Abnormal lipid metabolism down-regulates adenosine triphosphate synthase β-subunit protein expression in corpus cavernosum smooth musclein vitroandin vivo

Andrologia ◽  
2013 ◽  
Vol 46 (5) ◽  
pp. 487-494 ◽  
Author(s):  
Z.-H. Liu ◽  
L.-P. Yu ◽  
T. Xu ◽  
X.-W. Zhang ◽  
Y.-Q. Yuan ◽  
...  
Andrologia ◽  
2020 ◽  
Vol 52 (11) ◽  
Author(s):  
Lixian Cheng ◽  
Xue Yi ◽  
Ying Shi ◽  
Shuwei Yu ◽  
Liyuan Zhang ◽  
...  

2007 ◽  
Vol 10 (5-6) ◽  
pp. 273-278 ◽  
Author(s):  
◽  
Jie Mei ◽  
Miejung Park ◽  
David A. York ◽  
Charlotte Erlanson-Albertsson

Author(s):  
Liping Yang ◽  
Yixuan Hou ◽  
Yan-e Du ◽  
Qiao Li ◽  
Fanlin Zhou ◽  
...  

AbstractThe aberrant classical miRNAs are considered to play significant roles in tumor progression. However, it remains unclear for nonclassical miRNAs, a set of Drosha-independent miRNAs in the process of various biology. Here, we reveal that a nonclassical miR-4646-5p plays a pivotal role in gastric cancer (GC) metastasis. MiR-4646-5p, one of Drosha-independent mirtronic miRNA, is aberrant up-regulated in Drosha-low expressed GC and Drosha-knockdown gastric cancer cells. Mirtronic miR-4646-5p is a specific transcription splicing product of intron 3 of the host gene Abhd16a with the aid of SRSF2. The enhanced miR-4646-5p can stabilize HIF1A by targeting PHD3 to positive feedback regulate Abhd16a and miR-4646-5p itself expressions. ABHD16A, as an emerging phosphatidylserine-specific lipase, involves in lipid metabolism leading to lysophosphatidylserines (lyso-PSs) accumulation, which stimulates RhoA and downstream LIMK/cofilin cascade activity through GPR34/Gi subunit, thus causes metastasis of gastric cancer. In addition, miR-4646-5p/PHD3/HIF1A signaling can also up-regulate RhoA expression and synergistically promote gastric cancer cell invasion and metastasis. Our study provides new insights of nonclassical mirtronic miRNA on tumor progress and may serve as a new diagnostic biomarker for gastric cancer. MiR-4646-5p and its host gene Abhd16a mediated abnormal lipid metabolism may be a new target for clinical treatment of gastric cancer.


2021 ◽  
Vol 12 (5) ◽  
pp. 2323-2334
Author(s):  
Shihong Zheng ◽  
Peichang Cao ◽  
Zequn Yin ◽  
Xuerui Wang ◽  
Yuanli Chen ◽  
...  

Apigenin prevented the DDC-induced abnormal lipid metabolism, liver damage and liver fibrosis by reducing inflammation and oxidative stress. Apigenin might be a potential drug for the treatment of cholestatic liver diseases.


2011 ◽  
Vol 106 (4) ◽  
pp. 491-501 ◽  
Author(s):  
Manar Aoun ◽  
Francoise Michel ◽  
Gilles Fouret ◽  
Audrey Schlernitzauer ◽  
Vincent Ollendorff ◽  
...  

Accumulation of muscle TAG content and modification of muscle phospholipid fatty acid pattern may have an impact on lipid metabolism, increasing the risk of developing diabetes. Some polyphenols have been reported to modulate lipid metabolism, in particular those issued from red grapes. The present study was designed to determine whether a grape polyphenol extract (PPE) modulates skeletal muscle TAG content and phospholipid fatty acid composition in high-fat–high-sucrose (HFHS) diet-fed rats. Muscle plasmalemmal and mitochondrial fatty acid transporters, GLUT4 and lipid metabolism pathways were also explored. The PPE decreased muscle TAG content in HFHS/PPE diet-fed rats compared with HFHS diet-fed rats and induced higher proportions of n-3 PUFA in phospholipids. The PPE significantly up-regulated GLUT4 mRNA expression. Gene and protein expression of muscle fatty acid transporter cluster of differentiation 36 (CD36) was increased in HFHS diet-fed rats but returned to control values in HFHS/PPE diet-fed rats. Carnitine palmitoyltransferase 1 protein expression was decreased with the PPE. Mitochondrial β-hydroxyacyl CoA dehydrogenase was increased in HFHS diet-fed rats and returned to control values with PPE supplementation. Lipogenesis, mitochondrial biogenesis and mitochondrial activity were not affected by the PPE. In conclusion, the PPE modulated membrane phospholipid fatty acid composition and decreased muscle TAG content in HFHS diet-fed rats. The PPE lowered CD36 gene and protein expression, probably decreasing fatty acid transport and lipid accumulation within skeletal muscle, and increased muscle GLUT4 expression. These effects of the PPE are in favour of a better insulin sensibility.


1997 ◽  
Vol 325 (3) ◽  
pp. 793-800 ◽  
Author(s):  
Dean C. NG ◽  
Richard C. CARLSEN ◽  
Donal A. WALSH

Neural influences on the co-ordination of expression of the multiple subunits of skeletal muscle phosphorylase kinase and their assembly to form the holoenzyme complex, α4β4γ4δ4, have been examined during denervation and re-innervation of adult skeletal muscle and during neonatal muscle development. Denervation of the tibialis anterior and extensor digitorum longus muscles of the rat hindlimb was associated with a rapid decline in the mRNA for the γ subunit, and an abrupt decrease in γ-subunit protein. The levels of the α- and β-subunit proteins in the denervated muscles also declined rapidly, their time course of reduction being similar to that for the γ-subunit protein, but they did not decrease to the same extent. In contrast with the rapid decline in γ-subunit mRNA upon denervation, α- and β-subunit mRNAs stayed at control innervated levels for approx. 8–10 days, but then decreased rapidly. Their decline coincided very closely with the onset of re-innervation. Re-innervation of the denervated muscles, which occurs rapidly and uniformly after the sciatic nerve crush injury, produced an eventual slow and prolonged recovery of the mRNA for all three subunits and parallel increases in each of the subunit proteins. A similar co-ordinated increase of both subunit mRNA and subunit proteins of the phosphorylase kinase holoenzyme was observed during neonatal muscle development, during the period when the muscles were attaining their adult pattern of motor activity. The phosphorylase kinase holoenzyme remains in a non-activated form during all of these physiological changes, as is compatible with the presence of the full complement of the regulatory subunits. These data are consistent with a model whereby the transcriptional and translational expression of phosphorylase kinase γ subunit occurs only with concomitant expression of the α and β subunits. This would ensure that free and unregulated, activated γ subunit alone, which would give rise to unregulated glycogenolysis, is not produced. The data also suggest that control of phosphorylase kinase subunit expression and the formation of the holoenzyme in skeletal muscle is provided by the motor nerve, probably through imposed levels or patterns of muscle activity.


Author(s):  
Gaston Zilleruelo ◽  
S. L. Hsia ◽  
Michael Freundlich ◽  
Carolyn Abitbol ◽  
Milan Novak ◽  
...  

2019 ◽  
Vol 20 (2) ◽  
pp. 76-81
Author(s):  
Jhouharotul Faradisah ◽  
Diah Purwaningsari

Dyslipidemia is an abnormal lipid metabolism which may cause fat degeneration on hepatocytes cells and elevated triglyceride serum level. Dyslipidemia can be prevented by the consumption of high antioxidant food. Noni(Morinda citrifolia) contains many antioxidant such as flavanoid, kuersetin, tannin, and saponin, which are able to prohibit the elevation of ROS.This research is aimed to find out the effect of noni(Morinda citrifolia) extract in reducing the number of hepatocyte’s cells with fat degeneration and decreasing the triglyceride level which is elevated due to high cholesterol diet induction.In this study white rats divided randomly into 4 groups, control group (K-), high cholesterol diet induced group (K+), high cholesterol diet induced with 100 mg/Kg BW noni extract group (P1), high cholesterol diet induced with 200 mg/Kg BW noni extract group (P2). The result shows that noni  extract with dose 100 mg/Kg BW and  200 mg/Kg BWcan reduce the number of hepatocytes cells with fat degeneration (p= 0,026 and p=0,027) and decrease the level of triglyceride serum (p=0,036 and p=0,010).The conclusion is noni extract with dose 100 mg/KgBW reduces effectively  the number of hepatocyte’s cells with fat degeneration and decreases the level of triglyceride serum which increase because of high cholesterol diet. 


Sign in / Sign up

Export Citation Format

Share Document