Na<sup>+</sup>-K<sup>+</sup>-ATPase α2-gene and skeletal muscle characteristics in response to long-term overfeeding

Ukkola, Olavi; Joanisse, Denis R.; Tremblay, Angelo; Bouchard, Claude

doi:10.1152/japplphysiol.00942.2002

Cited by 18 publications

(8 citation statements)

References 21 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…In addition, it seems that the enzyme is fully activated during exercise (41)(42)(43). The absolute OGDH activity values measured in skeletal muscle of adults in the present study was similar to those previously reported (42,44). However, to our knowledge, the activity of this enzyme has not yet been reported in children.…”

supporting

confidence: 91%

Anaerobic and Aerobic Enzyme Activities in Human Skeletal Muscle from Children and Adults

et al. 2005

View full text Add to dashboard Cite

Literature has shown that children have lower anaerobic capacity and oxidize more lipids during aerobic activity compared with adults. The purpose of the present study was to examine the effects of age on the activity of marker enzymes for anaerobic and aerobic metabolism in human skeletal muscle from relatively sedentary children and adults. The m. obliquus internus abdominis was analyzed for anaerobic [creatine kinase, adenylate kinase, and lactate dehydrogenase (LDH)] and aerobic (carnitine palmitoyltransferase and 2-oxoglutarate dehydrogenase) enzyme activities in 32 male individuals. The subjects were divided into two groups: children (3-11 y; n ϭ 20) and adults (29 -54 y; n ϭ 12). LDH activity was higher in adults (118.2 Ϯ 20.1) compared with children (27.8 Ϯ 10.1) mol · min Ϫ1 · g Ϫ1 wet weight (p Ͻ 0.0002). Creatine kinase activity was 28% (p Ͻ 0.0003) lower in children than in adults, and adenylate kinase activity was 20% (p Ͻ 0.006) lower in children than in adults. In addition, we found higher 2-oxoglutarate dehydrogenase activity in adults compared with children (p Ͻ 0.04), with no effect of age on carnitine palmitoyltransferase activity (NS). When samples were expressed relative to protein content, only LDH activity remained significantly lower in children compared with adults (p Ͻ 0.0001). In conclusion, the lower LDH activity observed in children compared with adults may partially explain decreased anaerobic and lactate generation capacity of the children studied. However, the mechanisms for the relatively deficient anaerobic enzyme activities of children are not clear. The functional characteristics of human skeletal muscle are partially dependent on fiber type; however, modifications to the nature and the capacity of the energy-delivering metabolic pathways can occur independent of fiber type. It is widely known that metabolic enzymes in skeletal muscle have the ability to respond to physiologic stimuli such as exercise (1-4), as well as pathologic processes such as muscular dystrophy, acute respiratory failure, mitochondrial myopathy, denervation, and inactivity (5-9). Although there is some controversy regarding fiber type differences between children and adults (10 -13), there are only minor increases in the proportion of type II fibers with age (10 -12), with no difference in ultrastructure (13). Moreover, there is still disagreement over the effect of age on the enzymatic capacity of skeletal muscle, particularly during the maturation from the pediatric to the adult age group.It has been reported that phosphofructokinase (PFK) was 3-fold lower in the skeletal muscle of children (11-13 y) compared with adults (24 -52 y); however, succinate dehydrogenase activity was not significantly altered by age (11,14). Other studies that have examined anaerobic enzyme activity in children have reported lower glycolytic [PFK, lactate dehydrogenase (LDH)] and higher aerobic (succinate dehydrogenase, fumarase) enzyme activities in children compared with younger adults (14,15). In contrast, one report demon...

show abstract

supporting

confidence: 91%

Anaerobic and Aerobic Enzyme Activities in Human Skeletal Muscle from Children and Adults

et al. 2005

View full text Add to dashboard Cite

show abstract

“…In addition, candidate genes in two of our linkage regions have previously been associated with obesity. These associations include the APOA2 (31,32) and ATP1A2 (33,34,35) genes located in our chromosome 1 linkage region () and SLC6A3 (36) located in one of our chromosome 5 (1–5 Mb) linkage regions ().…”

Section: Discussionmentioning

confidence: 99%

Linkage and Genome‐wide Association Analysis of Obesity‐related Phenotypes: Association of Weight With the MGAT1 Gene

Johansson

Marroni

Hayward

et al. 2010

Obesity

View full text Add to dashboard Cite

As major risk‐factors for diabetes and cardiovascular diseases, the genetic contribution to obesity‐related traits has been of interest for decades. Recently, a limited number of common genetic variants, which have replicated in different populations, have been identified. One approach to increase the statistical power in genetic mapping studies is to focus on populations with increased levels of linkage disequilibrium (LD) and reduced genetic diversity. We have performed joint linkage and genome‐wide association analyses for weight and BMI in 3,448 (linkage) and 3,925 (association) partly overlapping healthy individuals from five European populations. A total of four chromosomal regions (two for weight and two for BMI) showed suggestive linkage (lod >2.69) either in one of the populations or in the joint data. At the genome‐wide level (nominal P < 1.6 × 10−7, Bonferroni‐adjusted P < 0.05) one single‐nucleotide polymorphism (SNP) (rs12517906) (nominal P = 7.3 × 10−8) was associated with weight, whereas none with BMI. The SNP associated with weight is located close to MGAT1. The monoacylglycerol acyltransferase (MGAT) enzyme family is known to be involved in dietary fat absorption. There was no overlap between the linkage regions and the associated SNPs. Our results show that genetic effects influencing weight and BMI are shared across diverse European populations, even though some of these populations have experienced recent population bottlenecks and/or been affected by genetic drift. The analysis enabled us to identify a new candidate gene, MGAT1, associated with weight in women.

show abstract

“…Body fatness‐related phenotypes (fat mass, percentage of body fat, sum of skinfolds) showed associations with markers in AGRP (87), AR (118), ATP1A2 (92), CNTFR (119), ESR1 (94), FOXC2 (96), IRS2 (101), LIPE (103), PPARA (109), and PPARG (113). Phenotypes reflecting body fat distribution (abdominal visceral fat, waist circumference, waist‐to‐hip girth ratio, sagittal diameter) were associated with ADRB2 (120, 121), APM1 (89), APOA1 (90), AR (122), CYP19A1 (123), DF (124), ESR1 (94), HSD11B1 (98), IL6 (99), IRS2 (101), LIPC (102), MACS2 (104), PPARG (113, 114), TGFB1 (117), and UCP1 (125).…”

Section: Qtls From Crossbreeding Experimentsmentioning

confidence: 99%

The Human Obesity Gene Map: The 2003 Update

et al. 2004

Self Cite

View full text Add to dashboard Cite

This is the tenth update of the human obesity gene map, incorporating published results up to the end of October 2003 and continuing the previous format. Evidence from single‐gene mutation obesity cases, Mendelian disorders exhibiting obesity as a clinical feature, quantitative trait loci (QTLs) from human genome‐wide scans and animal crossbreeding experiments, and association and linkage studies with candidate genes and other markers is reviewed. Transgenic and knockout murine models relevant to obesity are also incorporated (N = 55). As of October 2003, 41 Mendelian syndromes relevant to human obesity have been mapped to a genomic region, and causal genes or strong candidates have been identified for most of these syndromes. QTLs reported from animal models currently number 183. There are 208 human QTLs for obesity phenotypes from genome‐wide scans and candidate regions in targeted studies. A total of 35 genomic regions harbor QTLs replicated among two to five studies. Attempts to relate DNA sequence variation in specific genes to obesity phenotypes continue to grow, with 272 studies reporting positive associations with 90 candidate genes. Fifteen such candidate genes are supported by at least five positive studies. The obesity gene map shows putative loci on all chromosomes except Y. Overall, more than 430 genes, markers, and chromosomal regions have been associated or linked with human obesity phenotypes. The electronic version of the map with links to useful sites can be found at http://obesitygene.pbrc.edu.

show abstract

Na⁺-K⁺-ATPase α2-gene and skeletal muscle characteristics in response to long-term overfeeding

Abstract: and skeletal muscle characteristics in response to long-term overfeeding.

Cited by 18 publications

References 21 publications

Anaerobic and Aerobic Enzyme Activities in Human Skeletal Muscle from Children and Adults

Anaerobic and Aerobic Enzyme Activities in Human Skeletal Muscle from Children and Adults

Linkage and Genome‐wide Association Analysis of Obesity‐related Phenotypes: Association of Weight With the MGAT1 Gene

The Human Obesity Gene Map: The 2003 Update

Contact Info

Product

Resources

About

Na+-K+-ATPase α2-gene and skeletal muscle characteristics in response to long-term overfeeding

Abstract: and skeletal muscle characteristics in response to long-term overfeeding.

Cited by 18 publications

References 21 publications

Anaerobic and Aerobic Enzyme Activities in Human Skeletal Muscle from Children and Adults

Anaerobic and Aerobic Enzyme Activities in Human Skeletal Muscle from Children and Adults

Linkage and Genome‐wide Association Analysis of Obesity‐related Phenotypes: Association of Weight With the MGAT1 Gene

The Human Obesity Gene Map: The 2003 Update

Contact Info

Product

Resources

About

Na⁺-K⁺-ATPase α2-gene and skeletal muscle characteristics in response to long-term overfeeding