Your browser doesn't support javascript.
loading
Show: 20 | 50 | 100
Results 1 - 3 de 3
Filter
1.
Diabetes & Metabolism Journal ; : 327-336, 2017.
Article in English | WPRIM | ID: wpr-123921

ABSTRACT

Obesity and diabetes has become a major epidemic across the globe. Controlling obesity has been a challenge since this would require either increased physical activity or reduced caloric intake; both are difficult to enforce. There has been renewed interest in exploiting pathways such as uncoupling protein 1 (UCP1)-mediated uncoupling in brown adipose tissue (BAT) and white adipose tissue to increase energy expenditure to control weight gain. However, relying on UCP1-based thermogenesis alone may not be sufficient to control obesity in humans. On the other hand, skeletal muscle is the largest organ and a major contributor to basal metabolic rate and increasing energy expenditure in muscle through nonshivering thermogenic mechanisms, which can substantially affect whole body metabolism and weight gain. In this review we will describe the role of Sarcolipin-mediated uncoupling of Sarcoplasmic Reticulum Calcium ATPase (SERCA) as a potential mechanism for increased energy expenditure both during cold and diet-induced thermogenesis.


Subject(s)
Humans , Adipose Tissue, Brown , Adipose Tissue, White , Basal Metabolism , Diabetes Mellitus , Energy Intake , Energy Metabolism , Hand , Metabolism , Motor Activity , Muscle, Skeletal , Obesity , Sarcoplasmic Reticulum Calcium-Transporting ATPases , Thermogenesis , Weight Gain
2.
Academic Journal of Second Military Medical University ; (12): 1248-1252, 2013.
Article in Chinese | WPRIM | ID: wpr-839511

ABSTRACT

ATP2A2 is a member of ATP2As family, it encodes SERCA2b, a sarco (endo) plasmic reticulum calcium transport ATPases (SERCAs). As the main function of SERCA2b is to transport calcium from the cytosol to the sarco(endo) plasmic reticulum, it plays a vital role in numerous calcium-related signaling pathways involving control of tumor growth, differentiation, angiogenesis, metastasis and apoptosis. Recent studies have identified the accurate change of ATP2A2 expression in some tumors, which makes the first step in investigating how ATP2A2 participates in tumorigenesis and whether it can be taken as a new tumor marker and target for treatment. Here we made a comprehensive review on the role of ATP2A2 in tumorigenesis, and it is believed that the abnormal expression of ATP2A2 can damage the calcium homeostasis between cytosol and sarco (endo) plasmic reticulum, accelerating malignant proliferation, migration and angiogenesis of the tumor. Moreover, we also discussed the prospect of research and application of ATP2A2.

3.
Medical Journal of Chinese People's Liberation Army ; (12)1983.
Article in Chinese | WPRIM | ID: wpr-564973

ABSTRACT

Objective To investigate the therapeutic effects of recombinant adeno-associated virual gene serotype 1(rAAV1) mediated transfer of sarcoplasmic reticulum Ca2+ ATPase(SERCA2a) on beagle dogs with heart failure(HF).Methods The chronic HF model was reproduced in beagle dogs by giving rapid right ventricular pacing(230 beats/min) for 30 days.A reduced rate(180 beats/min)was continued for another 30 days.Sixteen beagle dogs were divided into four groups(4 each): control group,HF group,HF+EGFP group and HF+SERCA2a group.After rapid pacing for 30 days,rAAV1-EGFP(1?1012vg/ml) and rAAV1-SERCA2a(1?1012vg/ml) were respectively delivered via intramyocardial routes,while no treatment was given to the animals in both control and HF groups.At the end of the study,haemodynamics,echocardiography and the protein expression of SRCA2a were measured respectively.The apoptosis index of cardiac myocyte was evaluated by TUNEL.Bax expression was assessed by immunohistochemistry.Results After gene transfer of SERCA2a in HF beagle dogs for 30 days,the heart function was improved along with an increase in SERCA2a expression.Left ventricular systolic function was significantly increased,including the left ventricular systolic pressure(LVSP),left ventricular maximal rate of pressure rise(LV+dp/dtmax),left ventricular maximal rate of pressure decline(LV-dp/dtmax,P

SELECTION OF CITATIONS
SEARCH DETAIL