The genetic basis of obesity complications

Abstract

Intensive research is currently being performed into the genetic background of excess body mass complications such as diabetes, cardiovascular disorders, especially atherosclerosis and coronary heart disease. Chronic inflammation is an important process in the pathogenesis of obesity, wherein there is an aberrant expression of genes encoding adipokines. Visceral tissue is characterized by a higher expression and secretion of interleukin-8, interleukin-1ß and plasminogen activator inhibitor 1 in the subcutaneous tissue secretion of leptin prevails. An important complication of obesity is obstructive sleep apnea, often observed in PraderWilli syndrome. The genetic background of sleep apnea may be a polymorphism of the SREBF1 gene. The consequence of excess body mass is metabolic syndrome, which may be related to the occurrence of the rs926198 variant of gene encoding caveolin-1. The genes of transcription factor TCF7L2 and PPAR-γ2 take part in the pathogenesis of diabetes development. It has been demonstrated that oncogenes FOS, FOSB, and JUN may be co-responsible not only for obesity but also for osteoporosis and colorectal cancer. It has been shown that weight loss causes a modification in the expression of about 100 genes involvedt in the production of substances such as cytokines and other responsible for chronic inflammation in obesity. In future studies on the complications of obesity, such scientific disciplines as proteomics, peptidomics, metabolomics and transcriptomics should be used. The aim of this study is to present the current state of knowledge about the genetic basis of obesity complications.

Candidate SNP Markers of Atherogenesis Significantly Shifting the Affinity of TATA-Binding Protein for Human Gene Promoters Show Stabilizing Natural Selection as a Sum of Neutral Drift Accelerating Atherogenesis and Directional Natural Selection Slowing It

“…Human gene LEP codes for leptin, which is also called obesity hormone because laboratory animals with a protein-damaging mutation in this gene are abnormally obese [119], as shown in Table 5. As readers can see in this table, within the human leptin promoter, we identified two unannotated SNPs able to cause obesity that can accelerate atherogenesis in line with a review article [120] found in PubMed using its keyword search utility [38]. In addition, here we found three unannotated SNPs increasing the LEP level (and thus protecting against both obesity and atherosclerosis [121]) as candidate SNP markers of an atherogenesis slowdown (e.g., rs34104384, Table 5).…”

“…Human gene APOA1 for apolipoprotein A1 carries a known SNP marker (APOA1:−35A>C) of hematuria, fatty liver, and obesity [122], and is a commonly accepted risk factor of atherogenesis acceleration [120]. Indeed, this prediction is consistent with the outcome of treatment of atherosclerosis using exogenous apolipoprotein A1 [123] as well as by both a low-protein diet and exercise increasing the endogenous APOA1 level in obese post-menopausal women [124].…”

Effect of One-Year Growth Hormone Therapy on Cardiometabolic Risk Factors in Boys with Obesity

“…A recent study indicated that excessive gain of gestational weight, gestational diabetes mellitus, breast feeding for a period of less than 6 months, and hypertensive disorders of pregnancy may lead to maternal and childhood obesity [2]. Skrypnik et al [3] presented the current state of knowledge about the genetic basis of obesity complications. Early attention and detection of these risk factors may prevent the development of obesity and its complications.…”

Socio-demographic and behavioural determinants of body mass index among an adult population in rural Northern Ghana: the AWI-Gen study

“…Reported lifestyle factors include alcohol consumption, smoking [18,19] and physical inactivity [20]. The role of genetic factors in determining BMI has also been extensively reported in the literature [21,22]. Several cross-sectional and longitudinal studies in non-African countries have also observed a positive association between BMI and pesticide exposure [23–27].…”