Lack of association between polymorphism of the human cyclic GMP-dependent protein kinase gene and obesity. Int J Obes (Lond)

Section on Statistical Genetics, Department of Biostatistics, University of Alabama at Birmingham, Birmingham, AL 35294, USA.
International Journal of Obesity (Impact Factor: 5). 08/2005; 29(7):872-4. DOI: 10.1038/sj.ijo.0802973
Source: PubMed


To investigate whether genetic variation in the cyclic GMP-dependent protein kinase gene (PRKG1) is associated with obesity.
The study included 143 individuals from New York City area, NY, USA. The subjects were sampled on the basis of body mass index (BMI): obese (BMI ranging from 33.8 to 89.5 kg/m(2)), and nonobese (BMI ranging from 16.0 to 29.4 kg/m(2)). The association between C2276T polymorphism in PRKG1 gene and obesity was tested using linear regression analysis.
BMI levels were predicted by linear regression models adjusted for demographic factors. An analysis was performed twice: in individuals of all ethnic backgrounds and in European-Americans only. In both cases, genotype did not have a significant effect.
We found no evidence that the C2276T polymorphism in the PKRG1 gene is associated with obesity.

Download full-text


Available from: Marla B Sokolowski, Oct 04, 2015
16 Reads
  • Source
    • "Function of FAM86D is still unknown. We confirmed intronic gain at PRKG1 in one EC, which is involved in fatty acid metabolism [33]. We found loss at ANKS1B, while overexpression of ANKS1B is reported in pre-B cell acute lymphocytic leukaemia [34]. "
    [Show abstract] [Hide abstract]
    ABSTRACT: Ollier disease is a rare, non-hereditary disorder which is characterized by the presence of multiple enchondromas (ECs), benign cartilaginous neoplasms arising within the medulla of the bone, with an asymmetric distribution. The risk of malignant transformation towards central chondrosarcoma (CS) is increased up to 35%. The aetiology of Ollier disease is unknown. We undertook genome-wide copy number and loss of heterozygosity (LOH) analysis using Affymetrix SNP 6.0 array on 37 tumours of 28 Ollier patients in combination with expression array using Illumina BeadArray v3.0 for 7 ECs of 6 patients. Non-recurrent EC specific copy number alterations were found at FAM86D, PRKG1 and ANKS1B. LOH with copy number loss of chromosome 6 was found in two ECs from two unrelated Ollier patients. One of these patients also had LOH at chromosome 3. However, no common genomic alterations were found for all ECs. Using an integration approach of SNP and expression array we identified loss as well as down regulation of POU5F1 and gain as well as up regulation of NIPBL. None of these candidate regions were affected in more than two Ollier patients suggesting these changes to be random secondary events in EC development. An increased number of genetic alterations and LOH were found in Ollier CS which mainly involves chromosomes 9p, 6q, 5q and 3p. We present the first genome-wide analysis of the largest international series of Ollier ECs and CS reported so far and demonstrate that copy number alterations and LOH are rare and non-recurrent in Ollier ECs while secondary CS are genetically unstable. One could predict that instead small deletions, point mutations or epigenetic mechanisms play a role in the origin of ECs of Ollier disease.
    Orphanet Journal of Rare Diseases 01/2011; 6(1):2. DOI:10.1186/1750-1172-6-2 · 3.36 Impact Factor
  • Source
    • "prkg1 is homologous to D. melanogaster for. Although a polymorphism in prkg1 has not yet been found between obese and healthy-weight human populations (Zakharkin et al. 2005), some evidence suggests a link between cGK1 and obesity. prkg1 is expressed at higher levels in adipocytes of obese women (Engeli et al. 2004). "
    [Show abstract] [Hide abstract]
    ABSTRACT: Successful foraging is necessary for procurement of nutritional resources essential for an animal's survival. Maintenance of foraging and food acquisition is dependent on the ability to balance food intake and energy expenditure. This review examines the role of cGMP-dependent protein kinase (PKG) as a regulator of foraging behaviour, food acquisition, and energy balance. The role of PKG in food-related behaviours is highly conserved among worms, flies, bees, ants, and mammals. A growing body of literature suggests that PKG plays an integral role in the component behaviours and physiologies underlying foraging behaviour. These include energy acquisition, nutrient absorption, nutrient allocation, nutrient storage, and energy use. New evidence suggests that PKG mediates both neural and physiological mechanisms underlying these processes. This review illustrates how investigating the role of PKG in energy homeostasis in a diversity of organisms can offer a broad perspective on the mechanisms mediating energy balance.
    Genome 02/2009; 52(1):1-7. DOI:10.1139/G08-090 · 1.42 Impact Factor
  • Source
    [Show abstract] [Hide abstract]
    ABSTRACT: In natural environments where food abundance and quality can change drastically over time, animals must continuously alter their food acquisition strategies. Although genetic variation contributes to this plasticity, the specific genes involved and their interactions with the environment are poorly understood. Here we report that natural variation in the Drosophila gene, foraging (for), which encodes a cGMP-dependent protein kinase (PKG), affects larval food acquisition in an environmentally dependent fashion. When food is plentiful, the wild-type rover (for(R)) allele confers lower food intake and higher glucose absorption than both the wild-type sitter (for(s)) allele and the mutant for(s2) allele. When food is scarce, for(R), for(s) and for(s2) larvae increase food intake to a common maximal level, but for(R) larvae retain their increased absorption efficiency. Changes in for expression can induce corrective behavioral modifications in response to food deprivation. When reared in environments with low food levels, for(R) larvae have higher survivorship and faster development than for(s) and for(s2) larvae. Together, these results show that natural variation in for has far reaching implications affecting a suite of phenotypes involved in the regulation of food acquisition.
    Journal of Experimental Biology 11/2007; 210(Pt 20):3547-58. DOI:10.1242/jeb.006924 · 2.90 Impact Factor
Show more