scholarly journals Therapeutic targets during mitochondrial lipid metabolism

2020 ◽  
Vol 36 (3) ◽  
pp. 205-208 ◽  
Author(s):  
William Wang ◽  
Liyang Li ◽  
Xiangdong Wang
2018 ◽  
Vol 50 (5) ◽  
pp. 1726-1739 ◽  
Author(s):  
Jing Tian ◽  
Wenzhu Tang ◽  
Ming Xu ◽  
Chen Zhang ◽  
Pei Zhao ◽  
...  

Background/Aims: Shengmai San (SMS), prepared from Panax ginseng, Ophiopogon japonicus, and Schisandra chinensisin, has been widely used to treat ischemic disease. In this study, we investigated whether SMS may exert a beneficial effect in diabetic cardiomyopathy through improvement of mitochondrial lipid metabolism. Methods: A leptin receptor-deficient db/db mouse model was utilized, and lean age-matched C57BLKS mice served as non-diabetic controls. Glucose and lipid profiles, myocardial structure, dimension, and function, and heart weight to tibial length ratio were determined. Myocardial ultrastructural morphology was observed with transmission electron microscopy. Protein expression and activity of oxidative phosphorylation (OXPHOS) complex were assessed using western blotting and microplate assay kits. We also observed cellular viability, mitochondrial membrane potential, OXPHOS complex activity, and cellular ATP level in palmitic acid-stimulated H9C2 cardiomyocytes. Changes in the sirtuin (SIRT1)/AMP-activated protein kinase (AMPK)/peroxisome proliferator-activated receptor gamma coactivator 1-alpha (PGC-1α) pathway and mitochondrial uncoupling signaling were assessed using western blotting and quantitative real-time PCR. Results: Leptin receptor-deficient db/db mice exhibit obesity, hyperglycemia, and hyperlipidemia, accompanied by distinct myocardial hypertrophy and diastolic dysfunction. SMS at a dose of 3 g/kg body weight contributed to a recovery of diabetes-induced myocardial hypertrophy and diastolic dysfunction. SMS administration led to an effective restoration of mitochondrial structure and function both in vivo and in vitro. Furthermore, SMS markedly enhanced SIRT1 and p-AMPKα protein levels and decreased the expression of acetylated-PGC-1α and uncoupling protein 2 protein. SMS also restored the depletion of NRF1 and TFAM levels in diabetic hearts and H9C2 cardiomyocytes. Conclusion: The results indicate that SMS may alleviate diabetes-induced myocardial hypertrophy and diastolic dysfunction by improving mitochondrial lipid metabolism.


2018 ◽  
Vol 20 (suppl_5) ◽  
pp. v348-v348
Author(s):  
Huda Alfardus ◽  
Maria de los Angeles Estevez Cebrero ◽  
Jonathan Rowlinson ◽  
Anbarasu Lourdusamy ◽  
Richard Grundy ◽  
...  

2018 ◽  
Vol 20 (suppl_6) ◽  
pp. vi40-vi40
Author(s):  
Huda Alfardus ◽  
Maria de los Angeles Estevez Cebrero ◽  
Jonathan Rawlinson ◽  
Anbarasu Lourdusamy ◽  
Richard Grundy ◽  
...  

2013 ◽  
Vol 1 (2) ◽  
pp. 16
Author(s):  
Ashlyn Williams ◽  
Lindsey Crawford ◽  
Amit K Tiwari ◽  
Temesgen Samuel ◽  
Gemechu Wirtu DVM, PhD

2017 ◽  
Vol 37 (1) ◽  
pp. 262-273 ◽  
Author(s):  
J. H. (Han) van der Kolk ◽  
J. J. Gross ◽  
V. Gerber ◽  
R. M. Bruckmaier

Nutrients ◽  
2021 ◽  
Vol 13 (12) ◽  
pp. 4315
Author(s):  
Kristyn Dunlop ◽  
Ousseynou Sarr ◽  
Nicole Stachura ◽  
Lin Zhao ◽  
Karen Nygard ◽  
...  

Low birth weight (LBW) offspring are at increased risk for developing insulin resistance, a key precursor in metabolic syndrome and type 2 diabetes mellitus. Altered skeletal muscle vasculature, extracellular matrix, amino acid and mitochondrial lipid metabolism, and insulin signaling are implicated in this pathogenesis. Using uteroplacental insufficiency (UPI) to induce intrauterine growth restriction (IUGR) and LBW in the guinea pig, we investigated the relationship between UPI-induced IUGR/LBW and later life skeletal muscle arteriole density, fibrosis, amino acid and mitochondrial lipid metabolism, markers of insulin signaling and glucose uptake, and how a postnatal high-fat, high-sugar “Western” diet (WD) modulates these changes. Muscle of 145-day-old male LBW glucose-tolerant offspring displayed diminished vessel density and altered acylcarnitine levels. Disrupted muscle insulin signaling despite maintained whole-body glucose homeostasis also occurred in both LBW and WD-fed male “lean” offspring. Additionally, postnatal WD unmasked LBW-induced impairment of mitochondrial lipid metabolism, as reflected by increased acylcarnitine accumulation. This study provides evidence that early markers of skeletal muscle metabolic dysfunction appear to be influenced by the in utero environment and interact with a high-fat/high-sugar postnatal environment to exacerbate altered mitochondrial lipid metabolism, promoting mitochondrial overload.


2020 ◽  
Vol 178 ◽  
pp. 114091 ◽  
Author(s):  
Mercedes Dávalos-Salas ◽  
John M. Mariadason ◽  
Matthew J. Watt ◽  
Magdalene K. Montgomery

2018 ◽  
Vol 20 (suppl_3) ◽  
pp. iii280-iii280
Author(s):  
H Alfardus ◽  
M de los Angeles Estevez Cebrero ◽  
J Rawlinson ◽  
A Lourdusamy ◽  
R Grundy ◽  
...  

2021 ◽  
Vol 12 ◽  
Author(s):  
Shi-Feng Huang ◽  
Xiao-Fei Peng ◽  
Lianggui Jiang ◽  
Ching Yuan Hu ◽  
Wen-Chu Ye

Lipid metabolism is an essential biological process involved in nutrient adjustment, hormone regulation, and lipid homeostasis. An irregular lifestyle and long-term nutrient overload can cause lipid-related diseases, including atherosclerosis, myocardial infarction (MI), obesity, and fatty liver diseases. Thus, novel tools for efficient diagnosis and treatment of dysfunctional lipid metabolism are urgently required. Furthermore, it is known that lncRNAs based regulation like sponging microRNAs (miRNAs) or serving as a reservoir for microRNAs play an essential role in the progression of lipid-related diseases. Accordingly, a better understanding of the regulatory roles of lncRNAs in lipid-related diseases would provide the basis for identifying potential biomarkers and therapeutic targets for lipid-related diseases. This review highlighted the latest advances on the potential biomarkers of lncRNAs in lipid-related diseases and summarised current knowledge on dysregulated lncRNAs and their potential molecular mechanisms. We have also provided novel insights into the underlying mechanisms of lncRNAs which might serve as potential biomarkers and therapeutic targets for lipid-related diseases. The information presented here may be useful for designing future studies and advancing investigations of lncRNAs as biomarkers for diagnosis, prognosis, and therapy of lipid-related diseases.


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