR-143 in the mesenteric fat was significantly up-regulated (3.3-fold, p<0.05) in HFD mice compared to NC mice. MiR-143 expression levels were positively correlated with body weight (R=0.577, p=0.0011) and the mesenteric fat weight (R=0.608, p=0.0005). We also measured expression levels in the mesenteric fat of PPARγ and AP2, whose expression are deeply involved in the development of obesity, insulin resistant and arteriosclerosis. The expression levels of miR-143 were closely correlated with those of PPARγ (R=0.600, p=0.0040) and AP2 (R=0.630, p=0.0022). These findings provide the first evidence for up-regulated expression of miR-143 in the mesenteric fat of HFD-induced obese mice, which might contribute to regulated expression of genes involved in the pathophysiology of obesity.

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