AIMTo investigate the effects of exercise on phosphorylated and total ERK1/2, and mRNA of ERK2.

METHODSMale rats were randomly divided into control and trained groups. The trained rats were submitted to 1 h or 1.5 h of exercise daily and had a fragment of their excised gastroenemius muscle, 24 h or 48 h after the last training session. The train lasted for 7 weeks. The changes in the expressions of ERK1/2 and p-ERK1/2 were determined by Western blotting.The expression of ERK2 mRNA was determined by RT-PCR.

RESULTSExercise led to a marked increase in p-ERK1/2 of trained groups as compared with controls, and increased ERK1/2 protein expression of training 1.5 h/d, 24 h and 48 h after the last training session. ERK2 mRNA was increased by exercise 1 h/d, 24 h and exercise 1.5 h/d, 24 h and 48 h after the last training session. Glucose tolerance test found that blood insulin concentration was decreased with exercise training.

CONCLUSIONEndurance exercise could increase muscle responsiveness to insulin by improving the total ERK1/2 and p-ERK1/2, ERK2 mRNA expression.

Animals ; Glucose Tolerance Test ; Insulin ; physiology ; Male ; Mitogen-Activated Protein Kinase 1 ; metabolism ; Muscle, Skeletal ; metabolism ; Phosphorylation ; Physical Conditioning, Animal ; physiology ; RNA, Messenger ; genetics ; Rats ; Rats, Sprague-Dawley

AIMTo investigate the effects of exercise on JNK phosphorylation, protein and gene expression.

METHODSMale rats were randomly divided into control and trained groups. The trained rats were submitted to 1 h or 1.5 h of exercise daily and had a fragment of their excised gastrocenemius muscle, 24 h or 48 h after the last training session. The train lasted for 7 weeks. The changes in the expressions of JNK and p-JNK were determined by Western blotting. The expression of JNK mRNA was determined by RT-PCR.

RESULTSGlucose tolerance test found that blood insulin concentration was decreased with exercise training. Exercise led to a marked increase in p-JNK of trained groups 24 hours after exercise in rats that exercised for 1 hour per day and 24 and 48 hours after the exercise in those that exercised for 1.5 hours per day as compared with controls, and the protein expression of JNK significantly increased 24 and 48 hours after the exercise in rats that exercised for 1.5 hours per day. JNK mRNA was increased by exercise 1.5 h/d, 24 h after the last training session.

CONCLUSIONExercise could increase muscle responsiveness to insulin, improving the total JNK and p-JNK and mRNA expression.

Animals ; Glucose Tolerance Test ; Insulin ; physiology ; JNK Mitogen-Activated Protein Kinases ; genetics ; metabolism ; Male ; Muscle, Skeletal ; metabolism ; Phosphorylation ; Physical Conditioning, Animal ; physiology ; RNA, Messenger ; genetics ; metabolism ; Rats ; Rats, Sprague-Dawley

BACKGROUNDCongenital long QT syndrome (LQTS) is an ion channelopathy associated with genetic mutations. It is well known that most LQTS patients (91%) have a single mutation. The purpose of this study was to investigate the clinical characteristics of congenital LQTS patients with bigenic mutations in Taiwan, China.

METHODSCongenital LQTS patients were recruited consecutively at Taiwan University Hospital in Taiwan from 2003 to 2009. The diagnosis of LQTS was defined by an LQTS Schwartz score greater than 4. Mutation screening in KCNQ1, KCNH2, KCNE1, and SCN5A was performed using direct sequencing.

RESULTSThree of 16 LQTS patients (18.7%) were identified with bigenic mutations. One patient had missense mutations in KCNQ1 and KCNH2, the second in KCNQ1 and KCNE1, and the third in KCNH2 and SCN5A. The mean age at onset of LQTS for patients with bigenic mutations was (17 ± 3) years, and all of these patients were female. Two of them experienced seizure and one presented with syncope, although one of them had a family history of syncope. The mean QTc interval was (515 ± 17) ms, similar to those with single mutation or SNPs ((536 ± 74) ms, P = 0.63). Compared to those LQTS patients with single mutation or SNPs, a significantly higher percentage of LQTS patients with bigenic mutations presented with seizure and were younger at onset of the first index event (P = 0.03 and 0.001, respectively), but lower percentage of them presented with sudden cardiac death (P = 0.03).

CONCLUSIONSAlthough the percentage of bigenic mutations in LQTS is less than 10% in Caucasian populations, we identified 3 of 16 LQTS patients (18.7%, 95% confidence interval: 0.04-0.46) with bigenic mutations in Taiwan. However, the severity of their clinical presentations was not higher than those patients with single mutation or SNPs.

Adolescent ; Adult ; Aged ; ERG1 Potassium Channel ; Ether-A-Go-Go Potassium Channels ; genetics ; Female ; Genotype ; Humans ; KCNQ1 Potassium Channel ; genetics ; Long QT Syndrome ; genetics ; pathology ; Male ; Middle Aged ; Mutation ; NAV1.5 Voltage-Gated Sodium Channel ; genetics ; Polymorphism, Single Nucleotide ; genetics ; Potassium Channels, Voltage-Gated ; genetics ; Young Adult