Relevant bibliographies by topics / Obesity – Genetic aspects

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  1. Journal articles
  2. Dissertations / Theses
  3. Books
  4. Book chapters

Academic literature on the topic 'Obesity – Genetic aspects'

Author: Grafiati
Published: 4 June 2021
Last updated: 20 February 2023

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Journal articles on the topic "Obesity – Genetic aspects"

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BOUCHARD, CLAUDE, and LOUIS PÉRUSSE. "Genetic Aspects of Obesity." Annals of the New York Academy of Sciences 699, no. 1 Prevention an (October 1993): 26–35. http://dx.doi.org/10.1111/j.1749-6632.1993.tb18834.x.

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Johnson, P. R., M. R. C. Greenwood, B. A. Horwitz, and J. S. Stern. "Animal Models of Obesity: Genetic Aspects." Annual Review of Nutrition 11, no. 1 (July 1991): 325–53. http://dx.doi.org/10.1146/annurev.nu.11.070191.001545.

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Barness, Lewis A., John M. Opitz, and Enid Gilbert-Barness. "Obesity: Genetic, molecular, and environmental aspects." American Journal of Medical Genetics Part A 143A, no. 24 (2007): 3016–34. http://dx.doi.org/10.1002/ajmg.a.32035.

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Sadaf Farooqi, I. "Genetic and hereditary aspects of childhood obesity." Best Practice & Research Clinical Endocrinology & Metabolism 19, no. 3 (September 2005): 359–74. http://dx.doi.org/10.1016/j.beem.2005.04.004.

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Tyrtova, Ludmila Viktorovna, Natalja Vladimirovna Parshina, and Kristina Vladimirovna Skobeleva. "Genetic and Epigenetic Aspects of Obessity and Metabolic Syndrom in Child." Pediatrician (St. Petersburg) 4, no. 2 (June 15, 2013): 3–11. http://dx.doi.org/10.17816/ped423-11.

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In a review article analyzes the role of heredity in the occurrence of obesity and metabolic syndrome. Debut of hyperphagia and severe obesity from early childhood are typical for monogenic forms and syndromes. Many nonspecific candidate-genes in combination form a polygenic basis for the accumulation of excess body fat, especially under the influence of irrational diet and low physical activity. Examined the role of epigenetic factors in the individual genetic variants in fetus, predisposing to obesity and metabolic syndrome after birth. Discuss the possibilities of early prevention of obesity and metabolic syndrome.
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Marklová, Eliška. "Genetic Aspects of Diabetes Mellitus." Acta Medica (Hradec Kralove, Czech Republic) 44, no. 1 (2001): 3–6. http://dx.doi.org/10.14712/18059694.2019.79.

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Practically all types of diabetes mellitus (DM) result from complex interactions of genetic and environmental factors. Multifactorial and polygenic Type 1 DM is strongly influenced by genes controlling the immune system, mainly HLA-DQ and DR. In addition to this, many other predisposition loci, interacting with each other, have some influence on susceptibility to DM. Heterogeneous Type 2 DM, accounting for about 85 % of all diabetic patients, is supposed to be induced by multiple genes defects involved in insulin action and/or insulin secretion. Other genetically influenced traits like obesity and hyperlipidemia are strongly associated with the Type 2. The group called Other specific types of DM include monogenic forms MODY 1-5 and many various subtypes of the disease, where the specific gene mutations have been identified. Both genetic and intrauterine environmental influences are likely to contribute to the abnormalities defined as Gestational DM.
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Clément, Karine, and Arnaud Basdevant. "Pathophysiological Aspects of Human Obesity – What We Know in 2010." European Endocrinology 06 (2010): 10. http://dx.doi.org/10.17925/ee.2010.06.00.10.

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Obesity, a disease of both developed and developing countries, is spreading at an epidemic pace. According to the World Health Organization (WHO), obesity is defined as an increase or abnormal accumulation of body fat mass to the extent that an individual’s health will be negatively affected. Overweight (i.e. body mass index [BMI] >25kg/m2) is considered to be a significant risk factor for the development of many chronic diseases. Environmental, behavioural, genetic and biological factors interact to cause obesity, which can be viewed as a set of phenotypes that evolve over time in stages that need to be precisely measured. This article provides a clinical viewpoint on some biological processes that may explain some of the stages in the development of human obesity, its chronic maintenance and the occurrence of complications, with a focus on brain structures, genetics, the profound alterations in adipose tissue biology and the recent revival in thinking in terms of brown adipose tissue.
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Oral, Onur, George Nomikos, and Nikitas Nomikos. "Evaluation of Genetics of Obesity and MC4R Deficiency: A Gene-oriented Approach to Obesity." Journal of Endocrinology Research 3, no. 1 (April 2, 2021): 41. http://dx.doi.org/10.30564/jer.v3i1.2977.

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Obesity is a multifactorial and complex health problem that is affected by several factors including genetic, environmental, social,behavioural, and biological aspects. Even though the influence of other environmental and behavioural factors such as sedentary lifestyle, high-calorie nutritional intake, and the inadequate expenditure of energy are acknowledged as important aspects that cause obesity, the issue of inheritance is indisputable. The study aims to investigate the effects of inheritance on obesity and examine how understanding and detecting genetic reasons behind obesity may benefit the treatment and prevention of the obesity epidemic. The relationship between common gene variants and obesity is now being studied through the emergence of GWAS. It is undeniable that genetic mutations and gene deficiencies particularly MC4R deficiency are significant factors. The process of detecting genes that create a tendency to obesity is currently being studied. It may be possible to prevent and treat obesity with the detection of certain genes.
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Kozak, LP, and RA Koza. "Mitochondrial uncoupling proteins and obesity: Molecular and genetic aspects of UCP1." International Journal of Obesity 23, S6 (June 1999): S33—S37. http://dx.doi.org/10.1038/sj.ijo.0800941.

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Kireeva, Victoria Vladimirovna, Svetlana Aleksandrovna Lepekhova, Lyubov Nazirovna Mansurova, and Saryuna Chingisovna Dugarova. "EPIGENETIC AND MOLECULAR AND GENETIC ASPECTS OF OBESITY AS A RISK FACTOR OF CARDIOVASCULAR CATASTROPHES." EurasianUnionScientists 5, no. 7(76) (August 20, 2020): 39–44. http://dx.doi.org/10.31618/esu.2413-9335.2020.5.76.926.

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The review provides current information of obesity in the pathogenesis of cardiovascular diseases the leading cause of death. Showing the genetic basis for the development of metabolic syndrome. The question of external influence on genes, mutations in which lead to the development of obesity is determined. The question of the possible role of exogenous destroyers in the development of metabolic syndrome is considered. The main genes involved in monogenic and polygenic variants of obesity are identified. The review shows that to prevent the development of metabolic syndrome, it is necessary to form risk groups and to take mandatory preventive activity in these groups. Pathogenetic significance determines the attention of clinicians to this pathology, and the molecular and genetic aspects of formation the cardiovascular diseases dictate the need for personalized medicine to predict and prevent, and pharmacogenetics to correct obesity, metabolic syndrome and the cardiovascular system as a whole.
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Dissertations / Theses on the topic "Obesity – Genetic aspects"

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Rask-Andersen, Mathias. "Obesity Genetics : Functional Aspects of Four Genetic Loci Associated with Obesity and Body Mass." Doctoral thesis, Uppsala universitet, Funktionell farmakologi, 2013. http://urn.kb.se/resolve?urn=urn:nbn:se:uu:diva-204449.

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Obesity is a complex disorder which has reached epidemic proportions in many parts of the world. Twin studies have demonstrated a high heritability for obesity. The subsequent appli-cation of genome wide association studies (GWAS) in the last decade have identified at least 32 genetic loci associated with body mass and obesity. Despite these great advances, these loci are almost exclusively completely naïve in a functional context. Genetic variations within the gene encoding the fat mass and obesity associated gene (FTO) are the strongest and most consistently observed genetic variants associated with obesity and body mass throughout various studied populations from all parts of the world. The identification of association of FTO with obesity has spurred immense interest in the function of the FTO protein and the functional consequences of its variants. However, the implications of genetic variants at other genetic loci on protein molecular function and body mass development remain undetermined. This thesis aims to examine more closely four of the genetic loci associated with obesity; in proximity of, or associated with: FTO, TMEM18, MAP2K5 and STK33, in two cohorts of children of European descent: a case-control of clinically obese children and normal weight controls from the Stockholm area; and a cross sectional cohort of Greek children. These smaller cohorts allow for studies of more specific effects of genetic variants as individuals in these cohorts can be more carefully studied. TMEM18 gene expression was also studied in the rat-brain where a positive correlation was observed between the body weight of the animal and TMEM18 expression. We also employed next generation sequencing to more carefully study obesity-associated genetic loci related to FTO and TMEM18. We utilized a novel strategy in this project to study genetic variation in the entire FTO- and TMEM18 genes, as well as in the GWAS-identified BMI-associated loci located downstream from TMEM18. This analysis was performed on a case-control cohort of Swedish children (n = ~1000). Through this analysis, we were able to observe genetic variants within intron 1 of the FTO gene to be the main genetic variants asso-ciated with obesity at this locus. We also observed, for the first time, obesity-associated genetic variants within the gene encoding TMEM18. To analyze the potential functional context of FTO we used an in silico approach, utilizing public information databases on mRNA co-expression and protein-protein interaction. Based on our findings, we speculate on a wider functional role of FTO in extracellular ligand-induced neuronal plasticity, possibly via interaction or modulation of the BDNF/NTRK2 signaling pathway.
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Day, Felix Ranulf. "Discovery and application of genetic variants for obesity related traits." Thesis, University of Cambridge, 2014. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.708350.

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Vogels, Neeltje. "On the weighty issue of obesity: physiological, behavioral and genetic aspects." Maastricht : Maastricht : Universitaire Pers Maastricht ; University Library, Universiteit Maastricht [host], 2006. http://arno.unimaas.nl/show.cgi?fid=5231.

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Swarbrick, Michael. "Candidate genes for obesity and related phenotypes." University of Western Australia. Dept. of Pathology, 2002. http://theses.library.uwa.edu.au/adt-WU2004.0033.

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The current epidemic of obesity poses a substantial threat to public health worldwide. Obesity is associated with many deleterious health conditions, including type 2 diabetes, hypertension, dyslipidaemia, respiratory conditions, arthritis, and some forms of cancer. Moreover, the rising prevalence of obesity has been accompanied by a substantial increase in the cost of treating these conditions. Obesity results from a complex interaction between behavioural, environmental, and genetic factors. While the recent increase in the prevalence of obesity is largely due to behavioural factors (for example, physical inactivity); it has also been observed that genetic factors make a large contribution to individual susceptibility. In fact, studies indicate that as much as 50 - 80% of the variation in measures of obesity can be attributed to the effects of genes. Furthermore, closer examination of this genetic component using segregation analysis has indicated the presence of common genes for obesity, with large effects on the phenotype. However, these putative major genes for obesity have not yet been identified. The aim of this thesis was to investigate the role of three distinct genetic loci in obesity and related cardiovascular factors, including type 2 diabetes and dyslipidaemia. The aim of the first investigation was to test whether a common polymorphism (Pro12Ala) in the gene encoding peroxisome proliferator-activated receptor gamma 2 (PPAR-γ2) was associated with obesity and other cardiovascular risk factors in a large group of Caucasian subjects. PPAR-γ2 is an adipogenic transcription factor, which also regulates insulin sensitivity in adipose tissue. No association was observed between the Pro12Ala polymorphism and obesity in Caucasians, but obese subjects carrying the Ala allele displayed an altered blood lipid profile compared with obese Pro/Pro subjects. As the Pro12Ala polymorphism may exacerbate the risk of cardiovascular disease by modifying blood lipid profile in obesity, this relationship was examined further in a separate population. The aim of the second investigation was to determine whether the Pro12Ala polymorphism was associated with obesity, dyslipidaemia, diabetes and carotid intima-medial wall thickening in a population at high risk of developing cardiovascular disease. Australian Aboriginal people display high rates of mortality from cardiovascular disease, and it is possible that their increased susceptibility is due to genetic factors. However, the results from the Aboriginal population confirmed the results of the first study: there was no intrinsic association between the Pro12Ala variant and obesity. In addition, the Ala allele was not associated with deleterious changes in blood lipid profile, as it was in Caucasians. The aim of the third investigation was to confirm the presence of a quantitative trait locus (QTL) for obesity on chromosome 20q13. Highly polymorphic genetic markers in this region were tested for linkage and association with several measures of obesity in a Caucasian population. None of the measures of obesity were linked to or associated with markers spanning 20q13, suggesting that this chromosomal region does not contain a major locus for obesity in this Caucasian population. In the fourth investigation, the 5' sequence of Agouti Signalling Protein (ASIP) was identified. ASIP is a candidate gene for obesity, as it is expressed at high levels in adipocytes, and may participate in several obesity-related processes. Three new exons and two alternative promoters were identified for the ASIP gene. These results may lead to greater understanding of the role of ASIP in obesity and adipocyte metabolism; and may also be used to direct further research into genetic variation within this candidate gene. In conclusion, extensive study of two established candidate genetic loci revealed no association with measures of obesity. Therefore, it is likely that loci other than these make significant contributions to obesity in humans. Further investigation of novel candidate genes, such as ASIP, may allow the identification of novel genetic polymorphisms and new pathways important for the genetic basis of obesity.
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Ong, Kwok-leung, and 王國良. "Genetic variants of obesity- and inflammation-related genes in hypertension: genetic association studiesusing candidate gene approach." Thesis, The University of Hong Kong (Pokfulam, Hong Kong), 2010. http://hub.hku.hk/bib/B45200555.

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Yeung, Chun-yu, and 楊振宇. "Adipocyte- and epidermal-fatty acid-binding proteins in relation to obesity and its medical complications." Thesis, The University of Hong Kong (Pokfulam, Hong Kong), 2009. http://hub.hku.hk/bib/B44204565.

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Lefebvre, Francois L. "The effect of intermittent feeding programs and genetic line on adiposity in broiler chickens /." Thesis, McGill University, 1987. http://digitool.Library.McGill.CA:80/R/?func=dbin-jump-full&object_id=63892.

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Rong, Rong, and 榮蓉. "Genetics of obesity in Hong Kong Chinese: a candidate gene approach focusing on the melanocortin-4 receptor andadiponectin." Thesis, The University of Hong Kong (Pokfulam, Hong Kong), 2005. http://hub.hku.hk/bib/B31459729.

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Cheung, Yu-yan Chloe, and 張語殷. "Obesity and type 2 diabetes susceptibility genes identified from recent genome-wide association studies: impact on Southern Chinese." Thesis, The University of Hong Kong (Pokfulam, Hong Kong), 2011. http://hub.hku.hk/bib/B47849617.

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Background and objectives: Recent genome-wide association (GWA) studies conducted in Caucasian populations have significantly expanded the list of confirmed and potential susceptibility genes for obesity and type 2 diabetes. The major objective of this thesis was to establish the role of the previously identified obesity- and T2DM-susceptibility genes in the Hong Kong Southern Chinese population. Major findings: In a cross-sectional case-control study of Southern Chinese which involved 470 obese cases and 700 normal-weight controls, significant associations with obesity were demonstrated in 7 of 13 single nucleotide polymorphisms (SNPs) that have shown significant associations with obesity and/or body mass index (BMI) in previous Caucasian GWA studies. These SNPs are located within or near the GNPDA2, FTO, MC4R, KCTD15, SFRS10-ETV5-DGKG, SEC16B-RASAL2 and NEGR1 loci. The combined genetic risk score (GRS) of the 13 studied SNPs was associated with an increased risk for obesity. The GNPDA2 rs10938397, FTO rs8050136, and MC4R rs17782313, which showed the most significant associations with obesity, were further examined for their associations with persistent central obesity and the metabolic syndrome (MetS). Both rs8050136 and rs10938397 were significantly associated with persistent central obesity. rs10938397 was also associated with the MetS. The combined GRS of these 3 SNPs showed significant associations with both persistent central obesity and persistent MetS. Nineteen multimarker-tagging SNPs that span a well-defined LD block of the FTO gene were evaluated for their associations with obesity in a case-control study which involved 249 cases and 400 controls. rs16952522 was found to be significantly associated with obesity, in addition to the well-known SNP rs8050136. These 2 SNPs were nominally associated with T2DM, although the associations were abolished after adjustment for age, sex and BMI. However, the GA haplotype composed of the risk alleles of these 2 SNPs was significantly associated with T2DM, independent of BMI. Seventeen previously identified T2DM-associated SNPs were investigated for the associations with glycaemic progression in an 8-year follow-up study which involved 518 cases and 998 controls. Their combined GRS was associated with an increased risk for glycaemic progression. A significant association with glycaemic progression was found with CDKN2A/B rs10811661. Moreover, KCNJ11 rs5219 and IGF2BP2 rs11711477 also showed potential associations with glycaemic progression. In the subsequent 12-year follow-up study, which involved 200 cases and 903 controls, the CDKN2A/B rs10811661 showed a significant independent association with incident T2DM. The KCNJ11 E23K (rs5219) variant was examined for its association with diabetes development in a 12-year prospective study. It was found to be significantly associated with the development of prediabetes but not with the development of T2DM. However, in a meta-analysis which involved 15680 subjects across different populations, this variant could indeed predict T2DM. Conclusions: The findings of this thesis have provided novel evidence supporting the role of the GWA studies-identified obesity- and T2DM-associated genetic variants as genetic markers of obesity and T2DM among Southern Chinese in Hong Kong, and suggest that the GNPDA2, FTO and MC4R genes confer susceptibility to obesity and that the CDKN2A/B and KCNJ11 genes may play a role in diabetes development.
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Medicine
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Doctor of Philosophy
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Williams, Helen. "Investigation of the metabolic functions of Klf3 and Klf8 using mouse models." Thesis, The University of Sydney, 2011. https://hdl.handle.net/2123/28935.

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Obesity is a disease characterised by an excess of white adipose tissue. It leads to increased risk of several associated disorders including cardiovascular disease and type 2 diabetes mellitus. The number of people who are obese is increasing worldwide and as such much research is conducted on obesity and associated disorders. The use of animal models in the study of obesity allows understanding of involvement of specific genes in fat formation and related processes. This can be used to identify targets for prevention or treatment of obesity. Kriippel—like factors are a family of transcription factors that have been implicated in a number of roles, one of which is metabolism. The Klf3'/' mouse has decreased adipose tissue but the metabolic implications of this had not been determined. Klf8 has high homology to Klf3 in the zinc finger region and was suspected to have a role in metabolism and fat formation. A metabolic role for Klf8 had not been investigated. In this thesis, the metabolic profiles of Klf3— and Klf8—deficient mice were examined. Klf3'/' male mice were found to be resistant to diet-induced weight gain. They maintained lower WAT mass and smaller adipocytes. In addition, these mice had reduced hepatic steatosis and improved glucose tolerance and circulating hormone levels. Klf88W male and Klf8+/g’ female mice had no clear phenotype suggesting Klf8 either has roles in areas other than metabolism, or that functional redundancy occurs, thus compensating for the decreased Klf8. These studies show that Klf3 could potentially be targeted for treatments of obesity as mice lacking this protein are lean, resistant to diet-induced obesity and appear metabolically healthy.
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Books on the topic "Obesity – Genetic aspects"

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1966-, Clément Karine, and Sorensen Thorkild I. A, eds. Genetics of obesity. New York: Informa Healthcare, 2007.

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Claude, Bouchard, ed. The Genetics of obesity. Boca Raton, Fla: CRC Press, 1994.

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Grant, Struan F. A. The genetics of obesity. New York: Springer, 2014.

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The genetics of obesity. New York: Rosen, 2009.

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Simons, Rae. Too many Sunday dinners: Family and diet. Broomall, Pa: Mason Crest Publishers, 2011.

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Lustig, Robert H. Obesity Before Birth: Maternal and prenatal influences on the offspring. Boston, MA: Springer Science+Business Media, LLC, 2011.

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Freemark, Michael. Pediatric obesity: Etiology, pathogenesis, and treatment. New York: Humana Press, 2010.

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Wood, Philip A. How fat works. Cambridge, MA: Harvard University Press, 2005.

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How fat works. Cambridge, Mass: Harvard University Press, 2006.

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Arterburn, Stephen. Hand me-down genes and second-hand emotions: You can overcome the genetic and family factors that can lead to depression, alcoholism, obesity, and suicide. New York: Simon & Schuster, 1994.

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Book chapters on the topic "Obesity – Genetic aspects"

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Larder, Rachel, Chung Thong Lim, and Anthony P. Coll. "Genetic aspects of human obesity." In Clinical Neuroendocrinology, 93–106. Elsevier, 2014. http://dx.doi.org/10.1016/b978-0-444-59602-4.00006-x.

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Bray, G. A., and C. Bouchard. "Obesity, Determinants of: Genetic Aspects." In International Encyclopedia of the Social & Behavioral Sciences, 10775–81. Elsevier, 2001. http://dx.doi.org/10.1016/b0-08-043076-7/03368-4.

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Bravo-Sagua, Roberto, Marcela Reyes, Sergio Lavandero, and Mariana Cifuentes. "Calcium in Obesity and Related Diseases." In Molecular, Genetic, and Nutritional Aspects of Major and Trace Minerals, 35–44. Elsevier, 2017. http://dx.doi.org/10.1016/b978-0-12-802168-2.00004-x.

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Mistri, Shradha. "Relations between Dietary Habits, Lifestyle and Leading Obesity." In Psychology and Patho-physiological Outcomes of Eating [Working Title]. IntechOpen, 2021. http://dx.doi.org/10.5772/intechopen.98307.

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Obesity, hypertension, depression currently in the rise are some of the many problems faced by a common person due to poor dietary and sleeping habits along with some genetic disorders. An extensive study has been done over two years with 205 subjects regarding their eating & sleeping habits and their mental & physical state on a day-to-day basis. The subjects include both males and females ranging from 15 years of age to 70 above. Altogether 12.68% of people suffer from obesity while just 51.21% of them have an appropriate weight. Women below the age of 25 have shown an overpowering presence of PCOS affecting their health and 38.53% of the population showcasing suffering from hypertension and 14.14% suffering from depression. Sleep has yet proven to be a defining factor in wellbeing. 17.07% of the population exhibit signs of sleep deprivation while just 63.9% of the population sleep over 7 hours daily. Like many other countries, in India, the shift from traditional healthy food to fast food & processed food is taking place, resulting in various health problems like obesity, heart problems, arthritis, weakness, diabetes, high blood pressure, difficulty in breathing, stroke & so on. The aim of this meta-analysis was to quantify the effects of nutrition, mental health and exercise on the various aspects of a person’s well-being.
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Benlier, Necla, Nevhiz Gundogdu, and Mehtap Ozkur. "Human Genetic Polymorphisms Associated with Susceptibility to COVID-19 Infection and Response to Treatment." In Genetic Polymorphisms - New Insights [Working Title]. IntechOpen, 2021. http://dx.doi.org/10.5772/intechopen.99877.

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Clinicians and researchers observing the natural history of endemic and epidemic infections have always been fascinated by the vagaries of these diseases, in terms of both the changing nature of the disease severity and phenotype over time and the variable susceptibility of hosts within exposed populations. SARS-CoV-2, the virus that causes COVID-19 and is believed to originate from bats, quickly transformed into a global pandemic. The pandemic of the novel severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) has been posing great threats to the global health in many aspects. Currently, there are no proven effective vaccines or therapeutic agents against the virus. Comprehensive understanding of the biology of SARS-CoV-2 and its interaction with hosts is fundamentally important in the fight against SARS-CoV-2. Advanced age, male sex, and comorbidities such as hypertension and cardiovascular disease as well as diabetes and obesity have been identified as risk factors for more severe COVID-19. However, which and to what extent specific genetic factors may account for the predisposition of individuals to develop severe disease or to contract the infection remains elusive. The increasing availability of data from COVID-19 patient populations is allowing for potential associations to be established between specific gene loci and disease severity, susceptibility to infection, and response to current/future drugs.
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Tatarchuk, Tatyana, Tetiana Tutchenko, and Olga Burka. "Special Considerations on Hyperandrogenism and Insulin Resistance in Nonobese Polycystic Ovaries Syndrome." In Androgens [Working Title]. IntechOpen, 2022. http://dx.doi.org/10.5772/intechopen.103808.

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PCOS is a widespread phenotypically inhomogeneous endocrinopathy with significant health consequences and incompletely elucidated pathogenesis. Though visceral adiposity and insulin resistance (IR) is a well-proved pathogenic set of factors of PCOS, not all women with obesity and IR have PCOS and not all PCOS women are obese and have IR, which is explained by certain genetic backgrounds. The reported prevalence of nonobese PCOS (NonObPCOS) is about 20–30%, but it may be higher because especially in lean women with nonclassical phenotypes PCOS diagnosis is often delayed or unrecognized. Unlike obese PCOS, NonObPCOS management is less clear and is limited to symptomatic treatment. This chapter presents in structured fashion the existing results on the prevalence of NonObPCOS, as well as on special aspects of body composition, IR, and hyperandrogenism pathogenesis, including adrenal contribution in NonObPCOS.
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Owen, Katharine R. "Diagnosis of Non Type 1, Non Type 2 Forms of Diabetes." In Oxford Textbook of Endocrinology and Diabetes 3e, edited by John A. H. Wass, Wiebke Arlt, and Robert K. Semple, 1965–70. Oxford University Press, 2021. http://dx.doi.org/10.1093/med/9780198870197.003.0249.

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Diabetes that is neither type 1 nor type 2 in aetiology accounts for around 5% of cases, with a wide range of causes. The widest differential diagnosis is in the young adult group. Non-type 1/type 2 diabetes includes monogenic causes of both beta-cell dysfunction (MODY, neonatal diabetes, mitochondrial diabetes) and insulin resistance (lipodystrophy, insulin receptor defects and monogenic obesity), as well as pancreatic, endocrine, and syndromic causes. It is important to make the correct aetiological diagnosis as this is likely to affect treatment and other aspects of management as well as defining the risk of diabetes in family members. Apart from clinical features and basic biochemistry, there are a number of investigations which can help with determining aetiology. These include beta-cell antibodies, assessment of endogenous insulin secretion using C-peptide, specific biomarkers, and genetic testing. Combining some of these features has led to the development of an online probability model for MODY. It is important to understand the roles and limitations of these tests and tools in clinical practice.
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Rho, Jonathan, Paul Percelay, Sophie Pilkinton, T. J. Hollingsworth, Ilyse Kornblau, and Monica Jablonski. "An Overview of Age-Related Macular Degeneration: Clinical, Pre-Clinical Animal Models and Bidirectional Translation." In Animal Models in Medicine and Biology [Working Title]. IntechOpen, 2021. http://dx.doi.org/10.5772/intechopen.96601.

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Age-related macular degeneration (AMD) is a multifactorial disease that results from a complex and unknown interplay among environmental, genetic, and epidemiologic factors. Risk factors include aging, family history, obesity, hypercholesterolemia, and hypertension, along with cigarette smoking, which is the most influential modifiable risk factor. Single nucleotide polymorphisms (SNPs) in numerous genes such as complement factor H (CFH) pose some of the known genetic risks. The pathophysiology in AMD is incompletely understood, but is known to involve oxidative stress, inflammation, dysregulated antioxidants, lipid metabolism, and angiogenesis. Animal models have been integral in expanding our knowledge of AMD pathology. AMD is classified as non-exudative or exudative. Because there is no perfect animal model that recapitulates all aspects of the human disease, rodents, rabbits, and non-human primates offer different advantages and disadvantages to serve as models for various aspects of the disease. Scientific advances have also allowed for the creation of polygenic pre-clinical models that may better represent the complexity of AMD, which will likely expand our knowledge of disease mechanisms and serve as platforms for testing new therapeutics. There have been, and there continues to be, many drugs in the pipeline to treat both exudative and non-exudative AMD. However, Food and Drug Administration (FDA)-approved therapies for exudative AMD that mainly target angiogenic growth factors are the only therapeutics currently being used in the clinics. There remains no FDA-approved therapy for the non-exudative form of this disease. This chapter contains a basic overview and classification of AMD and multiple animal models of AMD are highlighted. We include an overview of both current FDA-approved treatments and those in development. Lastly, we conclude with a summary of the important role of pre-clinical studies in the development of therapeutics for this highly prevalent disease.
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"method normally found in the UK is, at the moment, slightly different. This system is called solidarity; everyone shares the cost of insurance, across the entire gamut of risk. Even so, there have been modifiers which have crept in, such as smoking or obesity. In the case of smoking it is a self-inflicted injury and, for the most part so is obesity, but not always. Generally speaking, genetic information can be ignored using this model. So we return to our original supposition: why not test everyone and modify their premiums accordingly, which is what the insurance industry would like? Well, to begin with this would be a ‘cherry picking’ exercise. Whatever is said it can be assumed that the truth, now or later, is that if insurance companies were allowed to assess individual risk someone would end up as uninsurable, while those that probably do not need insurance will be quite happily given it. So if the claim is that there is no intention to increase profits, which it has been stated to be, why bother? Is it altruism on the part of insurance companies to put premiums up for one group and down for another? This brings us to point two. If there is no desire to increase profits, why not retain the actuarial system currently in place? Actuarial tables have been used for centuries and give a good guide to the numbers of any age cohort who will die at any given time. This system works for both the insured and the insurer; to change it is to load the dice in a game of chance in favour of the dice holder. The insurers want to bet on a certainty; the rest of us want access to affordable insurance. This is the point where the legal challenge should be pursued. Discrimination in any form is both undesirable and dangerous. It is undesirable because we may lose a significant resource in the shape of our genetic diversity. After all, we have seen that some genes which are routinely described as ‘disease genes’ have turned out to confer additional fitness to the unaffected carriers, such as sickle cell anaemia (malaria resistance) and cystic fibrosis (tuberculosis resistance). It is also dangerous because we cannot tell what path this sort of action could lead us down; eugenics is not a very sensible route for humanity to take. A primary concern in this sort of testing is that the individuals that are making judgments on the results of these tests are simply not capable of making them. With any genetic test counselling is essential; without it the misery which can be caused within a family can be immense. Such things should be challenged before the situation becomes uncontrollable. During the Human Genome Project it was discovered that in excess of 1.4 million single nucleotide polymorphisms (SNPs) are present in the human genome. Many of these are of considerable importance in testing for specific genetic conditions, even down to such things as adverse reactions to specific drugs. This will be of enormous benefit because although an adverse reaction may be a simple headache or weight loss, such a reaction can be so severe as to result in death. But SNPs have another practical application in the criminal justice system. They can be used in large panels to produce a DNA profile for identification. But even now it is reported that an American company, DNAPrint Genomics in Florida is patenting a test which tests for SNPs that correlate with eye colour. They are not trying to determine eye colour by looking at the genes which actually code for eye colour in their entirety, but at single bases differences which indicate the." In Genetics and DNA Technology: Legal Aspects, 115. Routledge-Cavendish, 2013. http://dx.doi.org/10.4324/9781843146995-23.

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10

Kakkar, Shama, Runjhun Tandon, and Nitin Tandon. "How Can Flaxseed be Utilized as Functional Food." In Vegetable Growing [Working Title]. IntechOpen, 2021. http://dx.doi.org/10.5772/intechopen.100201.

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Although vegetables and fruits are unquestionably important components of food, incorporating herbs and spices into one’s diet has become a must to improve one’s health in today’s world. Due to rising popularity among health-conscious consumers, studies on functional foods such as herbs are a growing field in food science. Flaxseed (Linum Usitatissimum L.), which comes from the flax plant, an annual herb, is gaining interest as a functional food ingredient due to its high levels of alpha-linolenic acid (ALA), lignans, and fiber. Flaxseed consumption in the diet helps to prevent serious illnesses such as heart disease, cancer, diabetes, obesity, gastrointestinal, renal, and bone problems. Type II diabetes, in particular, is one of the great healthcare challenges of the twenty-first century, as it has engulfed children, adolescents, and young adults alike. While standard risk factors for type II diabetes are genetics, living style, and behavioral aspects, this article focuses on preventing or controlling the disease through dietary changes. To the best of our knowledge, review articles on the commercial use of flaxseed in the formulation of numerous food products with low glycemic index and their impact on diabetes are hardly available. The data from the previous 5 years is used to compile this report.
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