scholarly journals Pyridoxine and Atherosclerosis: Role of Pyridoxine in the Metabolism of Lipids and Glycosaminoglycans in Rats Fed Normal and High Fat, High Cholesterol Diets Containing 16 % Casein

1978 ◽  
Vol 31 (1) ◽  
pp. 7 ◽  
Author(s):  
PL Vijayammal ◽  
PA Kurup
Keyword(s):  
Body Weight ◽  
Normal Diet ◽  
Low Doses ◽  
High Cholesterol ◽  
High Fat ◽  
High Doses

The effect of administration of low and high doses of pyridoxine on the metabolism of lipids and glycosaminoglycans has been studied in rats fed normal and high fat, high cholesterol diets. Low doses of pyridoxine (0'005 mg/100 g body weight) caused increased concentrations of cholesterol and triglycerides in the serum and aorta in animals fed normal and high fat, high cholesterol diets. Administration of high doses of pyridoxine (5'0 mg/100 g body weight) caused decrease in the concentration of these lipids in these tissues except in the case of the aorta in the animals fed a normal diet.

scholarly journals Neuroprotective role of Ginkgobiloba and Rosuvastatin in CA1 region of Hippocampus against high fat diet induced neurotoxicity

2021 ◽  
Vol 8 (3) ◽  
pp. 179-189
Author(s):  
Anil Kumar ◽  
Anand Acharya ◽  
Subhadra Devi Velichety ◽  
Rajesh Vaderav
Keyword(s):  
Body Weight ◽  
Spatial Learning ◽  
High Fat Diet ◽  
Diet Group ◽  
Normal Diet ◽  
High Fat ◽  
Ca1 Region ◽  
Group I ◽  
Branching Points

Diet rich in fat is one of the main risk factor for the development of Alzheimer’s disease. Studies have shown that diet rich in fat disrupts memory and learning. The present study evaluates the ameliorative role of Ginkgobiloba and Rosuvastatin against high fat diet induced neurotoxicity in CA1 (Corona Ammonis) region of hippocampus. Animals were randomly divided into six groups. Group I received normal diet, Group II received high fat diet, Group III & IV were treated with Ginkgobiloba 50mg/kg and 100mg/kg body weight, and Group V & VI were treated with Rosuvastatin 10mg/kg and 20 mg/kg body weight. All the rats were subjected to spatial learning (Morris water maze). Subsequently, rats were sacrificed and brains were removed. Golgi staining was done and CA1 neurons of hippocampus were traced using camera lucida. Dendritic branching points and dendritic intersections were quantified. Lipid profile and Super oxide (SOD) was also estimated.There was enhancement of spatial learning in treatment group rats. Furthermore, a significant increase in dendritic length and branching points was observed in CA1 region along with significant decrease in the Superoxide dismutase in rats treated with higher dose of Ginkgobiloba and Rosuvastatin. Present study concludes that Ginkgobiloba and Rosuvastatin in higher dose have protective role against high fat diet induced neurotoxicity in CA1 region.

scholarly journals Decitabine: A Historical Review of the Development Process of an Epigenetic Drug

2020 ◽  
Vol 7 ◽  
Author(s):  
Cihan Zamur ◽  
Uğur Topal
Keyword(s):  
Development Process ◽  
Historical Review ◽  
Low Doses ◽  
Combination Therapies ◽  
Action Mechanism ◽  
Epigenetic Effect ◽  
Epigenetic Drug ◽  
Patient Responses ◽  
High Doses

Decitabine (5-aza-2p-deoxycytidine) is a hypomethylation agent with a double-action mechanism, these are the reactivation of silenced genes; exhibiting differentiation at low doses and showing cytotoxicity at high doses. Decitabine was used as a classic anticancer drug in the original studies in the 1980s, 1500 to 2500 mg/m2 per cycle was the maximum clinically tolerated dose. The dosage was reassessed after a better understanding of epigenetics in cancer and the role of decitabine in epigenetic (hypomethylation) therapy was obtained, in about 1/20th of the previous doses (i.e., 'optimal biological' doses modulating hypomethylation). It has been found that decitabine (100 to 150 mg / m2 per cycle) can be used in patients with myelodysplastic syndromes (MDS) and other myeloid tumors, with manageable side effects. Combination therapies which amplify the epigenetic effect of decitabine will most likely improve the patient responses and allow it to be used in the treatment of other malignancies.

Abstract 404: NLR Family, Pyrin Domain-containing 3 Knockout Rescues Cardiac Dysfunction Induced by High-fat Diet Feeding

2017 ◽  
Vol 121 (suppl_1) ◽  
Author(s):  
Matthew R Peterson ◽  
Samantha Haller ◽  
Tracy Ta ◽  
Luiza Bosch ◽  
Aspen Smith ◽  
...  
Keyword(s):  
Body Weight ◽  
Blood Glucose ◽  
Inflammatory Response ◽  
Glucose Tolerance ◽  
High Fat Diet ◽  
Fasting Blood Glucose ◽  
Left Ventricular ◽  
Normal Diet ◽  
High Fat ◽  
Pyrin Domain

NLR family, pyrin domain-containing 3 (NLRP3) is a pattern recognition receptor responsible for perpetuating an inflammatory response through production of pro-inflammatory cytokines IL-1β and IL-18. It has been implicated in the sustained inflammatory response in obesity and multiple cardiovascular disease conditions. In order to investigate NLRP3 as a potential therapeutic target in metabolic syndrome, C57BL/6 wild-type (WT) and NLRP3 knockout (NLRP3-\-) mice were fed a normal diet (ND; 12% fat chow) or a high fat diet (HFD; 45% fat chow) for 5 months. At 5 months, echocardiography and glucose tolerance tests (GTTs) were performed. Cardiac function assessed by fractional shortening (FS) was significantly impaired by HFD feeding in the WT group (0.335 HFD vs. 0.456 ND; p<0.05) but not in the NLRP3-\- (0.449 HFD vs. 0.492 ND; p>0.05). FS was higher in NLRP3-\-HFD than in WT-HFD (p<0.05). Two-dimensional analysis shows the FS difference between NLRP3-\-HFD and WT-HFD was primarily explained by the difference in left ventricular end-systolic dimension (0.2716 cm WT vs. 0.1883 cm NLRP3-\-; p<0.05). Glucose tolerance measured by area under the curve (AUC) was significantly impaired by HFD feeding for both WT (23183 ND vs. 57298 HFD; p<0.001) and NLRP3-\- (23197 ND vs. 44626 HFD; p<0.001), but significantly better in the NLRP3-\-HFD than in WT-HFD (p<0.01). HFD feeding increased fasting blood glucose (FBG) for both WT (97.7 mg . dl -1 ND vs. 164.7 mg . dl -1 HFD; p<0.01) and NLRP3-\- (80.50 mg . dl -1 ND vs. 108.8 mg . dl -1 HFD; p<0.05), but significantly less in NLRP3-\- mice (NLRP3-\- vs. WT; p<0.05). For GTTs, body weight was significantly higher in the WT than NLRP3-\- fed HFD (47.93 g vs. 36.5 g; p<0.001). Body weight explained 92% of variation in glucose tolerance (p<0.0001) and 69% of variation in fasting blood glucose (p<0.0001). WT-HFD averaged 1.31X heavier than NLRP3-\-HFD, while the AUC for the IGTT was 1.28X larger for the WT-HFD than NLRP3-\-HFD. Body weights were not significantly different between genotypes at the time of echo. The results suggest that knockout of NLRP3 may be protective against HFD induced cardiovascular dysfunction. A protective effect on glucose tolerance is not strongly supported.

Abstract 17361: How Leptin Harms the Heart in High Fat Diet-Induced Obesity

Circulation ◽  
2020 ◽  
Vol 142 (Suppl_3) ◽  
Author(s):  
Maria Pini
Keyword(s):  
Body Weight ◽  
Mass Loss ◽  
Fat Mass ◽  
High Fat Diet ◽  
Cardiac Fibroblasts ◽  
High Fat ◽  
Wide Range ◽  
Plasma Leptin ◽  
Fat Mass Loss

Introduction: Sedentary lifestyle and excessive calorie intake are risk factors for CVD. We have demonstrated the cardioprotective effect of exercise in aged mice and the critical role of visceral adiposity and its profibrotic secretome in increasing cardiovascular risks in obesity and aging. The association between exercise, lowered plasma leptin and reduced inflammatory leukocytes has been recently shown in patients with atherosclerosis. It remains unclear whether elevated plasma leptin can preserve or alter cardiovascular function in obesity. Methods: We analyzed the effect of high fat diet (HFD) in C57BL/6J male mice on the heart in terms of function, structure, histology and key molecular markers. Two interventions were used: 1) active fat mass loss via exercise (daily swimming) during HFD; 2) passive fat mass loss via surgical removal of the visceral adipose tissue (VAT lipectomy) followed by HFD. Results: HFD increased body weight and adiposity, leading to higher plasma leptin, glucose and insulin levels, compared to control diet (CD) mice. HFD impaired left ventricle (LV) structure (hypertrophy, interstitial fibrosis) and cardiac function (echocardiography, in vivo hemodynamics). Atria of HFD mice had enhanced pro-inflammatory protein production. Exercise reduced circulating leptin levels in HFD mice by 50%, in line with fat mass loss. In contrast, lipectomy reduced visceral fat mass, but body weight, adiposity and plasma leptin did not change. Both exercise and VAT lipectomy improved cardiac contractility, reversed collagen deposition and oxidative stress in HFD mice. Both interventions downregulated LV pro-inflammatory markers. We proved the role of leptin in cardiac remodeling in vitro by incubating primary cardiac fibroblasts with hyperleptinemic plasma from HFD mice. Remarkably, plasma from HFD-EX (exercise) suppressed the fibro-proliferative and pro-inflammatory responses of cardiac fibroblasts. Conclusions: Leptin directly contribute to cardiac fibrosis in obesity via activation and proliferation of cardiac fibroblasts. Understanding how leptin signals to the heart might have implications in a wide range of CVD, potentially helping early stratification and personalized care.

Effects of Zinc Alpha2 Glycoprotein on Lipid Metabolism of Liver in High-Fat Diet-Induced Obese Mice

2017 ◽  
Vol 49 (10) ◽  
pp. 793-800 ◽  
Author(s):  
Guoqiang Fan ◽  
Yu Qiao ◽  
Shixing Gao ◽  
Jun Guo ◽  
Ruqian Zhao ◽  
...  
Keyword(s):  
Body Weight ◽  
Lipid Metabolism ◽  
High Fat Diet ◽  
Recombinant Plasmid ◽  
Diet Group ◽  
Normal Diet ◽  
Hormone Sensitive Lipase ◽  
High Fat ◽  
Hepatic Lipid ◽  
Protein Levels

AbstractZinc alpha2 glycoprotein (ZAG) is a new type of adipokine involved in adipose tissue mobilization, however, little is known about its lipid metabolism effect in liver. Therefore, we investigated the effects of ZAG in the regulation of hepatic lipid accumulation. Mice were randomly divided into two groups; one was fed a normal diet and another was fed a high-fat diet for eight weeks to establish obesity model. After that, the normal diet group was divided into ND (injection of pcDNA3.1) and NDZ (injection of ZAG recombinant plasmid) and the high-fat diet group was divided into HF (injection of pcDNA3.1) and HFZ (injection of ZAG recombinant plasmid). The mice were weighed once per week and injected with plasmid once every three days for eight times. The results showed that body weight and hepatic TG content were decreased dramatically in HFZ group compared with HF group. The stearoyl-CoAdesaturase1 (SCD1) and Acyl-CoA Synthetase-1 (ACSS1) protein levels in HFZ group were significantly decreased. Furthermore, phosphorylated hormone sensitive lipase (P-HSL) was significantly higher in HFZ group. In HFZ group, hepatic fatty acid translocase (CD36) and fatty acids binding protein-1 (FABP1) protein levels were reduced. In addition, the expression of phosphorylated protein kinase A (PPKA) in HFZ group was higher than the HF group. Meanwhile, NDZ group showed significantly decreased body weight and increased P-HSL level though the hepatic TG content showed no significantly changes compared with the ND group. Therefore, we conclude that ZAG may be beneficial for preventing high-fat-diet-induced hepatic lipid metabolic disorders.

TRPC6 deficiency causes increased body weight and glucose intolerance in mice fed a normal diet but does not amplify the obesogenic effect of a high fat diet

2020 ◽  
Vol 34 (S1) ◽  
pp. 1-1
Author(s):  
Zhen Wang ◽  
Lance T. Jaynes ◽  
Sydney P. Moak ◽  
Xuemei Dai ◽  
Yiling Fu ◽  
...  
Keyword(s):  
Body Weight ◽  
Glucose Intolerance ◽  
High Fat Diet ◽  
Normal Diet ◽  
High Fat

Oxidants and antioxidative defense

2002 ◽  
Vol 21 (2) ◽  
pp. 61-62 ◽  
Author(s):  
T Grune
Keyword(s):  
Free Radicals ◽  
Oxygen Free Radicals ◽  
Expression Patterns ◽  
Signal Transduction Pathways ◽  
Low Doses ◽  
The Past ◽  
Small Doses ◽  
Long Time ◽  
High Doses

The role of oxygen free radicals and other oxidants in several diseases has been well established over the past decade. Whereas it was long known that high doses of oxidants may damage or kill cells, the effect of low doses or long-time exposure to small flux rates of oxidants have been the focus of the free radical research until now. Here one has to take into account that most physiological and pathophysiological actions of oxidants and free radicals are based on the permanent action of small doses and flux rates. This includes effects of oxidants on signal transduction pathways and gene expression patterns. Therefore, only a few answers can be given today on the relevance of the effects of low doses of oxidants.

scholarly journals Angelica sinensis Suppresses Body Weight Gain and Alters Expression of the FTO Gene in High-Fat-Diet Induced Obese Mice

2017 ◽  
Vol 2017 ◽  
pp. 1-8 ◽  
Author(s):  
Tao Zhong ◽  
Xiao-Yue Duan ◽  
Hao Zhang ◽  
Li Li ◽  
Hong-Ping Zhang ◽  
...  
Keyword(s):  
Body Weight ◽  
High Fat Diet ◽  
Cpg Island ◽  
Body Weight Gain ◽  
Methylation Status ◽  
Normal Diet ◽  
Angelica Sinensis ◽  
Obese Mouse ◽  
Obese Mice ◽  
High Fat

The root of Angelica sinensis (RAS) is a traditional Chinese medicine used for preventing and treating various diseases. In this study, we assessed RAS supplementation effects on body weight and the FTO gene expression and methylation status in a high-fat-diet (HFD) induced obese mouse model. Female obese mice were divided into groups according to RAS dosage in diet as follows: normal diet, HFD diet (HC), HFD with low-dosage RAS (DL), HFD with medium-dosage RAS (DM), and HFD with high-dosage RAS (DH). After RAS supplementation for 4 weeks, body weight suppression and FTO expression in DH mice were significantly higher than in HC mice, whereas no significant change in FTO expression was detected between DM and DL mice or in their offspring. Bisulfite sequencing PCR (BSP) revealed that the CpG island in the FTO promoter was hypermethylated up to 95.44% in the HC group, 91.67% in the DH group, and 90.00% in the normal diet group. Histological examination showed that adipocytes in the DH group were smaller than those in the HC group, indicating a potential role of RAS in obesity. This study indicated that RAS could ameliorate obesity induced by HFD and that the molecular mechanism might be associated with the expression of the FTO gene.

scholarly journals The Correlation of Weight and Blood Cholesterol Levels of White Rat (Rattus Norvegicus) with High-Fat Diet

2016 ◽  
Vol 3 (3) ◽  
pp. 202-206
Author(s):  
Thatit Nurmawati
Keyword(s):  
Body Weight ◽  
Rattus Norvegicus ◽  
High Fat Diet ◽  
Egg Yolk ◽  
The Body ◽  
Blood Cholesterol ◽  
High Fat ◽  
Data Measurement ◽  
Cholesterol Levels

Cholesterol is an essential substance for the body. The role of cholesterol as material hormones,cell membranare needed by the body. This conditionchanges into a distrubtion if the cholesterollevels in the blood increase. Weight becomes one of this trigger. The consumption of high-fat foodsincrease weight which resulting in the increase of cholesterol cases. The purpose of this study was todetermine the level of correlations between weight and cholesterol levels after being given a high-fatdiet.The study used rats (Rattus norvegicus) sex male, 16 rats with age between 1-2 months. Rats weightrange between 100-150 gr and in healthy conditions. The giving of high-fat diet were in the form ofchicken feed, duck eggs, goat oil, lard and flour for 8 weeks. The data measurement done by scales andmeasuringcholesterol levels through the end of the tail by means of easy touch. The data analysis weredone to understand level of correlation between variables. The presentation of the data used tables. Theresults showed body weight of rats did not change after administration of a high-fat diet. The cholesterolslevels of the subjects were high. Theadministration of high-fat diet from egg yolk dan goat oilcouldincrease the level of cholesterol. There was a correlation between weight and cholesterol levels afterbeing given a high-fat diet (p <0.5). It was needed to repeatthe measurements to determine changes incholesterol levels and other factors that affect thigh blood to cholesterol levels.

scholarly journals Evaluation of voglibose on body weight in rats

2019 ◽  
Vol 8 (6) ◽  
pp. 1159
Author(s):  
Sarita Mulkalwar ◽  
Tanya Gupta ◽  
Vishwanath Kulkarni ◽  
A. V. Tilak ◽  
B. T. Rane ◽  
...  
Keyword(s):  
Diabetes Mellitus ◽  
Type 2 Diabetes ◽  
Type 2 Diabetes Mellitus ◽  
Body Weight ◽  
High Fat Diet ◽  
Normal Diet ◽  
High Fat ◽  
Diet Induced Obesity ◽  
Obesity Drugs

Background: As of 2018, 2.1 billion people nearly 30% of the world’s population are either obese or overweight. Worldwide obesity has nearly tripled since 1975. It is an emerging health problem with major adverse effects on health. It is a risk factor for many chronic diseases but is best known for its role in metabolic syndrome, which can lead to type 2 diabetes mellitus as well as cardiovascular diseases. Anti-obesity drugs are available but have many side effects. Voglibose, an antidiabetic drug, is an alpha glucosidase inhibitor which shows promising results in the reduction of body weight with minimal side effects.Methods: Voglibose (7 mg/kg) was administered to rats fed with normal laboratory chows and high fat diet to see its effect on body weight, body mass index, abdominal and thoracic circumference, and lipid profile at the end of 12 weeks.Results: Administration of voglibose significantly reduced food consumption, feed efficiency and increase in body weight induced by high fat diet in rats. Rats fed on normal diet also showed reductions in the same parameters, suggesting its weight lowering effect. Reductions in the anthropometric measurements, hypolipidemic effects and glucose lowering effects were also observed.Conclusions: Voglibose prevented high fat diet-induced obesity and improvement in metabolic profile, which ultimately has systemic effects on body weight in rats. Further studies are needed to see its potential therapeutic use in obese patients with type 2 diabetes mellitus, and related complications.

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