scholarly journals Quercetin Improves Glucose and Lipid Metabolism of Diabetic Rats: Involvement of Akt Signaling and SIRT1

2017 ◽  
Vol 2017 ◽  
pp. 1-10 ◽  
Author(s):  
Jing Peng ◽  
Qingde Li ◽  
Keye Li ◽  
Li Zhu ◽  
Xiaoding Lin ◽  
...  
Keyword(s):  
Diabetes Mellitus ◽  
Lipid Metabolism ◽  
Fasting Blood Glucose ◽  
Akt Signaling ◽  
Hepatic Glycogen ◽  
High Dose ◽  
Lipid Metabolism Disorder ◽  
Metabolism Disorder ◽  
Glucose And Lipid Metabolism ◽  
Quercetin Treatment

Glucose and lipid metabolism disorder in diabetes mellitus often causes damage to multiple tissues and organs. Diabetes mellitus is beneficially affected by quercetin. However, its concrete mechanisms are yet to be fully elucidated. In our study, diabetes was induced in Sprague-Dawley rats by STZ injection. The rats were randomly divided into normal control, diabetic model, low-dose quercetin treatment, high-dose quercetin treatment, and pioglitazone treatment groups. Fasting blood glucose was collected to evaluate diabetes. Immunohistochemistry and fluorometric assay were performed to explore SIRT1. Akt levels were measured through immunoprecipitation and Western blot. After 12 weeks of quercetin treatment, the biochemical parameters of glucose and lipid metabolism improved to varying degrees. Hepatic histomorphological injury was alleviated, and hepatic glycogen content was increased. The expression and activity of hepatic SIRT1 were enhanced, and Akt was activated by phosphorylation and deacetylation. These results suggested that the beneficial effects of quercetin on glucose and lipid metabolism disorder are probably associated with the upregulated activity and protein level of SIRT1 and its influence on Akt signaling pathway. Hence, quercetin shows potential for the treatment of glucose and lipid metabolism disorder in diabetes mellitus.

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.

Angelica sinensis polysaccharide regulates glucose and lipid metabolism disorder in prediabetic and streptozotocin-induced diabetic mice through the elevation of glycogen levels and reduction of inflammatory factors

2015 ◽  
Vol 6 (3) ◽  
pp. 902-909 ◽  
Author(s):  
Kaiping Wang ◽  
Peng Cao ◽  
Weizhi Shui ◽  
Qiuxiang Yang ◽  
Zhuohong Tang ◽  
...  
Keyword(s):  
Lipid Metabolism ◽  
Inflammatory Factors ◽  
Angelica Sinensis ◽  
Diabetic Mice ◽  
Lipid Metabolism Disorder ◽  
Metabolism Disorder ◽  
Glucose And Lipid Metabolism

Hypoglycemic and hypolipidemic effects of ASP in prediabetic and T2DM mice.

scholarly journals The role of miR-320 in glucose and lipid metabolism disorder-associated diseases

2021 ◽  
Vol 17 (2) ◽  
pp. 402-416
Author(s):  
Hengzhi Du ◽  
Yanru Zhao ◽  
Zhongwei Yin ◽  
Dao Wen Wang ◽  
Chen Chen
Keyword(s):  
Lipid Metabolism ◽  
Lipid Metabolism Disorder ◽  
Associated Diseases ◽  
Metabolism Disorder ◽  
Glucose And Lipid Metabolism

scholarly journals Tangduqing Granules Attenuate Insulin Resistance and Abnormal Lipid Metabolism through the Coordinated Regulation of PPARγ and DGAT2 in Type 2 Diabetic Rats

2019 ◽  
Vol 2019 ◽  
pp. 1-10
Author(s):  
Qinghua Zhang ◽  
Yingying Huang ◽  
Xiaojin Li ◽  
Hongyi Liu ◽  
Baichuan He ◽  
...  
Keyword(s):  
Insulin Resistance ◽  
Type 2 Diabetes ◽  
Lipid Metabolism ◽  
Insulin Sensitivity ◽  
Fasting Blood Glucose ◽  
Diabetic Rat ◽  
Lipid Metabolism Disorder ◽  
Metabolism Disorder ◽  
Type 2 Diabetic

Insulin resistance (IR) is a vital hallmark of type 2 diabetes mellitus, which is characterized by an impaired ability of insulin to promote glucose uptake and utilization. Lipid deposition is closely associated with impaired insulin sensitivity. PPARγ plays an important role in glucose homeostasis, adipocyte differentiation, and insulin sensitivity. Likewise, DGAT2 also exerts a crucial role in integrating carbohydrate and lipid metabolism in the liver. The present study is aimed at evaluating a Chinese medicinal formula, Tangduqing granules (TDQ), with multifaceted actions against lipid and glucose metabolism disorder and IR of type 2 diabetes. An animal model of type 2 diabetes was developed by high-fat diet feeding plus low-dose streptozotocin injection. After oral administration of TDQ for 5 weeks, the effects on glucose and lipid metabolism and the underlying mechanism were evaluated by biochemical, histological, RT-PCR, and western blotting methods. The results showed that TDQ decreased fasting blood glucose, ameliorated glucose tolerance, and improved IR. Besides, TDQ regulated hyperlipidemia symptoms, decreased serum lipid levels and liver TG, and reduced hepatic steatosis in a type 2 diabetic rat model. Furthermore, TDQ reversed diabetes-induced decrease in the mRNA and protein expression of PPARγ and elevation in the mRNA and protein levels of DGAT2 in the liver. In addition, we showed that interference of TDQ ameliorated palmitate-induced glucose and lipid metabolic abnormalities in HepG2 cells. TDQ are, therefore, a potential Chinese medicinal formula that relieves IR and lipid metabolism disorder might be through promotion of PPARγ and decrease of DGAT2 expression.

P0605 LIPID METABOLISM DISORDER AT WOMEN WITH GESTATIONAL DIABETES MELLITUS IN KOSOVA

2009 ◽  
Vol 20 ◽  
pp. S199
Author(s):  
Merita Emini Sadiku ◽  
Luljeta Begolli ◽  
Shqiponja Ponosheci ◽  
Nadije Morina ◽  
Ardiana Perjuci ◽  
...  
Keyword(s):  
Diabetes Mellitus ◽  
Lipid Metabolism ◽  
Gestational Diabetes ◽  
Gestational Diabetes Mellitus ◽  
Lipid Metabolism Disorder ◽  
Metabolism Disorder

scholarly journals Renal Injury by SARS-CoV-2 Infection: A Systematic Review

2020 ◽  
pp. 1-11
Author(s):  
Mo Wang ◽  
Huaying Xiong ◽  
Han Chen ◽  
Qiu Li ◽  
Xiong Zhong Ruan
Keyword(s):  
Lipid Metabolism ◽  
Immune Tolerance ◽  
Renal Injury ◽  
Thrombus Formation ◽  
Renal Involvement ◽  
Systemic Effects ◽  
Lipid Metabolism Disorder ◽  
Immune Clearance ◽  
Metabolism Disorder ◽  
Glucose And Lipid Metabolism

<b><i>Background:</i></b> SARS-CoV-2 infection can cause renal involvement, and severe renal dysfunction is more common among patients with chronic comorbid conditions, especially patients with chronic kidney disease. Angiotensin-converting enzyme 2 (ACE2) has been proven to be the major receptor of SARS-CoV-2 in kidneys, suggesting that ACE2-related changes may be involved in renal injury during the infection. In this review, we systematically reviewed the literature to summarize findings on the mechanism of renal injury caused by SARS-COV-2 infection, in order to provide a theoretical basis for renal protection therapy. <b><i>Summary:</i></b> For patients with SARS-CoV-2 infection, renal injury mainly manifests as increased serum creatinine, variable degrees of proteinuria and hematuria, and radiographic abnormalities of the kidneys. In this review, we summarize the pathogenesis of renal injury deriving from SARS-CoV-2 infection by focusing on its etiology, pathology, and clinical manifestations. The virus causes kidney injury by either direct infection or systemic effects, including host immune clearance and immune tolerance disorders, endothelium-mediated vasculitis, thrombus formation, glucose and lipid metabolism disorder, and hypoxia. <b><i>Key Messages:</i></b> Renal injury by SARS-CoV-2 is the result of multiple factors. Via highly expressed ACE2 in renal tissue, SARS-CoV-2 infection fundamentally initiates a mechanism of renal injury. Systemic effects such as host immune clearance and immune tolerance disorders, endothelial cell injury, thrombus formation, glucose and lipid metabolism disorder, and hypoxia aggravate this renal injury.

scholarly journals Multi-Omics Integration to Reveal the Mechanism of Hepatotoxicity Induced by Dictamnine

2021 ◽  
Vol 9 ◽  
Author(s):  
Can Tu ◽  
Ziying Xu ◽  
Lichun Tian ◽  
Zihui Yu ◽  
Tieshang Wang ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Lipid Metabolism ◽  
Weight Ratio ◽  
Control Group ◽  
High Dose ◽  
Down Regulation ◽  
Lipid Metabolism Disorder ◽  
Fatty Acid Binding ◽  
Female Mice ◽  
Metabolism Disorder

Herb-induced liver injury (HILI) has become a great concern worldwide due to the widespread usage of herbal products. Among these products is Dictamni Cortex (DC), a well-known Traditional Chinese Medicine (TCM), widely used to treat chronic dermatosis. Dictamni Cortex has drawn increasing attention because of its hepatotoxicity caused by the hepatotoxic component, dictamnine. However, the potential hepatotoxicity mechanism of dictamnine remains unclear. Therefore, this study aimed to use the multi-omics approach (transcriptomic, metabolomic, and proteomic analyses) to identify genes, metabolites, and proteins expressions associated with dictamnine-induced hepatotoxicity. A study on mice revealed that a high dose of dictamnine significantly increases serum aspartate aminotransferase (AST) activity, total bilirubin (TBIL), and direct bilirubin (DBIL) levels, the relative liver weight and liver/brain weight ratio in female mice (P &lt; 0.05 and P &lt; 0.01), compared to the normal control group. Liver histologic analysis further revealed a high dose of dictamnine on female mice caused hepatocyte vesicular steatosis characterized by hepatocyte microvesicles around the liver lobules. The expressed genes, proteins, and metabolites exhibited strong associations with lipid metabolism disorder and oxidative stress. Dictamnine caused increased oxidative stress and early hepatic apoptosis via up-regulation of glutathione S transferase a1 (GSTA1) and Bax/Bcl-2 ratio and down-regulation of the antioxidative enzymes superoxide dismutase (SOD), catalase, and glutathione peroxidase 1 (GPx-1). Besides, the up-regulation of Acyl-CoA synthetase long-chain family member 4 (ACSL4) and down-regulation of acetyl-coa acetyltransferase 1 (ACAT1) and fatty acid binding protein 1 (FABP-1) proteins were linked to lipid metabolism disorder. In summary, dictamnine induces dose-dependent hepatotoxicity in mice, which impairs lipid metabolism and aggravates oxidative stress.

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