scholarly journals Roles of MicroRNAs in Glucose and Lipid Metabolism in the Heart

2021 ◽  
Vol 8 ◽  
Author(s):  
Hengzhi Du ◽  
Yanru Zhao ◽  
Huaping Li ◽  
Dao Wen Wang ◽  
Chen Chen
Keyword(s):  
Lipid Metabolism ◽  
Insulin Signaling ◽  
Heart Development ◽  
Ischemia Reperfusion ◽  
Present Knowledge ◽  
Energy Substrate ◽  
Glucose And Lipid Metabolism ◽  
Overwhelming Evidence ◽  
Vascular Proliferation ◽  
Non Coding Rnas

MicroRNAs (miRNAs) are small non-coding RNAs that participate in heart development and pathological processes mainly by silencing gene expression. Overwhelming evidence has suggested that miRNAs were involved in various cardiovascular pathological processes, including arrhythmias, ischemia-reperfusion injuries, dysregulation of angiogenesis, mitochondrial abnormalities, fibrosis, and maladaptive remodeling. Various miRNAs could regulate myocardial contractility, vascular proliferation, and mitochondrial function. Meanwhile, it was reported that miRNAs could manipulate nutrition metabolism, especially glucose and lipid metabolism, by regulating insulin signaling pathways, energy substrate transport/metabolism. Recently, increasing studies suggested that the abnormal glucose and lipid metabolism were closely associated with a broad spectrum of cardiovascular diseases (CVDs). Therefore, maintaining glucose and lipid metabolism homeostasis in the heart might be beneficial to CVD patients. In this review, we summarized the present knowledge of the functions of miRNAs in regulating cardiac glucose and lipid metabolism, as well as highlighted the miRNA-based therapies targeting cardiac glucose and lipid metabolism.

scholarly journals Effects of chronic hyperinsulinemia on metabolic pathways and insulin signaling in the fetal liver

2020 ◽  
Vol 319 (4) ◽  
pp. E721-E733
Author(s):  
Paul J. Rozance ◽  
Amanda K. Jones ◽  
Stephanie L. Bourque ◽  
Angelo D’Alessandro ◽  
William. W. Hay ◽  
...  
Keyword(s):  
Lipid Metabolism ◽  
Amino Acid ◽  
Insulin Signaling ◽  
Carbon Metabolism ◽  
Fetal Liver ◽  
Whole Body ◽  
Ampk Activation ◽  
Fetal Sheep ◽  
Glucose And Lipid Metabolism ◽  
One Carbon Metabolism

The effect of chronic of hyperinsulinemia in the fetal liver is poorly understood. Here, we produced hyperinsulinemia with euglycemia for ∼8 days in fetal sheep [hyperinsulinemic (INS)] at 0.9 gestation. INS fetuses had increased insulin and decreased oxygen and amino acid (AA) concentrations compared with saline-infused fetuses [control (CON)]. Glucose (whole body) utilization rates were increased, as expected, in INS fetuses. In the liver, however, there were few differences in genes and metabolites related to glucose and lipid metabolism and no activation of insulin signaling proteins (Akt and mTOR). There was increased p-AMPK activation and decreased mitochondrial mass ( PGC1A expression, mitochondrial DNA content) in INS livers. Using an unbiased multivariate analysis with 162 metabolites, we identified effects on AA and one-carbon metabolism in the INS liver. Expression of the transaminase BCAT2 and glutaminase genes GLS1 and GLS2 was decreased, supporting decreased AA utilization. We further evaluated the roles of hyperinsulinemia and hypoxemia, both present in INS fetuses, on outcomes in the liver. Expression of PGC1A correlated only with hyperinsulinemia, p-AMPK correlated only with hypoxemia, and other genes and metabolites correlated with both hyperinsulinemia and hypoxemia. In fetal hepatocytes, acute treatment with insulin activated p-Akt and decreased PGC1A, whereas hypoxia activated p-AMPK. Overall, chronic hyperinsulinemia produced greater effects on amino acid metabolism compared with glucose and lipid metabolism and a novel effect on one-carbon metabolism in the fetal liver. These hepatic metabolic responses may result from the downregulation of insulin signaling and antagonistic effects of hypoxemia-induced AMPK activation that develop with chronic hyperinsulinemia.

scholarly journals Effect of He Qi San on DNA Methylation in Type 2 Diabetes Mellitus Patients with Phlegm-blood Stasis Syndrome

2019 ◽  
Vol 17 (1) ◽  
pp. 1213-1221
Author(s):  
Chu Shufang ◽  
Zhou Yinan ◽  
Li Huilin ◽  
Zhao Hengxia ◽  
Liu Deliang ◽  
...  
Keyword(s):  
Diabetes Mellitus ◽  
Type 2 Diabetes ◽  
Dna Methylation ◽  
Type 2 Diabetes Mellitus ◽  
Lipid Metabolism ◽  
Insulin Signaling ◽  
Blood Stasis ◽  
Blood Stasis Syndrome ◽  
Glucose And Lipid Metabolism

AbstractThis study was performed to elucidate the potential influence of He Qi San (HQS) on glucose and lipid metabolism in type 2 diabetes mellitus (T2DM) patients with phlegm-blood stasis syndrome (PBSS), and to determine DNA methylation changes. Sixty T2DM patients with PBSS were randomly divided into control and HQS groups. The control group received conventional treatments, and the HQS group received conventional treatments plus HQS. Glucose metabolism (FPG, 2hPG, FINS, and HbA1c) and lipid metabolism indexes (TG, TC and LDL-C) were determined. Genes with differential DNA methylation were subjected to GO and KEGG analyses. Glucose and lipid metabolism indexes in both groups were reduced, but were much more pronounced in the HQS group. Differential promoter CpG methylation regions were identified in 682 genes, including 426 genes with high-CpG promoters, 150 genes with intermediate CpG promoters, and 106 genes with low CpG promoters. Genes with differential DNA methylation were mainly enriched in the AMPK and insulin signaling pathways, terpenoid backbone biosynthesis, and renin secretion. We concluded that HQS remarkably improved indexes of glucose and lipid metabolism in T2DM patients with PBSS through regulating the DNA methylation of genes in the AMPK and insulin signaling pathways and terpenoid backbone biosynthesis.

The Role of Peroxisome Proliferator-Activated Receptor γ in Mediating Cardioprotection Against Ischemia/Reperfusion Injury

2017 ◽  
Vol 23 (1) ◽  
pp. 46-56 ◽  
Author(s):  
Chong-Bin Zhong ◽  
Xi Chen ◽  
Xu-Yue Zhou ◽  
Xian-Bao Wang
Keyword(s):  
Lipid Metabolism ◽  
Target Genes ◽  
Inflammatory Responses ◽  
Ischemia Reperfusion Injury ◽  
Ischemia Reperfusion ◽  
Peroxisome Proliferator ◽  
Peroxisome Proliferator Activated Receptor ◽  
Glucose And Lipid Metabolism ◽  
Cardioprotective Effects

Myocardial infarction (MI) is a serious cardiovascular disease resulting in high rates of morbidity and mortality. Although advances have been made in restoring myocardial perfusion in ischemic areas, decreases in cardiomyocyte death and infarct size are still limited, attributing to myocardial ischemia/reperfusion (I/R) injury. It is necessary to develop therapies to restrict myocardial I/R injury and protect cardiomyocytes against further damage after MI. Many studies have suggested that peroxisome proliferator-activated receptor γ (PPARγ), a ligand-inducible nuclear receptor that predominantly regulates glucose and lipid metabolism, is a promising therapeutic target for ameliorating myocardial I/R injury. Thus, this review focuses on the role of PPARγ in cardioprotection during myocardial I/R. The cardioprotective effects of PPARγ, including attenuating oxidative stress, inhibiting inflammatory responses, improving glucose and lipid metabolism, and antagonizing apoptosis, are described. Additionally, the underlying mechanisms of cardioprotective effects of PPARγ, such as regulating the expression of target genes, influencing other transcription factors, and modulating kinase signaling pathways, are further discussed.

scholarly journals Regulation of Glucose and Lipid Metabolism by Long Non-coding RNAs: Facts and Research Progress

2020 ◽  
Vol 11 ◽  
Author(s):  
Tie-Ning Zhang ◽  
Wei Wang ◽  
Ni Yang ◽  
Xin-Mei Huang ◽  
Chun-Feng Liu
Keyword(s):  
Lipid Metabolism ◽  
Research Progress ◽  
Glucose And Lipid Metabolism ◽  
Non Coding Rnas

GIP Signaling Integrates with Insulin Signaling to Regulate Glucose and Lipid Metabolism in Human Adipocytes

Diabetes ◽  
2018 ◽  
Vol 67 (Supplement 1) ◽  
pp. 37-OR
Author(s):  
AJIT REGMI ◽  
MELISSA K. THOMAS ◽  
M. DODSON MICHAEL ◽  
WILLIAM C. ROELL
Keyword(s):  
Lipid Metabolism ◽  
Insulin Signaling ◽  
Human Adipocytes ◽  
Glucose And Lipid Metabolism

scholarly journals Cross-talk between hypoxia and insulin signaling through Phd3 regulates hepatic glucose and lipid metabolism and ameliorates diabetes

2013 ◽  
Vol 19 (10) ◽  
pp. 1325-1330 ◽  
Author(s):  
Cullen M Taniguchi ◽  
Elizabeth C Finger ◽  
Adam J Krieg ◽  
Colleen Wu ◽  
Anh N Diep ◽  
...  
Keyword(s):  
Lipid Metabolism ◽  
Cross Talk ◽  
Insulin Signaling ◽  
Glucose And Lipid Metabolism ◽  
Hepatic Glucose
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