Glucose and lipid metabolism disorders in the chickens with dexamethasone-induced oxidative stress

2017 ◽  
Vol 102 (2) ◽  
pp. e706-e717 ◽  
Author(s):  
Z.-P. Lv ◽  
Y.-Z. Peng ◽  
B.-B. Zhang ◽  
H. Fan ◽  
D. Liu ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Lipid Metabolism ◽  
Glucose And Lipid Metabolism ◽  
Lipid Metabolism Disorders

Effects of VO2 nanoparticles on human liver HepG2 cells: Cytotoxicity, genotoxicity, and glucose and lipid metabolism disorders

NanoImpact ◽  
2021 ◽  
Vol 24 ◽  
pp. 100351
Author(s):  
Jia-Bei Li ◽  
Wen-Song Xi ◽  
Shi-Ying Tan ◽  
Yuan-Yuan Liu ◽  
Hao Wu ◽  
...  
Keyword(s):  
Lipid Metabolism ◽  
Hepg2 Cells ◽  
Human Liver ◽  
Glucose And Lipid Metabolism ◽  
Lipid Metabolism Disorders

SEX DIFFERENCES OF CARBOHYDRATE AND LIPID METABOLISM IMPAIRMENT IN RATS WITH TYPE 2 DIABETES MELLITUS

2018 ◽  
Vol 64 (2) ◽  
pp. 39-45 ◽  
Author(s):  
Nataliia Gorbenko ◽  
Oleksii Borikov ◽  
Olha Ivanova ◽  
K. V. Taran ◽  
T. S. Litvinova ◽  
...  
Keyword(s):  
Diabetes Mellitus ◽  
Type 2 Diabetes ◽  
Type 2 Diabetes Mellitus ◽  
Body Weight ◽  
Lipid Metabolism ◽  
Female Rats ◽  
Glucose And Lipid Metabolism ◽  
Carbohydrate And Lipid Metabolism ◽  
Lipid Metabolism Disorders

A sex difference of carbohydrate and lipid metabolism disorders in rats with type 2 diabetes has been studied. It was established that type 2 diabetes leads to a more pronounced deterioration in carbohydrate toleranceand insulin sensitivity in males compared to female rats, but the sex doesn’t affect basal glycemia and fructosamine levels. It was found that the increase of body weight and visceral fat in rats with type 2 diabetes is moremanifested in females than in males. It has been determined that hypertriglyceridemia is higher in diabeticmales compared to diabetic females, and the level of common lipids in the liver, both intact females and femaleswith type 2 diabetes, is lower than that of the males. The obtained results indicate a more expressive impairment of glucose and lipid metabolism in males compared to females with type 2 diabetes

Chlorpyrifos exposure induces lipid metabolism disorder at the physiological and transcriptomic levels in larval zebrafish

2019 ◽  
Vol 51 (9) ◽  
pp. 890-899
Author(s):  
Xiaoyu Wang ◽  
Jiajie Zhou ◽  
Manlu Shen ◽  
Jiayan Shen ◽  
Xinyue Zhang ◽  
...  
Keyword(s):  
Lipid Metabolism ◽  
Acid Synthesis ◽  
Treated Group ◽  
Heart Tissue ◽  
Lipid Metabolism Disorder ◽  
Larval Zebrafish ◽  
Metabolism Disorder ◽  
Glucose And Lipid Metabolism ◽  
Lipid Metabolism Disorders ◽  
Cellular Apoptosis

Abstract Chlorpyrifos (CPF) is a widely used insecticide in pest control, and it can affect aquatic animals by contaminating the water. In this study, larval zebrafish were exposed to CPF at concentrations of 30, 100 and 300 μg/l for 7 days. In the CPF-treated group, lipid droplet accumulation was reduced in larval zebrafish. The levels of triglyceride (TG), total cholesterol (TC), and pyruvate were also decreased after CPF exposure. Cellular apoptosis were significantly increased in the heart tissue after CPF exposure compared with the control. Transcription changes in cardiovascular genes were also observed. Through transcriptome analysis, we found that the transcription of 465 genes changed significantly, with 398 upregulated and 67 downregulated in the CPF-treated group, indicating that CPF exposure altered the transcription of genes. Among these altered genes, a number of genes were closely related to the glucose and lipid metabolism pathways. Furthermore, we also confirmed that the transcription of genes related to fatty acid synthesis, TC synthesis, and lipogenesis were significantly decreased in larval zebrafish after exposure to CPF. These results indicated that CPF exposure induced lipid metabolism disorders associated with cardiovascular toxicity in larval zebrafish.

scholarly journals Oral Bisphenol A Worsens Liver Immune-Metabolic and Mitochondrial Dysfunction Induced by High-Fat Diet in Adult Mice: Cross-Talk between Oxidative Stress and Inflammasome Pathway

Antioxidants ◽  
2020 ◽  
Vol 9 (12) ◽  
pp. 1201
Author(s):  
Claudio Pirozzi ◽  
Adriano Lama ◽  
Chiara Annunziata ◽  
Gina Cavaliere ◽  
Clara Ruiz-Fernandez ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Lipid Metabolism ◽  
Bisphenol A ◽  
Mitochondrial Dysfunction ◽  
Cross Talk ◽  
High Fat Diet ◽  
Additional Risk Factor ◽  
High Fat ◽  
Endocrine Disrupting Chemical ◽  
Glucose And Lipid Metabolism

Lines of evidence have shown the embryogenic and transgenerational impact of bisphenol A (BPA), an endocrine-disrupting chemical, on immune-metabolic alterations, inflammation, and oxidative stress, while BPA toxic effects in adult obese mice are still overlooked. Here, we evaluate BPA’s worsening effect on several hepatic maladaptive processes associated to high-fat diet (HFD)-induced obesity in mice. After 12 weeks HFD feeding, C57Bl/6J male mice were exposed daily to BPA (50 μg/kg per os) along with HFD for 3 weeks. Glucose tolerance and lipid metabolism were examined in serum and/or liver. Hepatic oxidative damage (reactive oxygen species, malondialdehyde, antioxidant enzymes), and mitochondrial respiratory capacity were evaluated. Moreover, liver damage progression and inflammatory/immune response were determined by histological and molecular analysis. BPA amplified HFD-induced alteration of key factors involved in glucose and lipid metabolism, liver triglycerides accumulation, and worsened mitochondrial dysfunction by increasing oxidative stress and reducing antioxidant defense. The exacerbation by BPA of hepatic immune-metabolic dysfunction induced by HFD was shown by increased toll-like receptor-4 and its downstream pathways (i.e., NF-kB and NLRP3 inflammasome) amplifying inflammatory cytokine transcription and promoting fibrosis progression. This study evidences that BPA exposure represents an additional risk factor for the progression of fatty liver diseases strictly related to the cross-talk between oxidative stress and immune-metabolic impairment due to obesity.

scholarly journals Decabromodiphenyl ether causes insulin resistance and glucose and lipid metabolism disorders in mice

2021 ◽  
Vol 12 (8) ◽  
pp. 1267-1281
Author(s):  
Ayiguli Alimu ◽  
Haiqiemuhan Abudureman ◽  
Yong-Zhi Wang ◽  
Mei-Yan Li ◽  
Jia-Sui Wang ◽  
...  
Keyword(s):  
Insulin Resistance ◽  
Lipid Metabolism ◽  
Decabromodiphenyl Ether ◽  
Glucose And Lipid Metabolism ◽  
Lipid Metabolism Disorders

scholarly journals Crtc1 Deficiency Causes Obesity Potentially via Regulating PPARγ Pathway in White Adipose

2021 ◽  
Vol 9 ◽  
Author(s):  
Yimeng Hu ◽  
Jian Lv ◽  
Yu Fang ◽  
Qiang Luo ◽  
Yuan He ◽  
...  
Keyword(s):  
Adipose Tissue ◽  
Lipid Metabolism ◽  
Direct Interaction ◽  
Underlying Mechanism ◽  
Fat Accumulation ◽  
Glucose And Lipid Metabolism ◽  
White Adipocytes ◽  
Transcription Cofactor ◽  
Lipid Metabolism Disorders ◽  
Normal Feeding

Obesity is characterized by excessive fat accumulation and associated with glucose and lipid metabolism disorders. Crtc1, a transcription cofactor regulating CREB activity, has been involved in the pathogenesis of metabolic syndrome; however, the underlying mechanism remains under debate. Here we generated a Crtc1–/– mouse line using the CRISPR/Cas9 system. Under normal feeding conditions, Crtc1–/– mice exhibited an obese phenotype resultant from the abnormal expansion of the white adipocytes. The development of obesity in Crtc1–/– mice is independent of alterations in food intake or energy expenditure. Moreover, Crtc1–/– mice were more prone to insulin resistance and dyslipidemia, as evidenced by higher levels of plasma glucose, insulin and FABP4 than wildtype mice. Transcriptome analysis in liver and epididymal white adipose tissue (eWAT) showed that the fat accumulation caused by Crtc1 deletion was mainly related to lipid metabolism in adipose tissue, but not in liver. GSEA and KEGG analysis identified PPAR pathway to be of the highest impact on lipid metabolism in eWAT. This regulation was independent of a direct interaction between CRTC1 and PPARγ. Our findings demonstrate a crucial role of Crtc1 in regulating lipid metabolism in adipose during development, and provide novel insights into obesity prevention and therapeutics.

scholarly journals Chronic folate deficiency induces glucose and lipid metabolism disorders and subsequent cognitive dysfunction in mice

PLoS ONE ◽  
2018 ◽  
Vol 13 (8) ◽  
pp. e0202910 ◽  
Author(s):  
Mei Zhao ◽  
Man Man Yuan ◽  
Li Yuan ◽  
Li Li Huang ◽  
Jian Hong Liao ◽  
...  
Keyword(s):  
Lipid Metabolism ◽  
Cognitive Dysfunction ◽  
Folate Deficiency ◽  
Glucose And Lipid Metabolism ◽  
Lipid Metabolism Disorders

Glucose and lipid metabolism disorders in children and adolescents with spinal muscular atrophy types 2 and 3

2021 ◽  
Vol 31 (4) ◽  
pp. 291-299
Author(s):  
Stefan A. Djordjevic ◽  
Vedrana Milic-Rasic ◽  
Vesna Brankovic ◽  
Ana Kosac ◽  
Ivana Dejanovic-Djordjevic ◽  
...  
Keyword(s):  
Lipid Metabolism ◽  
Spinal Muscular Atrophy ◽  
Children And Adolescents ◽  
Muscular Atrophy ◽  
Glucose And Lipid Metabolism ◽  
Lipid Metabolism Disorders

scholarly journals The effect of thyroxin on hepatic redox equilibrium and lipid metabolism in rats treated with doxorubicin

2014 ◽  
Vol 27 (4) ◽  
pp. 220-223
Author(s):  
Bartosz Czuba ◽  
Magdalena Fituch ◽  
Slawomir Mandziuk ◽  
Barbara Jodlowska-Jedrych ◽  
Wlodzimierz Matysiak ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Lipid Metabolism ◽  
Ketone Bodies ◽  
Cell Metabolism ◽  
Redox Status ◽  
Ros Generation ◽  
Redox Equilibrium ◽  
Lipid Metabolism Disorders ◽  
Liver Homogenates ◽  
Blood Ketone Bodies

Abstract The main side effects of the administration of doxorubicin, a widely used anticancer drug, is the generation of a reactive oxygen species (ROS) in normal cells. As a result, redox disorders and secondary oxidative stress are developed. Doxorubicin ROS generation is attributed to enzymes that are produced abundantly in hepatocytes. Oxidative stress has been a well-known risk factor of doxorubicin-related toxicity. However, in addition, according to the data collected in the last decade, changes in thyroxin status can propagate ROS generation, and, thus, initiate the doxorubicin hepatic effect. Moreover, both compounds have an impact on the cell metabolism. The aim of the study was to verify the thesis that thyroxin can modulate the effect of doxorubicin with regard to redox status and lipid metabolism disorders. In our work, we determined the ratio of NADP+/ NADPH and NAD+/NADH in liver homogenates, blood ketone bodies and triglycerides in the liver and blood in rats treated with doxorubicin and thyroxin. Our results indicate that thyroxin has an insignificant effect on NAD+/NADH, NADP+/NADPH ratios and on hepatic and blood triglycerides. Moreover, thyroxin administration normalized the level of blood ketone bodies that was disturbed by doxorubicin.

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