ArticleArchives of medical science : AMS2012
Population genetic analyses of susceptibility to increased body weight.
Article in Archives of medical science : AMS, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
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Who cites it
6 citing papers in PubMed, 9 citations in OpenAlex.
- Morphogenetic Variability as Potential Biomarker of Functional Outcome After Ischemic Stroke.Brain sciences · 2019Article
- Genetic and Environmental Dispositions for Cardiovascular Variability: A Pilot Study.Journal of clinical medicine · 2018Article
- Morphogenetic Variability and Hypertension in Ischemic Stroke Patients-Preliminary Study.Journal of clinical medicine · 2018Article
- Effect of feeding a high-fat diet independently of caloric intake on reproductive function in diet-induced obese female rats.Archives of medical science : AMS · 2016Article
- Indicators of the metabolic syndrome in obese adolescents.Archives of medical science : AMS · 2015Article
- Obesity risk factors in a representative group of Polish prepubertal children.Archives of medical science : AMS · 2014Article
Corrections and comments
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Authors and funding
9 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
introductionObesity is a complex condition with multifactorial origin. Assuming that such a state is genetically controlled, the aim of our study was to evaluate the degree of genetic homozygosity among overweight and obese individuals by the homozygously recessive characteristics (HRC) test. MATERIAL AND
methodsWe analysed the presence, distribution and individual combination of 15 selected genetically controlled recessive phenotype traits in a sample of 140 individuals with increased body mass index (overweight individuals n = 100 and obese individuals n = 40) and a control group of normal weight individuals (n = 300).
resultsOBESE INDIVIDUALS HAVE SIGNIFICANTLY HIGHER MEAN VALUES FOR GENETIC HOMOZYGOSITY THAN THOSE WITH NORMAL WEIGHT (NORMAL WEIGHT: 3.61 ±1.48; obese: 4.13 ±1.47, p < 0.05) and difference in the presence of certain individual combinations of evaluated phenotype traits (Σχ(2) = 76.9; p < 0.01). There was no difference in average homozygosity of such genetic markers between groups of normal weight and overweight individuals (normal weight: 3.61 ±1.48; overweight: 3.93 ±1.51, p > 0.05) and between groups of overweight and obese individuals (overweight: 3.93 ±1.51; obese: 4.13 ±1.47, p > 0.05). There is no difference in the presence of certain individual combinations of evaluated phenotype traits between overweight and obese individuals (Σχ(2) = 20.6; p > 0.05).
conclusionsThere is a populational genetic difference in the degree of genetic homozygosity and variability between the group of normal weight and group of obese individuals, indicating a possible genetic component. Overweight and obese individuals have a genetic predisposition, but different expression of genetic loads could be one of the possible explanations for different susceptibility to increase of fat mass and body mass index.
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