scholarly journals Exercise or Dietotherapy Is Not Better than Returning to a Regular Diet to Rebuild Lipid Homeostasis of Rats

2021 ◽  
Vol 2021 ◽  
pp. 1-9
Author(s):  
Yuan Yang ◽  
Nan-Jun Xu ◽  
Jia-Hui Li ◽  
Ling-Feng Zeng ◽  
Gui-Hong Liang ◽  
...  
Keyword(s):  
Weight Gain ◽  
High Fat Diet ◽  
Insulin Level ◽  
Normal Diet ◽  
Lipid Homeostasis ◽  
Control Group ◽  
High Fat ◽  
Serum Samples ◽  
Better Regulation ◽  
Rice Vinegar

Our aim was to explore the effects of dietary and behavior interventions on lipometabolism caused by an 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 and then intervened for another 4 weeks. Eight 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 in swimming group, and 7 were just for refeeding normal diet group. Then, the data of body weight was recorded and analyzed. Indexes of serum samples were tested by kits. AMPKα, HNF1α, and CTRP6 in pancreas, liver, cardiac, and epididymis adipose tissues were detected by western blot. According to our experiments, swimming and refeeding groups reflected a better regulation on lipid homeostasis mainly by upregulating 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 intervened 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 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.

The effectiveness comparisons of eugenosedin-A, glibenclamide and pioglitazone on diabetes mellitus induced by STZ/NA and high-fat diet in SHR

2021 ◽  
Author(s):  
Hui-Li Lin ◽  
Pei-Wen Cheng ◽  
Yi-Chen Tu ◽  
Bor-Chun Yeh ◽  
Bin-Nan Wu ◽  
...  
Keyword(s):  
Diabetes Mellitus ◽  
High Fat Diet ◽  
Lipid Synthesis ◽  
Normal Diet ◽  
Lipid Homeostasis ◽  
Control Group ◽  
Protective Effects ◽  
High Fat ◽  
Effective Agent ◽  
Treatment Groups

Abstract Objectives Eugenosedin-A (Eu-A), an adrenergic and serotonergic antagonist, is known to have anti-metabolic syndrome effects. In this study, we evaluated its protective effects against diabetes mellitus (DM) in spontaneous hypertensive rats (SHR) and compared it with two anti-diabetes medications, glibenclamide (Gli) and pioglitazone (Pio). Methods We divided 10-week-old SHRs into five groups: a control group fed a normal diet; an untreated DM group induced by injecting the SHRs with STZ/NA and feeding them a high-fat diet (HFD); and three treated groups (after giving STZ/NA and HFD) gavage given with Eu-A, Gli or Pio (5 mg/kg per day) for 4 weeks. Key findings The untreated DM group weighed less and had hyperglycaemia, hypoinsulinemia and hyperlipidemia. They were also found to have aberrant glucose-dependent insulin pathways, glucose metabolism and lipid synthesis proteins, while the controls did not. Eu-A, Gli and Pio ameliorated the above biochemical parameters in the treatment groups. Eu-A and Pio, but not Gli, improved hypertension and tachycardia. Conclusions Taken together, Eu-A ameliorated DM, hypertension and tachycardia by improving glucose, lipid homeostasis and anti-adrenergic, serotonergic activities. We concluded that Eu-A could be used in the development of an effective agent for controlling DM and its complications.

Particular Matter of Motor Vehicle Exposure and High-Fat Diet Effects on Kidney Histopathology, Creatinine, and Malondialdehyde (MDA) Levels in Wistar Rats

2021 ◽  
Vol 5 (3) ◽  
pp. 124-128
Author(s):  
Rizka Veni ◽  
Awal Prasetyo ◽  
Muflihatul Muniroh
Keyword(s):  
High Fat Diet ◽  
Wistar Rats ◽  
Motor Vehicle ◽  
Histopathological Change ◽  
Normal Diet ◽  
Control Group ◽  
High Fat ◽  
Control Group Design ◽  
Treatment Groups ◽  
Significant Difference

This study aims to analyze the effect of combination of motor vehicle particular matter exposure and high-fat diet in kidney histopathology, creatinine levels, and MDA levels in Wistar rats. This study used a posttest-only control group design. Eighteen healthy male Wistar rats were divided into three groups. The intervention groups received motor vehicle fume exposure for 100 s with normal diet (X1) or high-fat diet (X2), and the control group received no exposure (C). Data analysis was processed with a SPSS 25.0 computer program by using the one-way ANOVA test followed by post hoc LSD. The degree of kidney histopathological damage showed significant differences between the X1 and X2 groups when compared with the control group (p < 0.05). The results of the creatinine level examination found a significant difference between the X2 and C groups (p < 0.05) and the treatment groups X1 and X2 (p < 0.05). The results of kidney MDA level examination showed a significant difference between the treatment groups (X1 and X2) and the control group (p < 0.05). The combination of particular matter of motor vehicle fumes exposure and high-fat diet could induce kidney damage through histopathological change and increased creatinine levels and kidney MDA levels in Wistar rats.

Abstract 657: A New Translational Model of Hypercholesterolemia and Atherosclerosis: Effect of Statins on LDLR KO Miniature Swine

2014 ◽  
Vol 34 (suppl_1) ◽  
Author(s):  
Dale E Mais ◽  
Thomas Vihtelic ◽  
Chidozie Amuzie ◽  
Steven Denham ◽  
John R Swart ◽  
...  
Keyword(s):  
High Fat Diet ◽  
Clinical Chemistry ◽  
Small Animal ◽  
Normal Diet ◽  
Large Animal Model ◽  
Control Group ◽  
Large Animal ◽  
Wild Type ◽  
High Fat ◽  
Miniature Swine

Small animal models of atherosclerosis are commonly used in drug studies; however, the results often fail to translate into the clinic. A large animal model that more accurately reflects the human disease is needed. We recently developed a transgenic Yucatan pig model in which the LDL receptor (LDLR) gene is knocked out. Five groups of Yucatan pigs (N=4 per group), either wild type (LDLR+/+) or heterozygote (LDLR+/-) were fed a normal diet or a high fat diet for a six month period. One of the heterozygote/high fat diet groups in addition received a daily dose of a statin (atorvastatin) at 3 mg/kg. Every two weeks during the study a variety of clinical chemistry parameters were measured. At study termination, select arteries were collected, stained for lipid deposits and quantitated. In addition, sections of these arteries were prepared for immunohistochemistry to detect selected markers of macrophage infiltration into the atherosclerotic plaques. As expected, pigs fed a high fat diet gained significantly more weight at six months whether they were wild type or LDLR+/-. Atorvastatin appeared to attenuate this weight gain. There were significant increases in total cholesterol, HDL and LDL in pigs fed the high fat diet compared to their corresponding control group. The group receiving the atorvastatin had reduced values of these parameters compared to controls showing that a statin had a beneficial effect on lipid levels even in a high fat diet scenario. VLDL levels were not affected but there were triglyceride changes across the groups. Liver function was unchanged based on total bilirubin and AST while ALT measurements were altered in some of the groups. Immunohistochemistry and histomorphometry was performed on some arteries. Atorvastatin-induced amelioration of hypercholesterolemia in this model underscores its translational utility.

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.

scholarly journals Establishment of Type 2 Diabetes Mellitus Models Using High-Fat Diet and STZ in Bama Minipigs

2021 ◽  
Author(s):  
Yuqiong Zhao ◽  
Miaomiao Niu ◽  
Jia Yunxiao ◽  
Yuan Jifang ◽  
Xiang Lei ◽  
...  
Keyword(s):  
High Fat Diet ◽  
Low Dose ◽  
Normal Diet ◽  
Large Animal Model ◽  
Control Group ◽  
Large Animal ◽  
High Cholesterol ◽  
High Fat ◽  
Accelerated Atherosclerosis ◽  
Atherosclerotic Lesions

Abstract BackgroundIn the past 20 years, the number of adults with diabetes has tripled. For most of the researches are often conducted in rodent T2DM models, and effective drugs developed have low clinical conversion efficiency. Therefore, it is urgent to establish a large animal model to explore the pathogenesis of T2DM and formulate disease prevention and control strategies. MethodsThis study was designed to establish and validate a T2DM model in minipigs with notable hyperglycemia using a high-fat diet and low-dose streptozotocin (STZ)，and examined the influence of STZ infusion time, the difference between a high-fat diet and a high-cholesterol and high-fat diet, and the atherosclerotic lesions accelerated by diabetes. Male Bama minipigs (n=24) were randomly divided into 5 groups; the control group was fed with normal diet for 9 months; STZ+HFD group and STZ+HCFD group were infused with 90 mg/kg STZ and then fed with a high-fat diet or high-cholesterol and high-fat diet for 9 months, respectively; HFD + STZ group and HCFD + STZ group were fed with a high-fat diet or high-cholesterol and high-fat diet, respectively, for nine months (after 3 months, pigs were injected with 90 mg/kg STZ intravenously). ResultsThe results showed the serum glucose concentrations were within the normal range in all groups except for HFD + STZ group and HCFD + STZ group. Animals fed with a high-fat diet for 9 months, did not develop apparent atherosclerotic lesions; nevertheless, atherosclerotic lesions were seen in animals fed with high-cholesterol and high-fat diets. Moreover, hyperglycemia accelerated atherosclerosis (lesions on the intimal surface of the abdominal aorta, 0.44±0.29 vs. 0.28±0.26) in minipigs. ConclusionsHigh-fat/high-cholesterol and high-fat diet combined with low-dose streptozotocin successfully established T2DM in minipigs. High-fat diet could not induce apparent atherosclerosis lesions but high-cholesterol and high-fat diet could during the nine months period. Hyperglycemia accelerated atherosclerosis in the minipigs.

scholarly journals A Combination of Apple Vinegar Drink with Bacillus coagulans Ameliorates High Fat Diet-Induced Body Weight Gain, Insulin Resistance and Hepatic Steatosis

Nutrients ◽  
2020 ◽  
Vol 12 (9) ◽  
pp. 2504
Author(s):  
Raquel Urtasun ◽  
Joana Díaz-Gómez ◽  
Miriam Araña ◽  
María José Pajares ◽  
María Oneca ◽  
...  
Keyword(s):  
Body Weight ◽  
Weight Gain ◽  
Food Intake ◽  
High Fat Diet ◽  
Body Weight Gain ◽  
Bacillus Coagulans ◽  
Normal Diet ◽  
High Fat ◽  
Blood Biochemical ◽  
Traditional Remedy

Obesity is a worldwide epidemic characterized by excessive fat accumulation, associated with multiple comorbidities and complications. Emerging evidence points to gut microbiome as a driving force in the pathogenesis of obesity. Vinegar intake, a traditional remedy source of exogenous acetate, has been shown to improve glycemic control and to have anti-obesity effects. New functional foods may be developed by supplementing traditional food with probiotics. B. coagulans is a suitable choice because of its resistance to high temperatures. To analyze the possible synergic effect of Vinegar and B. coagulans against the metabolic alterations induced by a high fat diet (HFD), we fed twelve-week-old C57BL/6 mice with HFD for 5 weeks after 2 weeks of acclimation on a normal diet. Then, food intake, body weight, blood biochemical parameters, histology and liver inflammatory markers were analyzed. Although vinegar drink, either alone or supplemented with B. coagulans, reduced food intake, attenuated body weight gain and enhanced glucose tolerance, only the supplemented drink improved the lipid serum profile and prevented hepatic HFD-induced overexpression of CD36, IL-1β, IL-6, LXR and SREBP, thus reducing lipid deposition in the liver. The beneficial properties of the B. coagulans-supplemented vinegar appear to be mediated by a reduction in insulin and leptin circulating levels.

scholarly journals MON-642 Genetic Knockout of Intestinal Hexokinase Domain-Containing Protein 1 Affects Whole-Body Glycemic Control and Triglyceride Metabolism

2020 ◽  
Vol 4 (Supplement_1) ◽  
Author(s):  
Joseph Louis Zapater ◽  
Wasim Khan ◽  
Brian T Layden
Keyword(s):  
Glycemic Control ◽  
Olive Oil ◽  
High Fat Diet ◽  
Normal Diet ◽  
Whole Body ◽  
Lipid Homeostasis ◽  
Glucose Load ◽  
Wild Type ◽  
High Fat ◽  
Glucose And Lipid Homeostasis

Abstract Hexokinase domain-containing protein 1 (HKDC1) is a recently discovered putative fifth hexokinase that is widely expressed in a variety of human and mouse tissues. Previous work indicate that HKDC1 is important for whole-body glucose homeostasis and utilization in pregnancy and aging, and suggest roles for HKDC1 in nonalcoholic fatty liver disease development and progression of hepatocellular carcinoma. Prior work in the lab further showed that global heterozygous-deleted HKDC1 mice exhibit blunted uptake of triglycerides following an olive oil bolus compared to wild-type mice, suggesting a role for intestinal HKDC1 expression in intestinal lipid metabolism (unpublished results). To specifically study the significance of intestinal HKDC1 on whole-body glucose and lipid homeostasis, we utilized Cre-mediated recombination of HKDC1 in which Cre was expressed under the control of the villin gene promoter, creating a mouse model in which HKDC1 expression is specifically deleted in the intestinal epithelium. Quantitative RT-PCR data confirmed the knockout of HKDC1 within the mouse intestine in young and aged mice, while HKDC1 expression in other tissues was comparable to wild-type mice. Next, intestinal HKDC1 knockout mice and their wild-type littermate controls were either maintained on a normal diet or were switched to a high fat diet at 6 weeks of age to simulate the state of impaired glucose tolerance, and the effects of intestinal HKDC1 on glucose and lipid homeostasis were analyzed between 28-34 weeks of age. Mice fed a normal diet did not exhibit any differences in serum glucose or triglyceride during oral/intraperitoneal glucose tolerance tests or oral olive oil bolus, respectively, regardless of intestinal HKDC1 status. Interestingly, mice lacking intestinal HKDC1 that were on a high fat diet demonstrated improved overall glycemic control compared to wild-type mice after the administration of an oral glucose load, all while there were no changes in insulin levels, gluconeogenesis or insulin tolerance related to HKDC1 status. Additionally, introduction of an intraperitoneal glucose load to mice fed a high fat diet did not alter glucose control in the presence or absence of intestinal HKDC1. However, high fat diet-fed mice lacking intestinal HKDC1 did not have a significant increase in serum triglyceride following an oral olive oil bolus, while their stool fat and triglyceride content were comparable to wild-type. Collectively, these data indicate that intestinal HKDC1 has important roles in glucose and triglyceride metabolism within the intestinal epithelium, and further suggest a role in whole-body glucose homeostasis and in the development of insulin resistance and diabetes.

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

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