Genetic variation at the adipsin locus and response to long-term overfeeding

Ukkola, Olavi; Chagnon, Monique; Tremblay, Angelo; Bouchard, Claude

doi:10.1038/sj.ejcn.1601644

Cited by 16 publications

(8 citation statements)

References 21 publications

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“…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). Resting energy expenditure, thermic effect of feeding, and 24‐hour lipid oxidation phenotypes were associated with ADRB3 (126), IL6 (127), LEPR (128), PPARG (129), and PPARGC1 (130) markers, whereas adipocyte size and lipolysis showed associations with polymorphisms in LEPR (128), PLIN (131), and PPARGC1 (130).…”

Section: Qtls From Crossbreeding Experimentsmentioning

confidence: 99%

The Human Obesity Gene Map: The 2003 Update

et al. 2004

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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.

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Section: Qtls From Crossbreeding Experimentsmentioning

confidence: 99%

The Human Obesity Gene Map: The 2003 Update

et al. 2004

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“…However, in a review study published by Mlinar et al, the adipose level increases with insulin levels under the conditions of insulin resistance in which insulin is higher than normal (21), which contrasts with the results of the present study. Adipose levels are also considered as secondary signs of obesity (18). Also, Villa and (25) reported that women with PCOS do not have an increase in VAI.…”

Section: Discussionmentioning

confidence: 99%

The Effect of 12 Weeks of Intense Interval Training on Changes in Adipose Levels and Visceral Adiposity Index in Women with Polycystic Ovary Syndrome

Faryadian¹,

Behpoor²,

Taedibi³

2020

Int J Health Life Sci

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Background: Polycystic ovary syndrome is the most common endocrine disorder in women, which causes many disorders including diabetes. Objectives: The present study aimed to determine changes in adipose levels and visceral adiposity index after 12 weeks of intense interval training in women with polycystic ovary syndrome in Kermanshah city. Methods: This quasi-experimental study recruited 24 women with polycystic ovary in Kermanshah in 2017. First, 24 women were selected by convenience sampling and then they were divided into two groups of 12 patients. Interval training was performed continuously in the study group 3 sessions per week for 12 weeks. Serum levels of adipose and visceral adiposity index were determined before and after the exercise program through blood sampling and in laboratory conditions. Data was analyzed in SPSS software version 20 using paired t-test and independent t-test. Results: The results revealed no significant difference in adipose levels after 12 weeks of intense interval training in the study group (P < 0.05). But a significant difference was observed in visceral adiposity index before and after the intervention in the study group (P < 0.05). Conclusions:Intense interval training has a favorable effect on the visceral adiposity index in women with polycystic ovary syndrome and can be recommended as a safe treatment for these patients.

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“…Adipsin, a serine protease secreted by adipocytes and identical to complement factor D, is located on mouse chromosome 10 at 80.0 Mb. Although evidence for a primary role for adipsin in the etiology of obesity is lacking (20,21), a human twin study has shown that adipsin polymorphisms are correlated with response to overfeeding (22). Promelanin-concentrating hormone (Pmch), a hypothalamic peptide involved in feeding behavior, exists near the chromosome 10 locus peak at 47.0 cm.…”

Section: Discussionmentioning

confidence: 99%

Identification of quantitative trait loci affecting body composition in a mouse intercross

Vitarius

Sehayek

Breslow

2006

Proc. Natl. Acad. Sci. U.S.A.

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Gravimetric analysis and dual energy x-ray absorptiometry densitometry were used to determine lean, fat, and bone tissue traits in a F2 mouse population from a C57BL/6J and CASA/Rk intercross (B6CASAF2). These traits were used in a linkage analysis to identify quantitative trait loci that affect body composition. Linkage mapping showed that body weight (BW) loci on proximal chromosome 2 occurred in the same region as body length, lean tissue mass, and bone mineral content and on chromosome 13 in the same region as lean tissue mass, bone mineral density, and bone mineral content. Fat-related loci occurring on mid-chromosome 2 near 60 cM, proximal chromosome 6, and mid-chromosome 10 were distinct from BW, lean tissue, and bone tissue loci. In B6CASAF2 females, heterozygotes and CASA/Rk homozygotes at the chromosome 6 locus marker had higher body fat percentages, and this locus was responsible for 11% of the variance for body fat percentage. Female heterozygotes and C57BL/6J homozygotes at the chromosome 15 locus marker had higher bone mineral densities, and this locus could explain 8% of that trait's variance. A survey of the literature did not reveal any previous reports of fat-specific loci in the chromosomal 10 region near 42 cM reported in this study. The results of this study indicate that BW and BMI have limited usefulness as phenotypes in linkage or association studies when used as obesity phenotypes.body mass index ͉ bone mineral density ͉ dual energy x-ray absorptiometry ͉ lean tissue mass ͉ obesity

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Genetic variation at the adipsin locus and response to long-term overfeeding

Cited by 16 publications

References 21 publications

The Human Obesity Gene Map: The 2003 Update

The Human Obesity Gene Map: The 2003 Update

The Effect of 12 Weeks of Intense Interval Training on Changes in Adipose Levels and Visceral Adiposity Index in Women with Polycystic Ovary Syndrome

Identification of quantitative trait loci affecting body composition in a mouse intercross

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