• Title/Summary/Keyword: genetic obesity

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Obesity : Genetic vs Environmental Factors (비만 : 유전이냐 환경이냐)

  • Lee, Soyoung Irene;Jung, Han-Yong
    • Korean Journal of Biological Psychiatry
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    • v.10 no.1
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    • pp.45-53
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    • 2003
  • Debates relevant to the etiology of weight gain or obesity, i.e., the dichotomous understandings about whether obesity arises from the genetic predisposition or from the environmental influences, has long existed. This is an important issue because it is related to the therapists's prejudice when treating patients with obesity. In this review, the authors first discuss the environmental and the genetic factors that cause the obesity, and in the latter part, the interactions between genetic and environmental factors will be discussed. This issue is considered and described especially in a conceptual aspect for the therapists ultimately to understand how the genetic and the environmental factors interact to arise obesity. Conclusively, obesity is best understood as a complex, multifactorial, and chronic disabled state, which cause an individual with genetic predispostion to obesity under the environmental influences. In future, in favor of the accumulated knowledge about the genetic and environmental impacts and their interactions in detail, we will be able to provide a client-specific management or prevention of obesity.

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Obesity: Interactions of Genome and Nutrients Intake

  • Doo, Miae;Kim, Yangha
    • Preventive Nutrition and Food Science
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    • v.20 no.1
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    • pp.1-7
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    • 2015
  • Obesity has become one of the major public health problems all over the world. Recent novel eras of research are opening for the effective management of obesity though gene and nutrient intake interactions because the causes of obesity are complex and multifactorial. Through GWASs (genome-wide association studies) and genetic variations (SNPs, single nucleotide polymorphisms), as the genetic factors are likely to determine individuals' obesity predisposition. The understanding of genetic approaches in nutritional sciences is referred as "nutrigenomics". Nutrigenomics explores the interaction between genetic factors and dietary nutrient intake on various disease phenotypes such as obesity. Therefore, this novel approach might suggest a solution for the effective prevention and treatment of obesity through individual genetic profiles and help improve health conditions.

Relationship of Environmental Factors, Genetic Factors and Obesity with Sexual Maturity among Elementary School Girls (초등학교 여학생의 환경과 유전적 요인 및 비만도와 성적성숙도와의 관련성에 대한 연구)

  • Park, Jun-Hui;Kim, Yeong-Ok
    • Journal of the Korean Dietetic Association
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    • v.12 no.3
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    • pp.225-234
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    • 2006
  • The purpose of this study was to identify the factors that related to obesity among 6th grade elementary school girls. The study subjects were 337 girls residing in Seoul. Not only variables of nutritional environment such as eating habits, health related behavioral variables, nutritional feeding methods during infancy, and genetic factors but also sexual maturity had been included as a obesity related factors. Association between obesity and related variables were analyzed by $x^2$(Chi-square) test. The obesity prevalence of the study subjects were 16% based on Röhrer Index(RI). Fifty-three percent of the study subjects experienced menarche at the time of data collection. Result of analysis showed that not only the nutritional enviromental variables such as eating habits, specific food preferences, and habit of exercise but also genetic factors did not show any statistically significant association with obesity. Above finding may imply that more variables other than the variables included in this study might have influenced on the obesity of the children. However sexual maturity in term of breast development showed significant association with obesity.

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Joint Identification of Multiple Genetic Variants of Obesity in a Korean Genome-wide Association Study

  • Oh, So-Hee;Cho, Seo-Ae;Park, Tae-Sung
    • Genomics & Informatics
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    • v.8 no.3
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    • pp.142-149
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    • 2010
  • In recent years, genome-wide association (GWA) studies have successfully led to many discoveries of genetic variants affecting common complex traits, including height, blood pressure, and diabetes. Although GWA studies have made much progress in finding single nucleotide polymorphisms (SNPs) associated with many complex traits, such SNPs have been shown to explain only a very small proportion of the underlying genetic variance of complex traits. This is partly due to that fact that most current GWA studies have relied on single-marker approaches that identify single genetic factors individually and have limitations in considering the joint effects of multiple genetic factors on complex traits. Joint identification of multiple genetic factors would be more powerful and provide a better prediction of complex traits, since it utilizes combined information across variants. Recently, a new statistical method for joint identification of genetic variants for common complex traits via the elastic-net regularization method was proposed. In this study, we applied this joint identification approach to a large-scale GWA dataset (i.e., 8842 samples and 327,872 SNPs) in order to identify genetic variants of obesity for the Korean population. In addition, in order to test for the biological significance of the jointly identified SNPs, gene ontology and pathway enrichment analyses were further conducted.

Genetic Variations of Eight Candidate Genes in Korean Obese Group

  • Kang, Byung-Youn;Lee, Kang-Oh;Bae, Joon-Seol;Kim, Ki-Tae;Yoon, Moon-Young;Lim, Seok-Rhin;Seo, Sang-Beom;Shin, Jung-Hee;Lee, Chung-Choo
    • Environmental Mutagens and Carcinogens
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    • v.22 no.1
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    • pp.39-46
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    • 2002
  • Obesity is a complex metabolic disorder with a strong genetic component. There are many candidate genes for obesity and its related phenotypes. We studied genetic variations between Korean obese and lean groups. Polymorphisms investigated were the Msp I polymorphism of the $\alpha$$_{2A}$-adrenergic receptor ($\alpha$$_{2A}$-AR) gene, the Mnl I polymorphism of the $\alpha$$_2$-adrenergic receptor ($\alpha$$_2$-AR) gene, the BstO I polymorphism of the $\beta$$_3$-adrenergic receptor ($\beta$$_3$-AR) gene, the Pml I polymorphism of the lamin A/C (LMNA) gene, the Hga I polymorphism of the clearance receptor (NPRC) gene, the Msp I polymorphism of the leptin gene, BclI polymorphism of the uncoupling protein 1 (UCPI) gene and the Hha I polymorphism of the fatty acid binding protein 2 (FABP2) gene. Among these genetic markers, Pml I polymorphism at the LMNA gene and Bcl I polymorphism at the UCP1 gene were significantly associated with obesity. However, further studies are required whether thease findings are reproduced in large population, although two polymorphisms might be useful as genetic markers in the ethiology of obesity in Korean population.ion.

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Primary cilia in energy balance signaling and metabolic disorder

  • Lee, Hankyu;Song, Jieun;Jung, Joo Hyun;Ko, Hyuk Wan
    • BMB Reports
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    • v.48 no.12
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    • pp.647-654
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    • 2015
  • Energy homeostasis in our body system is maintained by balancing the intake and expenditure of energy. Excessive accumulation of fat by disrupting the balance system causes overweight and obesity, which are increasingly becoming global health concerns. Understanding the pathogenesis of obesity focused on studying the genes related to familial types of obesity. Recently, a rare human genetic disorder, ciliopathy, links the role for genes regulating structure and function of a cellular organelle, the primary cilium, to metabolic disorder, obesity and type II diabetes. Primary cilia are microtubule based hair-like membranous structures, lacking motility and functions such as sensing the environmental cues, and transducing extracellular signals within the cells. Interestingly, the subclass of ciliopathies, such as Bardet-Biedle and Alström syndrome, manifest obesity and type II diabetes in human and mouse model systems. Moreover, studies on genetic mouse model system indicate that more ciliary genes affect energy homeostasis through multiple regulatory steps such as central and peripheral actions of leptin and insulin. In this review, we discuss the latest findings in primary cilia and metabolic disorders, and propose the possible interaction between primary cilia and the leptin and insulin signal pathways which might enhance our understanding of the unambiguous link of a cell's antenna to obesity and type II diabetes.

Endocrine problems in children with Prader-Willi syndrome: special review on associated genetic aspects and early growth hormone treatment

  • Jin, Dong-Kyu
    • Clinical and Experimental Pediatrics
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    • v.55 no.7
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    • pp.224-231
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    • 2012
  • Prader-Willi syndrome (PWS) is a complex multisystem genetic disorder characterized by hypothalamic-pituitary dysfunction. The main clinical features include neonatal hypotonia, distinctive facial features, overall developmental delay, and poor growth in infancy, followed by overeating with severe obesity, short stature, and hypogonadism later in development. This paper reviews recent updates regarding the genetic aspects of this disorder. Three mechanisms (paternal deletion, maternal disomy, and deficient imprinting) are recognized. Maternal disomy can arise because of 4 possible mechanisms: trisomy rescue (TR), gamete complementation (GC), monosomy rescue (MR), and postfertilization mitotic nondisjunction (Mit). Recently, TR/GC caused by nondisjunction at maternal meiosis 1 has been identified increasingly, as a result of advanced maternal childbearing age in Korea. We verified that the d3 allele increases the responsiveness of the growth hormone (GH) receptor to endogenous GH. This paper also provides an overview of endocrine dysfunctions in children with PWS, including GH deficiency, obesity, sexual development, hypothyroidism, and adrenal insufficiency, as well as the effects of GH treatment. GH treatment coupled with a strictly controlled diet during early childhood may help to reduce obesity, improve neurodevelopment, and increase muscle mass. A more active approach to correct these hormone deficiencies would benefit patients with PWS.

Evaluation of Secondary Obesity (이차성 비만의 진단)

  • Kim, Bo-Yeon
    • Archives of Obesity and Metabolism
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    • v.1 no.2
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    • pp.53-58
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    • 2022
  • While the rising epidemic of obesity is primarily attributed to a sedentary lifestyle, poor dietary habits, and the aging of the population, secondary causes of obesity generally go undetected and untreated. These include endocrinological disorders, such as Cushing's syndrome, polycystic ovary syndrome, hypothalamic obesity, hypogonadism, and hypothyroidism, as well as genetic, syndromic, and drug-related obesity. We present an overview of the major disorders associated with obesity, highlighting the pathophysiologic mechanisms and discussing the diagnostic and treatment strategies that are most helpful to practicing physicians in recognizing and treating these generally under-detected and undertreated disorders.

Maternal and grandmaternal obesity and environmental factors as determinants of daughter's obesity

  • Shin, Mi Na;Lee, Kyung Hea;Lee, Hye Sang;Sasaki, Satoshi;Oh, Hea Young;Lyu, Eun Soon;Kim, Mi Kyung
    • Nutrition Research and Practice
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    • v.7 no.5
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    • pp.400-408
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    • 2013
  • Obesity may be the consequence of various environmental or genetic factors, which may be highly correlated with each other. We aimed to examine whether grandmaternal and maternal obesity and environmental risk factors are related to obesity in daughters. Daughters (n = 182) recruited from female students, their mothers (n = 147) and their grandmothers (n = 67) were included in this study. Multivariable logistic regression was used to analyze the association between the daughter's obesity and maternal, grandmaternal, and environmental factors. Maternal heights of 161-175cm (OD: 8.48, 95% CI: 3.61-19.93) and 156-160 cm (2.37, 1.14-4.91) showed positive associations with a higher height of daughter, compared to those of 149-155 cm. Mothers receiving a university or a higher education had a significant OR (3.82, 1.27-11.50) for a higher height of daughter compared to those having a low education (elementary school). Mother having the heaviest weight at current time (59-80 kg, 3.78, 1.73-8.28) and the heaviest weight at 20 years of age (51-65 kg, 3.17, 1.53-6.55) had significant associations with a higher height of daughters, compared to those having the lightest weight at the same times. There was no association between the height, weight, and BMI of daughters and the characteristics and education of her grandmothers. In conclusion, although genetic factors appear to influence the daughter's height more than environmental factors, the daughter's weight appears to be more strongly associated with individual factors than the genetic factors.

Chitinase 3-Like 1 (CHI3L1) Polymorphism Contributes to Visceral Obesity and Obesity-related Inflammation Induces Chi3l1 in Adipocytes

  • Kim, A Young;Jeong, Hyun Woo;Lee, Ji-Hae;Choi, Jin Kyu;Kim, Jeong Kee;Hwang, Jae Sung;Seo, Dae-Bang
    • Biomedical Science Letters
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    • v.24 no.1
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    • pp.23-29
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    • 2018
  • Abdominal obesity is considered as one of the most risky factors governing the development of metabolic diseases. Here we identify that human chitinase 3-like 1 (CHI3L1, also called YKL-40 in human) single nucleotide polymorphism (SNP), rs883125, is associated with abdominal obesity in Korean women. Korean women subjects with the rs883125 G/G or C/G genotype present higher waist-hip ratio than subjects with C/C genotype suggesting that human subjects who G nucleotide substitution at the rs883125 tended to more accumulate intra-abdominal fat at the abdominal cavity. In addition, Chi3l1 gene expression is increased in adipose tissue from obese mice and pro-inflammatory cytokine enhances Chi3l1 expression in adipocytes, indicating that Chi3l1 is greatly related with obesity and obesity-induced pro-inflammatory responses. Taken together, the minor allele of rs883125 is associated with a higher prevalence of abdominal obesity in Korean women. These findings suggest that genotype of rs883125 can be a biomarker of incident abdominal obesity and abdominal obesity-related metabolic diseases.