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EN
Obesity and overweight have become a global problem affecting not only high income countries but also developing countries. According to the World Health Organization (WHO) more than 1 billion adults are overweight and at least 300 million of them are obese. Experimental and clinical studies indicate that there is a relationship between iron metabolism and weight status. Iron deficiency is significantly more prevalent among obese individuals compared to non-obese ones. Adipose tissue produces many pro-inflammatory cytokines (interleukin-1, interleukin- 6, tumor necrosis factor-?) and adipokines (leptin, adiponectin, resistin) that influence iron homeostasis. According to recent studies, hepcidin, the main regulator of iron metabolism, can also be synthesized by the adipocytes. Development of iron deficiency among obese and overweight children has potentially harmful effects, which can lead to behavioral and learning problems as well as lowered resistance to infections. For this reason, screening for iron status among children with elevated BMI should be recommended.
EN
Adiponectin is an adipocyte-specific secretory protein, which seems to play a protective role in different models of vascular injury. Adiponectin infiltrates in the subendothelial space of injured vascular walls and suppresses the expression of adhesion molecules on endothelial cells, thus inhibiting the inflammatory processes that occur during the early phases of atherosclerosis. Adiponectin also suppresses lipid accumulation in macrophages and macrophage-to-foam cell transformation. The ability of adiponectin to act as an anti-inflammatory and anti-atherogenic factor has made this novel adipocytokine a promising therapeutic tool for the future.
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vol. 51
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issue 2
193-197
EN
The melanocortin-4 receptor (Mc4r) plays an important role in body-weight regulation. This study examines the methylation status and expression levels of the Mc4r gene in response to a standard and a high-fat diet in the obese Berlin fat mouse inbred (BFMI) line and the lean C57BL/6NCrl (B6) line of Mus musculus. The methylation status of CpG sites located within the Mc4r exon was analyzed by bisulfite genomic sequencing of genomic DNA of brain tissues, and gene expression analysis was performed by real-time PCR. In both lines, the methylation of CpGs 1-8 (near the transcription start) was lower than methylation of CpGs 9-16 (located towards the end of the selected amplicon). On the standard diet, the methylation status did not differ between the lines. In response to high-fat diet, methylation of the CpGs near the transcription start was decreased in both lines. The Mc4r gene expression, however, was only marginally increased in BMFI mice, whereas there was no change in B6 mice. The results suggest that a long-term high-fat diet might have an effect on the methylation status of the Mc4r gene. However, the effect of methylation on Mc4r expression seems to be a variable compensated by other regulating factors in a line-specific manner.
EN
A major challenge in the post-genomic era is to identify the physiological function of genes and elucidate the molecular basis for human disease. Genetic polymorphisms offer a convenient aveune for these efforts by providing evidence for the involvement of a given gene in human pathophysiology. Here we review the current evidence linking the low molecular weight protein tyrosine phosphatase (LMPTP) to several common diseases, including allergy, asthma, obesity, myocardial hypertrophy, and Alzheimer's disease. Based on the know effects of the genetic polymorphisms on the alternative mRNA splicing and enzyme levels of LMPTP, we discuss the possible molecular mechanisms of LMPTP involvement in these diseases.
EN
Thirteen candidate genes for human obesity were selected for cytogenetic mapping by FISH in the pig genome. Among them, 6 genes were assigned to chromosomes for the first time (NR3C1, GNB3, ADRB1, ADRB2, ADRB3 and UCP1). Location of the other 7 genes (INSIG2, LIPIN1, PLIN, NAMPT, ADIPOQ, UCP2 and UCP3), earlier mapped by somatic cell hybridization or with the use of a radiation hybrid panel, was verified (INSIG2) or more precisely described. The genes were assigned to the following chromosomes: INSIG2 to SSC15q12, LIPIN1 to SSC3q26, NR3C1 to SSC2q29, PLIN to SSC7q15, GNB3 to SSC5q21, NAMPT to SSC9q23, ADIPOQ to SSC13q41, ADRB1 to SSC14q28, ADRB2 to SSC2q29, ADRB3 to SSC15q13-14, UCP1 to SSC8q21-22, and both UCP2 and UCP3 to SSC9p24. Most of the genes were located within known QTL for pig fatness traits.
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vol. 51
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issue 2
153-168
EN
Fatnness traits are important in pig production since they influence meat quality and fattening efficiency. On the other hand, excessive fat accumulation in humans has become a serious health problem due to worldwide spread of obesity. Since the pig is also considered as an animal model for numerous human diseases, including obesity and metabolic syndrome, comparative genomic studies may bring new insights into genetics of fatness/obesity. Input of genetic factors into phenotypic variability of these traits is rather high and the heritability coefficient (h2) of these traits oscillates around 0.5. Genome scanning revealed the presence of more than 500 QTLs for fatness in the pig genome. In addition to QTL studies, many candidate gene polymorphisms have been analyzed in terms of their associations with pig fatness, including genes encoding leptin (LEP) and its receptor (LEPR), insulin-like growth factor 2 (IGF-2), fatty acid-binding proteins (FABP3 and FABP4), melanocortin receptor type 4 (MC4R), and the FTO (fat mass and obesity-associated) gene. Among them, a confirmed effect on pig fatness was found for a well-known polymorphism of the IGF-2 gene. In humans the strongest association with predisposition to obesity was shown for polymorphism of the FTO gene, while in pigs such an association seems to be doubtful. The development of functional genomics has revealed a large number of genes whose expression is associated with fat accumulation and lipid metabolism, so far not studied extensively in terms of the association of their polymorphism with pig fatness. Recently, epigenomic mechanisms, mainly RNA interference, have been considered as a potential source of information on genetic input into the fat accumulation process. The rather limited progress in studies focused on the identification of gene polymorphism related with fatness traits shows that their genetic background is highly complex.
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