miR-552-3p modulates transcriptional activities of FXR and LXR to ameliorate hepatic glycolipid metabolism disorder

2021 ◽  
Vol 74 (1) ◽  
pp. 8-19
Author(s):  
Lei Fan ◽  
Rongtao Lai ◽  
Ningning Ma ◽  
Yunxia Dong ◽  
Yu Li ◽  
...  
Keyword(s):  
Glycolipid Metabolism ◽  
Metabolism Disorder

scholarly journals miR-125a-5p ameliorates hepatic glycolipid metabolism disorder in type 2 diabetes mellitus through targeting of STAT3

Theranostics ◽  
2018 ◽  
Vol 8 (20) ◽  
pp. 5593-5609 ◽  
Author(s):  
Lina Xu ◽  
Yue Li ◽  
Lianhong Yin ◽  
Yan Qi ◽  
Huijun Sun ◽  
...  
Keyword(s):  
Diabetes Mellitus ◽  
Type 2 Diabetes ◽  
Type 2 Diabetes Mellitus ◽  
Glycolipid Metabolism ◽  
Metabolism Disorder

scholarly journals Glycolipid Metabolism Disorder in the Liver of Obese Mice Is Improved by TUDCA via the Restoration of Defective Hepatic Autophagy

2015 ◽  
Vol 2015 ◽  
pp. 1-11 ◽  
Author(s):  
Qinyue Guo ◽  
Qindong Shi ◽  
Huixia Li ◽  
Jiali Liu ◽  
Shufang Wu ◽  
...  
Keyword(s):  
Insulin Sensitivity ◽  
Insulin Signaling ◽  
Body Weight Gain ◽  
Obese Mice ◽  
Lower Blood Glucose ◽  
Glycolipid Metabolism ◽  
Metabolism Disorder ◽  
Reduced Body ◽  
Lower Blood ◽  
Important Regulator

Objective.Tauroursodeoxycholic acid (TUDCA) has been considered an important regulator of energy metabolism in obesity. However, the mechanism underlying how TUDCA is involved in insulin resistance is not fully understood. We tested the effects of TUDCA on autophagic dysfunction in obese mice.Material and Methods.500 mg/kg of TUDCA was injected into obese mice, and metabolic parameters, autophagy markers, and insulin signaling molecular were assessed by Western blotting and real-time PCR.Results.The TUDCA injections in the obese mice resulted in a reduced body weight gain, lower blood glucose, and improved insulin sensitivity compared with obese mice that were injected with vehicle. Meanwhile, TUDCA treatment not only reversed autophagic dysfunction and endoplasmic reticulum stress, but also improved the impaired insulin signaling in the liver of obese mice. Additionally, the same results obtained with TUDCA were evident in obese mice treated with the adenoviral Atg7.Conclusions.We found that TUDCA reversed abnormal autophagy, reduced ER stress, and restored insulin sensitivity in the liver of obese mice and that glycolipid metabolism disorder was also improved via the restoration of defective hepatic autophagy.

scholarly journals Rhus chinensis Mill. Fruits Ameliorate Hepatic Glycolipid Metabolism Disorder in Rats Induced by High Fat/High Sugar Diet

Nutrients ◽  
2021 ◽  
Vol 13 (12) ◽  
pp. 4480
Author(s):  
Zihuan Wu ◽  
Qingqing Ma ◽  
Shengbao Cai ◽  
Yilin Sun ◽  
Yuanyue Zhang ◽  
...  
Keyword(s):  
Chronic Diseases ◽  
Metabolic Disorders ◽  
Ethanol Extract ◽  
Key Factors ◽  
High Fat ◽  
Glycolipid Metabolism ◽  
High Sugar ◽  
Metabolism Disorder ◽  
Rhus Chinensis ◽  
Underlying Mechanisms

Hepatic glycolipid metabolism disorder is considered as one of the key factors in the pathogenesis of many chronic diseases. The objective of this study was to investigate the protective effect and underlying mechanisms of Rhus chinensis Mill. fruits against hepatic glycolipid metabolic disorders in rats induced by a high fat/high sugar diet. Results showed that ethanol extract, especially at a dose of 600 mg/kg b.w., could effectively ameliorate glycolipid metabolic disorders in rats. The biochemical indexes, including CAT, GSH and HOMA-IR, were significantly improved by the administration of ethanol extract. Immunohistochemistry and Western blot analysis revealed that ethanol extract up-regulated the expression levels of PI3K/AKT, PPAR-α, and the phosphorylation of IRS1 and AMPK proteins, and down-regulated the expressions of SREBP-1 and FAS proteins in the liver, which are closely related to hepatic glycolipid metabolism. Those findings suggested that R. chinensis Mill. fruits could be developed as functional foods and/or nutraceuticals for preventing or controlling some chronic diseases related to hepatic glycolipid metabolism disorder.

scholarly journals Citrus reticulatae pericarpium Extract Decreases the Susceptibility to HFD-Induced Glycolipid Metabolism Disorder in Mice Exposed to Azithromycin in Early Life

2021 ◽  
Vol 12 ◽  
Author(s):  
Hanqi Lu ◽  
Yanting You ◽  
Xinghong Zhou ◽  
Qiuxing He ◽  
Ming Wang ◽  
...  
Keyword(s):  
Gut Microbiome ◽  
High Fat Diet ◽  
Early Life ◽  
Underlying Mechanism ◽  
Inflammatory Factors ◽  
Glycolipid Metabolism ◽  
Metabolism Disorder ◽  
Adult Mice ◽  
Gut Microbe ◽  
Old Mice

BackgroundStudies have shown that gut microbe disorder in mice due to early-life antibiotic exposure promotes glycolipid metabolism disorder in adulthood. However, the underlying mechanism remains unclear and there is not yet an effective intervention or treatment for this process.PurposeThe study investigated whether early-life azithromycin (AZT) exposure in mice could promote high-fat diet (HFD)-induced glycolipid metabolism disorder in adulthood. Moreover, the effect of citrus reticulata pericarpium (CRP) extract on glycolipid metabolism disorder via regulation of gut microbiome in mice exposed to antibodies early in life were investigated.Methods and ResultsThree-week-old mice were treated with AZT (50 mg/kg/day) via drinking water for two weeks and then were fed a CRP diet (1% CRP extract) for four weeks and an HFD for five weeks. The results showed that early-life AZT exposure promoted HFD-induced glycolipid metabolism disorder, increased the levels of inflammatory factors, promoted the flora metabolism product trimethylamine N-oxide (TMAO), and induced microbial disorder in adult mice. Importantly, CRP extract mitigated these effects.ConclusionTaken together, these findings suggest that early-life AZT exposure increases the susceptibility to HFD-induced glycolipid metabolism disorder in adult mice, and CRP extract can decrease this susceptibility by regulating gut microbiome.

scholarly journals Kaempferide improves glycolipid metabolism disorder by activating PPARγ in high-fat-diet-fed mice

Life Sciences ◽  
2021 ◽  
Vol 270 ◽  
pp. 119133
Author(s):  
Heng Tang ◽  
Qingfu Zeng ◽  
Ting Tang ◽  
Yunjie Wei ◽  
Peng Pu
Keyword(s):  
High Fat Diet ◽  
High Fat ◽  
Glycolipid Metabolism ◽  
Metabolism Disorder

scholarly journals The Determinants for Adolescent Glycolipid Metabolism Disorder from Prenatal Period through Adolescence: a Cohort Study

2020 ◽  
Author(s):  
Xiao-Hua Liang ◽  
Jing-Yu Chen ◽  
Ping Qu ◽  
Xian Tang
Keyword(s):  
Risk Factors ◽  
Insulin Resistance ◽  
Cohort Study ◽  
Pubertal Development ◽  
Childhood And Adolescence ◽  
Healthy Children ◽  
Model Assessment ◽  
Prenatal Period ◽  
Glycolipid Metabolism ◽  
Metabolism Disorder

Abstract To explore the prevalence of and risk factors for glycolipid metabolism disorder (GLMD) from the prenatal period through childhood and adolescence. A bidirectional cohort study which was established in 2014 and followed between March 1 and July 20, 2019 were designed to evaluate the risk factors for GLMD. Two stage stratified cluster sampling was used to include participants from four communities in two counties in Chongqing. 2808 healthy children aged between 6 and 9 years in 2014 entered the cohort in 2014, and followed in 2019 with a follow-up rate of 70%. 2,136 samples (aged 11·68 ± 0·60 years) were included. The prevalence of insulin resistance (IR), prediabetes/diabetes and dyslipidemia was 21·02%, 7·19% and 21·61%, respectively. Subjects with an urban residence, no pubertal development, dyslipidemia in 2014, higher family income, higher parental education, low quality of life (QoL), and unstable neurotic and psychotic personalities had significantly elevated fasting insulin (FI) or homeostasis model assessment insulin resistance (HOMA-IR) levels; subjects with female sex, no pubertal development, dyslipidemia in 2014, obesity, gestational hypertension, maternal weight gain above Institute of Medicine guidelines, single parents, low QoL, introverted and unstable personality had increased triglyceride or triglyceride/high-density lipoprotein (HDL). Adolescent with rural residence and living convenience had higher HbA1c level. We observed that low QoL status, unstable and psychotic personality traits were associated with increased GLMD risk independent of obesity, suggesting that the community intervention to improve the QoL and psychological health of children is essential.

scholarly journals Kaempferide Improves Glycolipid Metabolism Disorder by Activating PPARγ in High-Fat-Diet-Fed Mice

2020 ◽  
Author(s):  
Qingfu Zeng ◽  
Heng Tang ◽  
Ting Tang ◽  
Peng Pu
Keyword(s):  
Signaling Pathway ◽  
High Fat Diet ◽  
Metabolic Diseases ◽  
Serum Insulin ◽  
High Fat ◽  
Glycolipid Metabolism ◽  
Metabolism Disorder ◽  
Pparγ Agonist ◽  
Underlying Mechanisms

Abstract Background: Kaempferide (Ka, 3,5,7-trihydroxy-4′-methoxyflavone), an active ingredient of Tagetes erecta L has been demonstrated to possess many pharmacological effects, including antioxidant, anti-inflammation, anticancer and antihypertension in previous study. However, there is no evidence of Ka on metabolic disorder in former studies. This study investigated the effects of Ka on glycolipid metabolism and explored the underlying mechanisms of action in vivo and vitro. Methods: High-fat diet (HFD) was used to induce the model of glycolipid metabolism disorder in mice.The hypolipidemic and hypoglycemic effect was detected by several indicators, like blood sample analysis blood glucose, serum insulin, HOMA index and intraperitoneal glucose tolerance tests (IPGTT). The signaling pathways of lipid metabolism (PPARγ/LXRα/ABCA1) and glucose metabolism (PPARγ/PI3K/AKT) were evaluated using Real-Time PCR and Western blot. The primary culture of hepatocytes was prepared to confirm the target of Ka by co-culturing with PPARγ agonist or inhibitor.Results: Administration of Ka at a dose of 10mg/kg for 16 weeks effectively attenuated obesity, hyperlipidemia, hyperglycemia and insulin resistance in HFD mice. Further studies revealed the hypolipidemic and hypoglycemic effects of Ka depended on the activation of PPARγ/LXRα/ABCA1 pathway and PPARγ/PI3K/AKT pathway, respectively. The primary hepatocyte test, co-cultured with PPARγ agonists or inhibitors, further confirmed the above signaling pathway and key protein. Conclusion: Ka played an important role in improving glycolipid metabolism disorder, which were causally associated with weight loss. The underlying mechanisms might are associated with the activation of PPARγ and its downstream signaling pathway. Our study helped to understand the pharmacological actions of Ka, and provides theoretical basis for Ka in the effective treatment of obesity, diabetes and other metabolic diseases.

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