Biomedical subjects

Jun Ren

Publications and source records attributed to Jun Ren.

180 records · Page 10Linked to original sources

PubMed2002

Overexpression of alcohol dehydrogenase exacerbates ethanol-induced contractile defect in cardiac myocytes.

Alcoholic cardiomyopathy is characterized by impaired ventricular function although its toxic mechanism is unclear. This study examined the impact of cardiac overexpression of alcohol dehydrogenase (ADH), which oxidizes ethanol into acetaldehyde (ACA), on ethanol-induced cardiac contractile defect. Mechanical and intracellular Ca(2+) properties were evaluated in ventricular myocytes from ADH transgenic and wild-type (FVB) mice. ACA production was assessed by gas chromatography. ADH myocytes exhibited similar mechanical properties but a higher efficiency to convert ACA compared with FVB myocytes. Acute exposure to ethanol depressed cell shortening and intracellular Ca(2+) in the FVB group with maximal inhibitions of 23.3% and 23.4%, respectively. Strikingly, the ethanol-induced depression on cell shortening and intracellular Ca(2+) was significantly augmented in the ADH group, with maximal inhibitions of 43.7% and 40.6%, respectively. Pretreatment with the ADH inhibitor 4-methylpyrazole (4-MP) or the aldehyde dehydrogenase inhibitor cyanamide prevented or augmented the ethanol-induced inhibition, respectively, in the ADH but not the FVB group. The ADH transgene also substantiated the ethanol-induced inhibition of maximal velocity of shortening/relengthening and unmasked an ethanol-induced prolongation of the duration of shortening/relengthening, which was abolished by 4-MP. These data suggest that elevated cardiac ACA exposure due to enhanced ADH expression may play an important role in the development of alcoholic cardiomyopathy.

Acetaldehyde↗

PubMed2002

Abrogated leptin-induced cardiac contractile response in ventricular myocytes under spontaneous hypertension: role of Jak/STAT pathway.

Leptin regulates cardiovascular function. Leptin levels are elevated in obesity and hypertension and may play a role in cardiovascular dysfunctions in these comorbidities. This study was designed to determine the influence of hypertension on the cardiac contractile response of leptin. Mechanical and intracellular Ca(2+) properties were evaluated using an IonOptix system in ventricular myocytes from spontaneously hypertensive (SHR) and age-matched Wistar Kyoto (WKY) rats. The contractile properties included peak shortening (PS), duration and maximal velocity of shortening/relengthening (TPS/TR(90), +/-dL/dt), and fura-fluorescence intensity change (DeltaFFI). NO and nitric oxide synthase (NOS) activity were assessed by the Griess and the (3)H-arginine/citrulline conversion assays, respectively. The leptin receptor (Ob-R) and the Janus kinase/signal transducer and activator of transcription (JAK/STAT) signaling pathway were evaluated by Western blot analysis. SHR animals displayed significantly elevated blood pressure and plasma leptin levels. Leptin elicited a concentration-dependent inhibition of PS and DeltaFFI in WKY, but not in SHR myocytes. Leptin did not affect TPS, TR(90), or +/- dL/dt. The difference in leptin-induced contractile response between the WKY and the SHR groups was abolished by the NOS inhibitor, Nomega-nitro-L-arginine methyl ester (L-NAME), but not by elevated extracellular Ca(2+). Either the JAK2 inhibitor AG-490 or the mitogen-activated protein (MAP) kinase inhibitor SB203580 abrogated the leptin-induced response in the WKY myocytes, whereas AG-490 unmasked a negative response in PS in the SHR myocytes. SHR myocytes displayed similar Ob-R protein abundance and basal NO levels, a blunted leptin-induced increase in NOS activity as well as enhanced basal STAT3 levels compared with the WKY group. These data indicate that the leptin-induced cardiac contractile response is abolished by spontaneous hypertension, possibly because of mechanisms involving altered JAK/STAT, MAP kinase signaling, and NO response.

Animals↗

PubMed2002

Nitric oxide synthase gene therapy for cardiovascular disease.

Gene therapy refers to the transfer of specific genes to the host tissue to intervene in a disease process, with resultant alleviation of the symptoms of a particular disease. Cardiovascular gene transfer is not only a powerful technique for studying the function of specific genes in cardiovascular biology and pathobiology, but also a novel and promising strategy for treating cardiovascular diseases. Since the mid-1990s, nitric oxide synthase (NOS), the enzyme that catalyzes the formation of nitric oxide (NO) from L-arginine, has received considerable attention as a potential candidate for cardiovascular gene therapy, because NO exerts critical and diverse functions in the cardiovascular system, and abnormalities in NO biology are apparent in a number of cardiovascular disease processes including cerebral vasospasm, atherosclerosis, postangioplasty restenosis, transplant vasculopathy, hypertension, diabetes mellitus, impotence and delayed wound healing. There are three NOS isoforms, i.e., endothelial (eNOS), neuronal (nNOS) and inducible (iNOS). All three NOS isoforms have been used in cardiovascular gene transfer studies with encouraging results. This review will discuss the rationale of NOS gene therapy in different cardiovascular disease settings and summarize the results of experimental NOS gene therapy from various animal models of cardiovascular disease to date.

Animals↗

PubMed2002

[Research on genetic variation of heart fatty acid-binding protein gene in ten pig breeds].

The genetic variation of heart fatty acid-binding protein (H-FABP) gene in 561 pigs including Duroc, Landrace, Large Yorkshire, Nanchang white pig, Erhualian, Meishan, Yushan black pig, Leping spotted pig, Jinhua black head-hind pig and Shanggao black head-hind pig were detected by PCR-RFLP with Hinf I, Hae III and Msp I. The results showed as follows: (1) Nanchang white pig presented only HH genotype while other breeds varied at the Hinf I-RFLP site; (2) The exotic breeds including Duroc, Landrace, Large Yorkshire and the native breed Nanchang white pig were proved to be polymorphic while the five Chinese local breeds presented no variation at the Hae III-RFLP site; (3) Among the tested breeds only Duroc presented variation at the Msp I-RFLP site. It is noted that all the Chinese local breeds present as AADD--genotypes.

Animals↗

PubMed2002

[Relationship of growth hormone (GH 2) genotypes with some production performances in pig].

The genotypes of 117 Nanchang White pigs and 361 Large Yorkshire pigs at GH 2 locus were detected by PCR-RFLP. The PCR products were cut by Apa I, and produced two alleles: A(449 + 101 + 55 bp), and B(316 + 133 + 101 + 49 bp). Effects of different genotypes on some important production traits involving the birth weight, 2-month body weight, 6-month body weight, corrected back-fat thickness, average back-fat thickness, feed to gain ratio and lean percentage were analyzed. The results showed that in Nanchang White pigs, no significant differences were observed between different genotypes and different growth and carcass traits; while in Large Yorkshire, the pigs with BB genotype had more lean percentage than pigs with AA genotype (P < 0.05).

Adipose Tissue↗

PubMed2002

[Studies of population genetic relationships among 24 Chinese and exotic pig breeds using AFLP analysis].

A total of 12 AFLP primer combinations were used to detect genetic variation of pooled DNA in a sample of 19 Chinese native pig breeds, 1 cultivated pig breed and 4 European and American pig breeds. The genetic similarity coefficient of 24 pig beeds was calculated from AFLP data, UPGMA cluster analysis was also performed. The 12 primer combinations generated more than 1000 bands, of which 208 bands were polymorphic, 17.3 polymorphic markers were detected by one primer combination on the average. Thirteen putative breed specific bands were produced in the pooled DNA of 8 pig breeds. The cultivated pig breed and 4 exotic pig breeds were clustere into one group, while 19 Chinese native pig breeds were gathered into the other group in the UPGMA tree. The result indicated that AFLP analysis had high assay efficiency index (Ai) and provided a valuable tool for assaying genetic diversity and breed characterization in pigs. Chinese native pig breeds and exotic pig breeds show remarkable genetic differentiation, which had farther genetic relationships. Nanchang White pig and Large White pig, Yushan Black pig and Yanshan Black pig had intimate genetic relationships with each other respectively, which were consistent with its breeding history, geographical distribution and RAPD analysis results. In addition, the reasons for cluster results of some pig breeds from AFLP data were not consistent with morphology, geographical distribution and existing classification were discussed.

Animals↗

PubMed2002

Ceramide attenuates high glucose-induced cardiac contractile abnormalities in cultured adult rat ventricular myocytes.

Ceramide, the metabolic product of signaling molecule sphingomyelin, has been implicated in cardiac Ca2+ regulation. To study the possible role of ceramide in the pathogenesis of diabetic cardiomyopathy, we examined the effects of ceramide on the cardiac contractility of cultured ventricular myocytes under control and simulated diabetic environments. Adult rat ventricular myocytes were maintained in normal (NG, 5.5 mM) or high glucose (HG, 25.5 mM) medium for 24 hr in the absence or presence of the membrane-permeant ceramide analog C2-ceramide, ceramide glucosyltransferase inhibitor D,L-threo-1-pheny-2-decanoylamino-3-morpholino-1-propanol (PDMP), or the inactive ceramide analog C2-dihydroceramide. Contractile indices analyzed included peak shortening (PS), time-to-PS (TPS), time-to-90% relengthening (TR90), maximal velocity of shortening/relengthening (+/- dL/dt), and intracellular Ca2+ fura-2 fluorescence intensity (FFI). Myocytes maintained in HG medium displayed reduced PS and +/- dL/dt associated with prolonged TR90 and normal TPS compared to NG myocytes. Interestingly, the HG-induced mechanical dysfunctions were significantly attenuated by C2-ceramide or PDMP. C2-ceramide did not affect the myocyte mechanics in NG myocytes although PDMP shortened TPS without affecting any other indices. The HG-induced contractile abnormalities were not altered by inactive ceramide analog C2-dihydroceramide (except +/- dL/dt). Fura-2 fluorescence recording revealed that HG reduced baseline as well as stimulated intracellular Ca2+ levels, which may be abolished by both C2-ceramide and PDMP. These data suggest that alteration of ceramide signaling may play a role in the pathogenesis of diabetic cardiomyopathy.

Animals↗

PubMed2002

Leptin, leptin resistance and endothelial dysfunction in pre-eclampsia.

Pre-eclampsia, or pregnancy-induced hypertension, is a major cause of maternal and fetal morbidity and mortality complicating 7-10% of pregnancies. Although mechanisms underlying pre-eclampsia are not well understood, endothelial dysfunction is considered to underscore many of the pre-eclamptic manifestations including hypertension, proteinuria and edema. Leptin, the obese gene product from adipocytes, is produced by the placenta during pregnancy. Serum leptin levels are elevated under normal pregnancy especially during the second trimester, which rapidly decreases and returns to normal after delivery, indicating the role of leptin as a gestational hormone for energy balance. Recent studies have revealed that the placental production of leptin may be pathologically augmented under pre-eclampsia although conflicting data also have been reported. Nevertheless, hyperleptinemia and possible further augmentation under pre-eclampsia may predispose to the development of maternal leptin resistance, which may be a component of insulin resistance predisposing the onset of endothelial dysfunction. This review summarizes recent findings regarding the putative changes of serum leptin levels during pre-eclampsia and the potential consequences on the vascular system.

Animals↗

PubMed2001

Measurement of Cardiac Mechanical Function in Isolated Ventricular Myocytes from Rats and Mice by Computerized Video-Based Imaging.

Isolated adult cardiac ventricular myocytes have been a useful model for cardiovascular research for more than 20 years. With the recent advances in cellular physiology and transgenic techniques, direct measurement of isolated ventricular myocyte mechanics is becoming an increasingly important technique in cardiac physiology that provides fundamental information on excitation-contraction coupling of the heart, either in drug intervention or pathological states. The goal of this article is to describe the isolation of ventricular myocytes from both rats and mice, and the use of real-time beat-to-beat simultaneous recording of both myocyte contraction and intracellular Ca(2+) transient.

Journal Article↗

PubMedDate not supplied

alpha2-Heremans Schmid glycoprotein, a putative inhibitor of tyrosine kinase, prevents glucose toxicity associated with cardiomyocyte dysfunction.

BACKGROUND: Diabetes leads to impaired glucose metabolism and insulin signaling in the heart, which may contribute to the development of diabetic cardiomyopathy. Insulin stimulates tyrosine phosphorylation of the insulin receptor and insulin receptor substrates. A two-fold increase in insulin-stimulated tyrosine phosphorylation has been reported in diabetic myocardium. The aim of the present study was to examine the effect of a putative inhibitor of tyrosine kinase phosphorylation, alpha(2)-Heremans Schmid glycoprotein (AHSG), on the mechanical dysfunction under a simulated diabetic environment. METHODS: Isolated ventricular myocytes from adult rats were maintained for 24 h in either normal glucose (NG, 5.5 mM) or high glucose (HG, 25.5 mM) medium with 10(-7) M insulin, and in the absence or presence of AHSG (50 micro g/ml). Contractile indices analyzed included: peak shortening (PS), time-to-PS (TPS), time-to-90% relengthening (TR(90)) and area underneath shortening and relengthening (Area/PS). RESULTS: Myocytes maintained in HG medium displayed reduced PS and prolonged TPS/TR(90), with enhanced area, compared to the NG myocytes. Interestingly, these HG-induced mechanical dysfunctions were abolished by AHSG. Removal of insulin from the culture medium did not affect the basal myocyte mechanics, but prevented AHSG from completely protecting against the HG-induced mechanical defects (i.e. HG-induced prolongation of TR(90) and area were only partially attenuated by AHSG in the absence of insulin). CONCLUSIONS: The present data support the notion of tyrosine phosphorylation in the pathogenesis of diabetic cardiomyopathy, and implicate the therapeutic value of tyrosine kinase phosphorylation inhibitors.

Animals↗

PubMedDate not supplied

Combined acetaldehyde and nicotine exposure depresses cardiac contraction in ventricular myocytes: prevention by folic acid.

Chronic alcoholism can progress to alcoholic cardiomyopathy characterized by ventricular dilation and impaired ventricular contractility. Nicotine abuse continues to remain a serious risk factor for cardiovascular diseases. However, little is know regarding the combined effects. This study was designed to examine the role of short-term combined exposure of the main alcohol metabolite acetaldehyde (ACA) and nicotine on cardiac contractile function in adult rat ventricular myocytes, and if folate exposure attenuates the effect of ACA/nicotine. Mechanical and intracellular Ca2+ properties were evaluated by an IonOptix SoftEdge system. Short-term (4-6 h) culture of myocytes with ACA (10 microM), nicotine (100 microM), or combination of the two in sealed vials with silicone septa depressed maximal velocity of shortening/relengthening, without affecting duration of shortening/relengthening and intracellular Ca2+ handling. Interestingly, the toxin-induced defects on myocyte mechanical properties were ablated with cotreatment of folate (100 microM), an essential vitamin required for DNA synthesis and repair. Collectively, these data provided evidence that ACA and nicotine, either alone or in combination, directly depressed cardiomyocyte mechanical function possibly through mechanisms related to DNA damage.

Acetaldehyde↗

PubMedDate not supplied

Enhanced stability of core-surface cross-linked micelles fabricated from amphiphilic brush copolymers.

"Stealth" nanoparticles made from polymer micelles have been widely explored as drug carriers for targeted drug delivery. High stability (i.e., low critical micelle concentration (CMC)) is required for their intravenous applications. Herein, we present a "core-surface cross-linking" concept to greatly enhance nanoparticle's stability: amphiphilic brush copolymers form core-surface cross-linked micelles (nanoparticles) (SCNs). The amphiphilic brush copolymers consisted of hydrophobic poly(epsilon-caprolactone) (PCL) and hydrophilic poly(ethylene glycol) (PEG) or poly(2-(N,N-dimethylamino)ethyl methacrylate) (PDMA) chains were synthesized by macromonomer copolymerization method and used to demonstrate this concept. The resulting SCNs were about 100 times more stable than micelles from corresponding amphiphilic block copolymers. The size and surface properties of the SCNs could be easily tailored by the copolymer's compositions.

Cross-Linking Reagents↗

PubMedDate not supplied

Influence of hypertension on tetrahydropapaveroline-induced vasorelaxation in rat thoracic aorta.

Tetrahydropapaveroline (THP), a condensation product of ethanol-derived acetaldehyde, has been shown to elicit a vasorelaxant response in rat thoracic aorta. This study examined the influence of hypertension on the THP-induced vasorelaxant responsiveness. Ring segments of thoracic aorta were isolated from Wistar-Kyoto (WKY) and spontaneously hypertensive rats (SHR) and isometric tension development was measured with a force transducer. In aorta, with or without intact endothelium, the contractile responses to potassium chloride (0-120 mM) were comparable between the WKY and the SHR groups. Hypertension did not affect the vasoconstrictive response to norepinephrine (0-10 microM) in vessels with intact endothelium, whereas it attenuated the norepinephrine-induced response in vessels without endothelium. THP (0.1-100 microM) elicited endothelium-intact as well as -denuded vasorelaxation in aorta from both WKY and SHR groups. Interestingly, the THP-induced endothelium-dependent vasorelaxation was significantly enhanced, whereas the THP-induced endothelium-independent vasorelaxation was not affected by hypertension. These data indicate that the THP-induced endothelium-dependent vasorelaxant response is altered by the hypertensive state.

Animals↗

PubMedDate not supplied

Influence of prenatal alcohol exposure on myocardial contractile function in adult rat hearts: role of intracellular calcium and apoptosis.

To assess the teratogenic action of ethanol on cardiac contractile function in offspring exposed to ethanol in utero, pregnant Sprague-Dawley rats were fed with ethanol during gestation. Left-ventricular papillary muscles and myocytes were isolated from the offspring of the ethanol-ingesting and control pregnant rats. Mechanical parameters measured were peak tension development (PTD, indicating the myocardial force-generating capacity), peak cell shortening (PS), time-to-PTD/PS (TPT/TPS), time-to-90% relaxation/re-lengthening (RT(90)/TR(90)), and maximal velocities of contraction/shortening and relaxation/re-lengthening (+/- VT and +/- dL/dt). Intracellular Ca(2+) levels and apoptosis were evaluated with fura-2 fluorescent dye and Caspase-3 activation assay, respectively. Offspring of the ethanol group displayed decreased heart weight associated with comparable body, liver and kidney weight, and papillary muscle weight/size, compared to the control group. However, prenatal ethanol exposure depressed myocardial PTD and +/- VT. The myocardium from the ethanol group also exhibited slightly but significantly shortened TPT, accompanied with normal RT(90). Muscles from both groups exhibited comparable responses to post-rest potentiation, increasing extracellular Ca(2+) concentration, noradrenaline and acute ethanol challenge. Ventricular myocytes from both the control and ethanol groups possessed similar PS, TPS, TR(90) and +/- dL/dt. Both resting and peak intracellular Ca(2+) levels were elevated in myocytes from the ethanol group. Additionally, acute ethanol application depressed caffeine-induced intracellular Ca(2+) rise in myocytes from both groups. Myocytes from the ethanol group displayed an enhanced Caspase-3 activation, compared to control myocytes. These results suggest that prenatal ethanol exposure alters myocardial contractile function and may contribute to the development of postnatal cardiac dysfunction through, in part, increased intracellular Ca(2+) loading and apoptosis.

Animals↗

PubMedDate not supplied

Gender disparity of streptozotocin-induced intrinsic contractile dysfunction in murine ventricular myocytes: role of chronic activation of Akt.

1. Clinical, epidemiological and experimental evidence suggests a 'female advantage' in the progression of cardiovascular diseases, including diabetic cardiomyopathy. It is speculated that this 'gender bias' may be due to gender-related differences in sex hormones and intrinsic myocardial contractile properties. 2. The present study was designed to examine the impact of diabetes and gender on cardiac contractile function and activation of the cardiac survival signalling molecule Akt. Short-term (2 weeks) diabetes was induced in adult mice of both genders with streptozotocin (STZ). Mechanical and intracellular Ca(2+) properties of isolated ventricular myocytes were evaluated using an IonOptix MyoCam system (IonOptix Corporation, Milton, MA, USA). Total and phosphorylated Akt were evaluated using western blot analysis. 3. Female mouse myocytes displayed smaller peak shortening (PS) amplitude and maximal velocity of shortening/relengthening (+/-dL/dt), longer time to PS and time to 90% relengthening compared with male counterparts. Diabetes significantly reduced PS, +/-dL/dt, prolonged TR(90), delayed intracellular Ca(2+) clearing and reduced sarcoplasmic reticulum (SR) Ca(2+) release in male mouse myocytes. All these abnormalities, with the exception of SR Ca(2+), release were masked by the female gender. 4. The negative staircase of PS with increased stimulus frequency (from 0.1 to 5.0 Hz) and protein carbonyl damage were comparable among all animal groups. 5. Female gender and diabetes independently enhanced phosphorylation of Akt without affecting total Akt expression. Interestingly, STZ-induced short-term diabetes failed to elicit additional phosphorylation of Akt in female hearts. 6. In summary, the present data revealed that STZ induced impaired cardiac contractile function and altered intracellular Ca(2+) handling in males, but not females, partially due to intrinsic mechanical differences and Akt activation status between genders.

Animals↗

PubMedDate not supplied

Cardiac-specific overexpression of catalase prolongs lifespan and attenuates ageing-induced cardiomyocyte contractile dysfunction and protein damage.

1. Oxidative stress plays a role in senescence-associated organ deterioration. This is supported by the beneficial effects of anti-oxidants against ageing-related organ damage, although their role in cardiac ageing has not been elucidated. 2. The aim of the present study was to examine the impact of cardiac-specific overexpression of catalase, an enzyme for H(2)O(2) detoxification, on cardiac contractile function and protein damage in young (3-4 months) and old (26-28 months) male mice. Lifespan was analysed using the Kaplan-Meier survival curve. Cardiomyocyte contractile indices at various stimulus frequencies (0.1-5.0 Hz) were analysed, including peak shortening (PS), time to 90% PS, time to 90% relengthening (TR(90)) and maximal velocity of shortening/relengthening (+/-dL/dt). Protein damage was assessed using protein carbonyl formation. Catalase transgenic mice showed longer lifespan than wild-type FVB mice. The catalase transgene itself did not alter bodyweight or organ weight, or myocyte function. Ageing depressed +/-dL/dt and prolonged TR(90), but had no effect on other indices in FVB mice. Increased frequency triggered decreases in PS amplitude were exaggerated in aged FVB myocytes. Interestingly, ageing-induced mechanical defects were significantly attenuated in myocytes from catalase mice. Protein carbonyl formation was elevated in aged FVB compared with young FVB mice, which was significantly diminished in catalase mice. The proteomes of the myocardium of young or old FVB and catalase mice were compared using two-dimensional gel electrophoresis and mass spectrometry. Six proteins with differential expression between young and old FVB groups were tentatively identified, some of which were reversed by catalase. 3. In summary, the present data suggest that catalase protects cardiomyocytes from ageing-induced contractile defects and protein damage.

Aging↗

PubMedDate not supplied

Controlled drug delivery system based on magnetic hollow spheres/polyelectrolyte multilayer core-shell structure.

A novel controlled drug delivery system was fabricated by coating chitosan/PAA multilayer onto magnetic hollow spheres via a "Layer-by-Layer" (LBL) assembly approach. Cefradine was used as a model drug to evaluate the drug release characteristics of this core-shell hollow structure and the results show that it exhibits a sustained release of the drug and the release rate can be regulated by the pH environment of release medium. It is believed that this core-shell hollow structure, which combines the advantage of controlled delivery as well as magnetic targeting, has commendable potential in drug delivery therapeutics.

Acrylic Resins↗

PubMedDate not supplied

Genetic variations of the porcine PRKAG3 gene in Chinese indigenous pig breeds.

Four missense substitutions (T30N, G52S, V199I and R200Q) in the porcine PRKAG3 gene were considered as the likely candidate loci affecting meat quality. In this study, the R200Q substitution was investigated in a sample of 62 individuals from Hampshire, Chinese Min and Erhualian pigs, and the genetic variations of T30N, G52S and V199I substitutions were detected in 1505 individuals from 21 Chinese indigenous breeds, 5 Western commercial pig breeds, and the wild pig. Allele 200R was fixed in Chinese Min and Erhualian pigs. Haplotypes II-QQ and IV-QQ were not observed in the Hampshire population, supporting the hypothesis that allele 200Q is tightly linked with allele 199V. Significant differences in allele frequencies of the three substitutions (T30N, G52S and V199I) between Chinese indigenous pigs and Western commercial pigs were observed. Obvious high frequencies of the "favorable" alleles 30T and 52G in terms of meat quality were detected in Chinese indigenous pigs, which are well known for high meat quality. However, the frequency of the "favorable" allele 199I, which was reported to have a greater effect on meat quality in comparison with 30T and 52G, was very low in all of the Chinese indigenous pigs except for the Min pig. The reasons accounting for this discrepancy remain to be addressed. The presence of the three substitutions in purebred Chinese Tibetan pigs indicates that the three substitutions were ancestral mutations. A novel A/G substitution at position 51 in exon 1 was identified. The results suggest that further studies are required to investigate the associations of these substitutions in the PRKAG3 gene with meat quality of Chinese indigenous pigs, and to uncover other polymorphisms in the PRKAG3 gene with potential effects on meat quality in Chinese indigenous pigs.

Adenine↗