Treatment with a melanocortin agonist improves abnormal lipid metabolism in streptozotocin-induced diabetic mice

Neuropeptides ◽  
2011 ◽  
Vol 45 (2) ◽  
pp. 123-129 ◽  
Author(s):  
Arnold Leckstrom ◽  
Pei San Lew ◽  
Nicole J. Poritsanos ◽  
Tooru M. Mizuno
2010 ◽  
Vol 104 (8) ◽  
pp. 1120-1128 ◽  
Author(s):  
Jeong Sook Noh ◽  
Hyun Young Kim ◽  
Chan Hum Park ◽  
Hajime Fujii ◽  
Takako Yokozawa

Oligonol was orally administered at 10 or 20 mg/kg body weight per d for 8 weeks to db/db mice with type 2 diabetes, and its effects were compared with those of the vehicle in db/db and m/m (misty, non-diabetic) mice. Serum and renal biochemical factors, protein expressions related to lipid metabolism and inflammation, and advanced glycation endproducts were measured. There were significant reductions in the serum lipid concentration, reactive oxygen species (ROS) and lipid peroxidation, as well as improvements in renal function parameters. In addition, oligonol treatment significantly decreased ROS levels and lipid peroxidation in the kidney. In particular, the renal lipid contents such as TAG and total cholesterol were significantly reduced in the oligonol-administered groups through the up-regulation of PPARα and down-regulation of sterol regulatory element-binding protein-1 in db/db mice. Moreover, oligonol inhibited non-fluorescent AGE formation and their receptor expression, suggesting that it could effectively inhibit AGE development caused by oxidative stress and/or dyslipidaemia in the kidney of db/db mice. Furthermore, augmented expressions of NF-κBp65, cyclo-oxygenase-2 and inducible NO synthase were down-regulated to the levels of m/m mice in the group given oligonol at 20 mg/kg. This means that oligonol would act as a regulator in the inflammatory response of type 2 diabetes. The present results suggest that oligonol could have renoprotective effects against abnormal lipid metabolism and ROS-related AGE formation in type 2 diabetes.


Diabetes ◽  
2020 ◽  
Vol 69 (Supplement 1) ◽  
pp. 1060-P
Author(s):  
LIXIN GUO ◽  
QI PAN ◽  
CHAO CHEN ◽  
SHUSHAN LIN ◽  
YU LI ◽  
...  

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.


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. 


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