scholarly journals Reduced Body Fat and Epididymal Adipose Apelin Expression Associated With Raspberry Ketone [4-(4-Hydroxyphenyl)-2-Butanone] Weight Gain Prevention in High-Fat-Diet Fed Mice

2021 ◽  
Vol 12 ◽  
Author(s):  
Lihong Hao ◽  
Nicholas T. Bello
Keyword(s):  
Gene Expression ◽  
Weight Gain ◽  
High Fat Diet ◽  
The United States ◽  
Metabolic Effects ◽  
Control Group ◽  
Oral Glucose ◽  
High Fat ◽  
Oral Gavage ◽  
Raspberry Ketone

Raspberry ketone [4-(4-hydroxyphenyl)-2-butanone] is a natural aromatic compound found in raspberries and other fruits. Raspberry ketone (RK) is synthetically produced for use as a commercial flavoring agent. In the United States and other markets, it is sold as a dietary supplement for weight control. The potential of RK to reduce or prevent excessive weight gain is unclear and could be a convergence of several different actions. This study sought to determine whether acute RK can immediately delay carbohydrate hyperglycemia and reduce gastrointestinal emptying. In addition, we explored the metabolic signature of chronic RK to prevent or remedy the metabolic effects of diet-induced weight gain. In high-fat diet (HFD; 45% fat)-fed male mice, acute oral gavage of RK (200 mg/kg) reduced hyperglycemia from oral sucrose load (4 g/kg) at 15 min. In HFD-fed female mice, acute oral RK resulted in an increase in blood glucose at 30 min. Chronic daily oral gavage of RK (200 mg/kg) commencing with HFD access (HFD_RK) for 11 weeks resulted in less body weight gain and reduced fat mass compared with vehicle treated (HFD_Veh) and chronic RK starting 4 weeks after HFD access (HFD_RKw4) groups. Compared with a control group fed a low-fat diet (LFD; 10% fat) and dosed with vehicle (LFD_Veh), glucose AUC of an oral glucose tolerance test was increased with HFD_Veh, but not in HFD_RK or HFD_RKw4. Apelin (Apln) gene expression in epididymal white adipose tissue was increased in HFD_Veh, but reduced to LFD_Veh levels in the HFD_RK group. Peroxisome proliferator activated receptor alpha (Ppara) gene expression was increased in the hepatic tissue of HFD_RK and HFD_RKw4 groups. Overall, our findings suggest that long term daily use of RK prevents diet-induced weight gain, normalizes high-fat diet-induced adipose Apln, and increases hepatic Ppara expression.

Probiotics lower plasma glucose in the high-fat fed C57BL/6J mouse

2010 ◽  
Vol 1 (2) ◽  
pp. 189-196 ◽  
Author(s):  
U. Andersson ◽  
C. Bränning ◽  
S. Ahrné ◽  
G. Molin ◽  
J. Alenfall ◽  
...  
Keyword(s):  
Gut Microbiota ◽  
Plasma Glucose ◽  
Short Chain Fatty Acids ◽  
Tolerance Test ◽  
Metabolic Effects ◽  
Control Group ◽  
Oral Glucose ◽  
Gut Health ◽  
High Fat ◽  
Early Diabetes

Today, the gut microbiota is considered a key organ in host nutritional metabolism and recent data have suggested that alterations in gut microbiota contribute to the development of type 2 diabetes and obesity. Accordingly, a whole range of beneficial effects relating to inflammation and gut health have been observed following administration of probiotics to both humans and different animal models. The objective of this study was to evaluate the metabolic effects of an oral probiotic supplement, Lactobacillus plantarum DSM 15313, to high-fat diet (HFD) fed C57BL/6J mice, a model of human obesity and early diabetes. The mice were fed the experimental diets for 20 weeks, after which the HFD had induced an insulin-resistant state in both groups compared to the start of the study. The increase in body weight during the HFD feeding was higher in the probiotic group than in the control group, however, there were no significant differences in body fat content. Fasting plasma glucose levels were lower in the group fed the probiotic supplement, whereas insulin and lipids were not different. Caecal levels of short-chain fatty acids were not significantly different between the groups. An oral glucose tolerance test showed that the group fed probiotics had a significantly lower insulin release compared to the control group, although the rate of glucose clearance was not different. Taken together, these data indicate that L. plantarum DSM 15313 has anti-diabetic properties when fed together with an HFD.

scholarly journals Preventive Effects of Kaempferol on High-Fat Diet-Induced Obesity Complications in C57BL/6 Mice

2020 ◽  
Vol 2020 ◽  
pp. 1-9
Author(s):  
Tieqiao Wang ◽  
Qiaomin Wu ◽  
Tingqi Zhao
Keyword(s):  
Insulin Resistance ◽  
Weight Gain ◽  
Blood Glucose ◽  
Gut Microbiota ◽  
Serum Cholesterol ◽  
High Fat Diet ◽  
Liver Weight ◽  
Control Group ◽  
High Fat ◽  
High Blood Glucose

Kaempferol is a dietary flavanol that regulates cellular lipid and glucose metabolism. Its mechanism of action in preventing hepatic steatosis and obesity-related disorders has yet to be clarified. The purpose of this research was to examine kaempferol’s antiobesity effects in high-fat diet- (HFD-) fed mice and to investigate its impact on their gut microbiota. Using a completely randomized design, 30 mice were equally assigned to a control group, receiving a low-fat diet, an HFD group, receiving a high-fat diet, and an HFD+kaempferol group, receiving a high-fat diet and kaempferol doses of 200 mg/kg in the diet. After eight weeks, the HFD mice displayed substantial body and liver weight gain and high blood glucose and serum cholesterol levels. However, treatment with kaempferol moderated body and liver weight gain and elevation of blood glucose and serum cholesterol and triglyceride levels. Examination of 16S ribosomal RNA showed that HFD mice exhibited decreased microbial diversity, but kaempferol treatment maintained it to nearly the same levels as those in the control group. In conclusion, kaempferol can protect against obesity and insulin resistance in mice on a high-fat diet, partly through regulating their gut microbiota and moderating the decrease in insulin resistance.

Molecular factors involved in the hypolipidemic- and insulin-sensitizing effects of a ginger (Zingiber officinale Roscoe) extract in rats fed a high-fat diet

2017 ◽  
Vol 42 (2) ◽  
pp. 209-215 ◽  
Author(s):  
Natalia de las Heras ◽  
María Valero-Muñoz ◽  
Beatriz Martín-Fernández ◽  
Sandra Ballesteros ◽  
Antonio López-Farré ◽  
...  
Keyword(s):  
Lipid Profile ◽  
Plasma Levels ◽  
High Fat Diet ◽  
Tissue Growth ◽  
Collagen I ◽  
Metabolic Effects ◽  
Control Group ◽  
Standard Diet ◽  
High Fat ◽  
Glucose Transporter 2

Hypolipidemic and hypoglycemic properties of ginger in animal models have been reported. However, information related to the mechanisms and factors involved in the metabolic effects of ginger at a hepatic level are limited. The aim of the present study was to investigate molecular factors involved in the hypoglycemic and hypolipidemic effects of a hydroethanolic ginger extract (GE) in the liver of rats fed a high-fat diet (HFD). The study was conducted in male Wistar rats divided into the following 3 groups: (i) Rats fed a standard diet (3.5% fat), the control group; (ii) rats fed an HFD (33.5% fat); and (iii) rats fed an HFD treated with GE (250 mg·kg−1·day−1) for 5 weeks (HFD+GE). Plasma levels of glucose, insulin, lipid profile, leptin, and adiponectin were measured. Liver expression of glycerol phosphate acyltransferase (GPAT), cholesterol 7 alpha-hydroxylase, peroxisome proliferator-activated receptors (PPAR), PPARα and PPARγ, glucose transporter 2 (GLUT-2), liver X receptor, sterol regulatory element-binding protein (SREBP1c), connective tissue growth factor (CTGF), and collagen I was measured. Data were analyzed using a 1-way ANOVA, followed by a Newman−Keuls test if differences were noted. The study showed that GE improved lipid profile and attenuated the increase of plasma levels of glucose, insulin, and leptin in HFD rats. This effect was associated with a higher liver expression of PPARα, PPARγ, and GLUT-2 and an enhancement of plasma adiponectin levels. Furthermore, GE reduced liver expression of GPAT, SREBP1c, CTGF, and collagen I. The results suggest that GE might be considered as an alternative therapeutic strategy in the management of overweight and hepatic and metabolic−related alterations.

scholarly journals HOX-7 suppresses body weight gain and adipogenesis-related gene expression in high-fat-diet-induced obese mice

2014 ◽  
Vol 14 (1) ◽  
Author(s):  
Heon-Myung Lee ◽  
Hong-Kun Rim ◽  
Jong-Hwan Seo ◽  
Yoon-Bum Kook ◽  
Sung-Kew Kim ◽  
...  
Keyword(s):  
Gene Expression ◽  
Body Weight ◽  
Weight Gain ◽  
High Fat Diet ◽  
Body Weight Gain ◽  
Obese Mice ◽  
Related Gene ◽  
High Fat

scholarly journals Evaluation of Beneficial Metabolic Effects of Berries in High-Fat Fed C57BL/6J Mice

2014 ◽  
Vol 2014 ◽  
pp. 1-12 ◽  
Author(s):  
Lovisa Heyman ◽  
Ulrika Axling ◽  
Narda Blanco ◽  
Olov Sterner ◽  
Cecilia Holm ◽  
...  
Keyword(s):  
High Fat Diet ◽  
Inflammatory Marker ◽  
Metabolic Effects ◽  
Control Group ◽  
High Fat ◽  
Hepatic Lipid Accumulation ◽  
Positive Effects ◽  
Low Fat Diet ◽  
Body Fat Content ◽  
Quercetin Glycosides

Objective. The aim of the study was to screen eight species of berries for their ability to prevent obesity and metabolic abnormalities associated with type 2 diabetes.Methods. C57BL/6J mice were assigned the following diets for 13 weeks: low-fat diet, high-fat diet or high-fat diet supplemented (20%) with lingonberry, blackcurrant, bilberry, raspberry, açai, crowberry, prune or blackberry.Results. The groups receiving a high-fat diet supplemented with lingonberries, blackcurrants, raspberries or bilberries gained less weight and had lower fasting insulin levels than the control group receiving high-fat diet without berries. Lingonberries, and also blackcurrants and bilberries, significantly decreased body fat content, hepatic lipid accumulation, and plasma levels of the inflammatory marker PAI-1, as well as mediated positive effects on glucose homeostasis. The group receiving açai displayed increased weight gain and developed large, steatotic livers. Quercetin glycosides were detected in the lingonberry and the blackcurrant diets.Conclusion. Lingonberries were shown to fully or partially prevent the detrimental metabolic effects induced by high-fat diet. Blackcurrants and bilberries had similar properties, but to a lower degree. We propose that the beneficial metabolic effects of lingonberries could be useful in preventing obesity and related disorders.

scholarly journals Regulating AMPKα and insulin level by Vinegar, Swimming and Refeeding on High-Fat Diet Rats to Rebuild Lipid Homeostasis

2020 ◽  
Author(s):  
Yuan Yang ◽  
Feng Zhang ◽  
Xiao Xiao ◽  
Chunlian Ma ◽  
Hua Liu ◽  
...  
Keyword(s):  
Weight Gain ◽  
High Fat Diet ◽  
Insulin Level ◽  
Diet Group ◽  
Normal Diet ◽  
Lipid Homeostasis ◽  
Control Group ◽  
High Fat ◽  
Better Regulation ◽  
Rice Vinegar

AbstractOur aims were to explore the effects of dietary and behavior interventions on lipometabolism caused by unhealthy high-fat diet and the best method to rebuild lipid homeostasis of this lifestyle. Apart from normal diet rats, 34 rats were fed with high-fat emulsion for 4 weeks before being divided into 4 groups and intervened for another 4 weeks. 8 of them were classified into high-fat control group and 9 were sorted into high-fat diet with rice vinegar group. Meanwhile, 10 were put into high-fat diet with swimming group and 7 were just for refeeding normal diet group. Then the data of body weight was recorded and analyzed. Serum, pancreas, liver, cardiac tissues and epididymis adipose were sampled as required. Indexes of serum were tested by kits. AMPKα, HNF1α, CTRP6 from tissues were detected by western blot. According to our experiments, Swimming and refeeding groups reflected a better regulation on lipid homeostasis mainly by up-regulating the expression of pancreas AMPKα. To be more specific, the refeeding rats showed lower T-CHO (P<0.001) and LDL-C (P<0.05), but higher weight gain (P<0.001),insulin level (P<0.01)and pancreas AMPKα (P<0.01)than high-fat control rats. Compared with rats experimented by swimming or rice vinegar, they showed higher weight gain (P<0.001),insulin level (P<0.01)and HNF1α, but lower of CTRP6. In summary, refeeding diet functioned better in regulating the lipometabolic level after high-fat diet. Whatever approach mentioned above we adopted to intervene, the best policy to keep the balance of lipid homeostasis is to maintain a healthy diet.

scholarly journals Kappa-Carrageenan Inhibited the High-Fat-Diet-Induced Obesity Through Up-Regulating the Hepatic Sirt1 Gene Expression

2021 ◽  
Vol 5 (Supplement_2) ◽  
pp. 503-503
Author(s):  
Zhiji Huang ◽  
Yafang Ma ◽  
Chunbao Li
Keyword(s):  
Gene Expression ◽  
Weight Gain ◽  
Energy Expenditure ◽  
Energy Intake ◽  
High Fat Diet ◽  
The Body ◽  
High Fat ◽  
Diet Induced Obesity ◽  
Sirt1 Gene ◽  
Kappa Carrageenan

Abstract Objectives Kappa-Carrageenan(CGN) is a widely used food additive in the meat industry and a highly viscous soluble dietary fiber which can hardly be fermented. It has been shown to be able to regulate the energy metabolism and inhibit diet-induced obesity. However, the mechanism is not well understood. The purpose of this study is to investigate the mechanisms of κ-carrageenan to inhibit the body weight gain. Methods A high-fat diet incorporated with lard, pork protein and CGN (2% or 4%, w/w) was given to C57BL/6J mice for 90 days. The energy intake and weight changes were measured every three days. After the dietary intervention, mice were sacrificed, liver and epididymal adipose tissues were taken for real-time polymerase chain reaction (RT-qPCR) analysis. Results The CGN in the high-fat diet restricted weight gain by decreasing liver and adipose mass without inhibiting energy intake.  The genes involving energy expenditure such as Acox1, Acadl, CPT-1A and Sirt1 were upregulated in the mice fed with carrageenan. However, the genes responsible for lipid synthesis were not significantly different compared to the diet-induced obese model. Conclusions The anti-obesity effect of the CGN in high-fat diet could be highly related to the enhancement of energy expenditure through up-regulating the downstream genes which promote β-oxidation by increasing the Sirt1 gene expression in liver. Funding Sources Ministry of Science and Technology of the People's Republic of China (10000 Talent Project)

scholarly journals Coenzyme Q10 Attenuates High-fat Diet-induced Non-alcoholic Fatty Liver Disease Through Activation of AMPK Pathway (P06-060-19)

2019 ◽  
Vol 3 (Supplement_1) ◽  
Author(s):  
Chen Ke ◽  
Ling Wenhua
Keyword(s):  
Liver Disease ◽  
Weight Gain ◽  
Fatty Liver ◽  
High Fat Diet ◽  
Fatty Liver Disease ◽  
Control Group ◽  
High Fat ◽  
Alcoholic Fatty Liver ◽  
Ampk Pathway ◽  
Alcoholic Fatty Liver Disease

Abstract Objectives To explore whether CoQ10 has an effect on NAFLD and the potential mechanism. Methods 2.1 Animal studies Thirty male C57BL/6 J mice (four weeks) were randomly distributed into three groups (n = 10): control group (10% Kcal from fat), the high-fat group (60% Kcal from fat), the CoQ10 group (CoQ10 1800 mg/kg, 60% Kcal from fat). The intervention time is 24 weeks. 2.2 Biochemical indicator Serum and liver biochemical markers were detected with appropriate test kits. 2.3 Histopathological evaluation H&E staining, immunohistochemistry and immunofluorescence were used to valuate the degree of NAFLD. Results 3.1 CoQ10 ameliorates high-fat diet-induced weight gain and dyslipidaemia. CoQ10 decreased the weight gain (Fig. 1A). In addition, CoQ10 reduced the high-fat diet-induced subcutaneous and visceral fat. Serum levels of TC and TG decreased in mice fed HFD with supplementation of CoQ10 (Fig. 1C). The level of HDL-c showed an unremarkable increase in mice supplemented with CoQ10, while LDL-c in this group decreased (Fig. 1D). 3.2 CoQ10 inhibited NAFLD induced by high-fat diet. The lipid droplet was reduced in the mice fed CoQ10(Fig. 2A). Analysis of Sirius Red staining showed that hepatic fibrosis was ameliorated in the mice fed CoQ10(Fig. 2B). Staining of macrophage marker, F4/80, and the leukocyte marker, CD45 showed that CoQ10 can alleviate inflammation(Fig.2C, D). CoQ10 also induce the injury of liver(Fig. 2E). 3.3 CoQ10 regulates liver lipid metabolism. CoQ10 reversed the increase of ACC and FAS and reversed the decrease of PPAR-α and CPT-1 both in mRNA and protein expression. CoQ10 could activate AMPK. Conclusions Co Q10 may attenuates high-fat diet-induced non-alcoholic fatty liver disease through activation of AMPK pathway. Funding Sources The key Project of National Natural Science Fund (grant number: 81730090). Supporting Tables, Images and/or Graphs

scholarly journals Hepatic Gene Expression Profile of Lipid Metabolism of Obese Mice after treatment with Anti-obesity Drug

2020 ◽  
Author(s):  
Maha Al-Qeraiwi ◽  
Manar Al-Rashid ◽  
Nasser Rizk ◽  
Abdelrahman El Gamal ◽  
Amena Fadl
Keyword(s):  
Gene Expression ◽  
Fatty Acid ◽  
High Fat Diet ◽  
Fat Metabolism ◽  
Control Group ◽  
Fatty Acid Transport ◽  
Hepatic Gene Expression ◽  
High Fat ◽  
Beta Oxidation ◽  
Hepatic Fat

Obesity is a global disorder with multifactorial causes. The liver plays a vital role in fat metabolism. Disorder of hepatic fat metabolism is associated with obesity and causes fatty liver. High fat diet intake (HFD) to mice causes the development of dietinduced obesity (DIO). The study aimed to detect the effects of anti-obesity drugs (sulforaphane; SFN and leptin) on hepatic gene expression of fat metabolism in mice that were fed HFD during an early time of DIO. Twenty wild types (WT) CD1 male mice aged ten weeks were fed a high fat diet. The mice were treated with vehicle; Veh (control group), and SFN, then each group is treated with leptin or saline. Four groups of treatment were: control group (vehicle + saline), Group 2 (vehicle + leptin), group 3 (SFN + saline), and group 4 (SFN + leptin). Body weight and food intake were monitored during the treatment period. Following the treatments of leptin 24 hour, fasting blood samples and liver tissue was collected, and Total RNA was extracted then used to assess the gene expression of 84 genes involved in hepatic fat metabolism using RT-PCR profiler array technique. Leptin treatment upregulated fatty acid betaoxidation (Acsbg2, Acsm4) and fatty acyl-CoA biosynthesis (Acot6, Acsl6), and downregulated is fatty acid transport (Slc27a2). SFN upregulated acylCoA hydrolase (Acot3) and long chain fatty acid activation for lipids synthesis and beta oxidation (Acsl1). Leptin + SFN upregulated fatty acid beta oxidation (Acad11, Acam) and acyl-CoA hydrolase (Acot3, Acot7), and downregulated fatty acid elongation (Acot2). As a result, treatment of both SFN and leptin has more profound effects on ameliorating pathways involved in hepatic lipogenesis and TG accumulation and lipid profile of TG and TC than other types of intervention. We conclude that early intervention of obesity pa could ameliorate the metabolic changes of fat metabolism in liver as observed in WT mice on HFD in response to anti-obesity treatment.

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