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Journal articles on the topic 'Obesity – Genetic aspects'
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1
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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Timasheva, Ya R., Zh R. Balkhiyarova, and O. V. Kochetova. "Current state of the obesity research: genetic aspects, the role of microbiome, and susceptibility to COVID-19." Problems of Endocrinology 67, no. 4 (September 16, 2021): 20–35. http://dx.doi.org/10.14341/probl12775.
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Obesity affects over 700 million people worldwide and its prevalence keeps growing steadily. The problem is particularly relevant due to the increased risk of COVID-19 complications and mortality in obese patients. Obesity prevalence increase is often associated with the influence of environmental and behavioural factors, leading to stigmatization of people with obesity due to beliefs that their problems are caused by poor lifestyle choices. However, hereditary predisposition to obesity has been established, likely polygenic in nature. Morbid obesity can result from rare mutations having a significant effect on energy metabolism and fat deposition, but the majority of patients does not present with monogenic forms. Microbiome low diversity significantly correlates with metabolic disorders (inflammation, insulin resistance), and the success of weight loss (bariatric) surgery. However, data on the long-term consequences of bariatric surgery and changes in the microbiome composition and genetic diversity before and after surgery are currently lacking. In this review, we summarize the results of studies of the genetic characteristics of obesity patients, molecular mechanisms of obesity, contributing to the unfavourable course of coronavirus infection, and the evolution of their microbiome during bariatric surgery, elucidating the mechanisms of disease development and creating opportunities to identify potential new treatment targets and design effective personalized approaches for the diagnosis, management, and prevention of obesity.
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Уксуменко, А., A. Uksumenko, Марина Антонюк, and Marina Antonyuk. "PATHOGENETIC ASPECTS OF THE PHENOTYPE OF BRONCHIAL ASTHMA ASSOCIATED WITH OBESITY." Bulletin physiology and pathology of respiration 1, no. 71 (March 25, 2019): 112–19. http://dx.doi.org/10.12737/article_5c89ac3a1c1ac3.25721118.
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Currently, in parallel with the increase in the prevalence of asthma, there is an increase in the number of obese patients. The results of numerous studies indicate that the asthma phenotype in combination with obesity has well-defined clinical features – a more severe course with frequent exacerbations and reduced control of the disease. The article considers the main pathogenetic mechanisms that determine the development of the asthma phenotype in combination with obesity. The influence of excess adipose tissue in the chest on respiratory mechanics, the correlation of gastroesophageal reflux disease and respiratory depression in sleep are described. It is shown that the phenotype of asthma with obesity is characterized by inflammation of adipose tissue, adipokine imbalance, insulin resistance, and disturbance of vitamin D metabolism. Gender peculiarities and genetic condition of asthma associated with obesity are considered. Understanding general mechanisms underlying the formation of asthma and obesity will undoubtedly contribute to the development of new therapeutic strategies.
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Clément, Karine. "Genetics of human obesity." Proceedings of the Nutrition Society 64, no. 2 (May 2005): 133–42. http://dx.doi.org/10.1079/pns2005416.
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The rapid development of new concepts and tools has led to a change in the way in which researchers carry out nutrition-related research. Obesity is determined by the interaction between predisposing genetic and environmental aspects, but at present the gene–gene and gene–environment interactions contributing to the development of this complex disease cannot be analysed in detail. The purpose of the present paper is to provide some examples of the knowledge that is available in the field of obesity genetics, and also the new strategies being developed that are aimed at studying the relative contribution of numerous genes to obesity and their responses to environmental changes. In the rare cases of monogenic obesities in which a major gene is the cause the molecular approach has proved extremely powerful in the identification of the genes responsible and in defining new syndromes. However, in the common forms of obesity (polygenic obesity) most studies have analysed genotype–phenotype associations without sometimes taking into account the influence of environmental factors (diet, sedentary lifestyle). Among the aspects limiting this integrated approach to obesity are the difficulty of having large enough samples and the expansion of biocomputing tools developed for accessing the question of multiple interactions with no a priori hypotheses. This picture is rapidly changing. Large databases of clinical data and DNA and biological sample banks with more precise environmental information and patient phenotypes are being compiled. The capacity for studying multiple genes simultaneously at the DNA or RNA levels is also possible. Finally, the tremendous progress in biocomputing will allow the integration of these different types of data (relating to environment, phenotype, genotype, gene expression) and will improve the ability to deal with this complex disease.
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Bogomolov, Pavel O., Kseniya Yu Kokina, Aleksander Yu Mayorov, and Ekaterina E. Mishina. "Genetic Aspects of Non-Alcoholic Fatty Liver Disease." Current pediatrics 17, no. 6 (January 31, 2019): 442–48. http://dx.doi.org/10.15690/vsp.v17i6.1974.
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Non-alcoholic fatty liver disease (NAFLD) is the most commonly diagnosed hepatopathy. There is an increase in the incidence of NAFLD in the structure of liver diseases in children and adolescents, which is directly related to the increasing prevalence of obesity. The spectrum of liver tissue changes in NAFLD ranges from benign hepatocellular steatosis to non-alcoholic steatohepatitis (NASH), fibrosis, cirrhosis of the liver, and hepatocellular carcinoma. With the increasing prevalence of NAFLD in children, we can expect an increase in the incidence of adverse outcomes among people of working age. The key problem for NAFLD is the prediction of disease outcomes. In epidemiological and genetic studies, the relationship between the morphological stage of NAFLD and hereditary factors is shown. Currently, there are three genes associated with NAFLD (PNPLA3, TM6SF2, and GCKR), which, together with the genes responsible for insulin resistance, lipid deposition, inflammation and fibrogenesis in hepatocytes, determine the phenotype of fatty liver disease. The article considers the modern understanding of the issues of genetics, development of liver steatosis and progression of NASH. It is expected that this knowledge can transform our risk stratification strategies in patients with NAFLD and help identify new therapeutic goals.
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Thibault, Louise, Stephen C. Woods, and Margriet S. Westerterp-Plantenga. "The utility of animal models of human energy homeostasis." British Journal of Nutrition 92, S1 (August 2004): S41—S45. http://dx.doi.org/10.1079/bjn20041141.
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The prevalence of obesity among adults and children has increased steadily over the last few years worldwide, reaching epidemic proportions. Particularly alarming is the link between obesity and the development of chronic disorders such as heart disease, type 2 diabetes, hypertension and some cancers (Bjorntorp, 1997). Environmental causes of obesity are thought to include a sedentary lifestyle and an abundance of highly palatable energy-dense foods (Hill et al. 2003). Genetic factors also contribute to susceptibility to obesity, although the genetic basis of most human obesities is thought to be polygenic (Comuzzie & Allison, 1998; Barsh et al. 2000). The present paper considers some of the animal models used to infer aspects of human obesity, with an emphasis upon their usefulness.
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Barak, Yaacov, and Suyeon Kim. "Genetic Manipulations of PPARs: Effects on Obesity and Metabolic Disease." PPAR Research 2007 (2007): 1–12. http://dx.doi.org/10.1155/2007/12781.
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The interest in genetic manipulations of PPARs is as old as their discovery as receptors of ligands with beneficial clinical activities. Considering the effects of PPAR ligands on critical aspects of systemic physiology, including obesity, lipid metabolism, insulin resistance, and diabetes, gene knockout (KO) in mice is the ideal platform for both hypothesis testing and discovery of new PPAR functions in vivo. With the fervent pursuit of the magic bullet to eradicate the obesity epidemic, special emphasis has been placed on the impacts of PPARs on obesity and its associated diseases. As detailed in this review, understanding how PPARs regulate gene expression and basic metabolic pathways is a necessary intermediate en route to deciphering their effects on obesity. Over a decade and dozens of genetic modifications of PPARs into this effort, valuable lessons have been learned, but we are left with more questions to be answered. These lessons and future prospects are the subject of this review.
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Gutiérrez-Cuevas, Jorge, Silvia Lucano-Landeros, Daniel López-Cifuentes, Arturo Santos, and Juan Armendariz-Borunda. "Epidemiologic, Genetic, Pathogenic, Metabolic, Epigenetic Aspects Involved in NASH-HCC: Current Therapeutic Strategies." Cancers 15, no. 1 (December 20, 2022): 23. http://dx.doi.org/10.3390/cancers15010023.
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Hepatocellular carcinoma (HCC) is the most common primary liver cancer and is the sixth most frequent cancer in the world, being the third cause of cancer-related deaths. Nonalcoholic steatohepatitis (NASH) is characterized by fatty infiltration, oxidative stress and necroinflammation of the liver, with or without fibrosis, which can progress to advanced liver fibrosis, cirrhosis and HCC. Obesity, metabolic syndrome, insulin resistance, and diabetes exacerbates the course of NASH, which elevate the risk of HCC. The growing prevalence of obesity are related with increasing incidence of NASH, which may play a growing role in HCC epidemiology worldwide. In addition, HCC initiation and progression is driven by reprogramming of metabolism, which indicates growing appreciation of metabolism in the pathogenesis of this disease. Although no specific preventive pharmacological treatments have recommended for NASH, dietary restriction and exercise are recommended. This review focuses on the molecular connections between HCC and NASH, including genetic and risk factors, highlighting the metabolic reprogramming and aberrant epigenetic alterations in the development of HCC in NASH. Current therapeutic aspects of NASH/HCC are also reviewed.
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Precenzano, Francesco, Daniela Smirni, Luigi Vetri, Pierluigi Marzuillo, Valentina Lanzara, Ilaria Bitetti, Margherita Siciliano, et al. "Childhood Obesity and Maternal Personality Traits: A New Point of View on Obesity Behavioural Aspects." Pediatric Reports 13, no. 3 (September 1, 2021): 538–45. http://dx.doi.org/10.3390/pediatric13030063.
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The epidemic spread of childhood obesity in Western society has interested many researchers, who agree in defining it as a multifactorial disease in which not only eating habits and sedentary lifestyle play a role, but also genetic predisposition. The aim of this study was to analyze the personality profile of a group of mothers of children with obesity and to compare this profile to that of a group of mothers of children without obesity. A total of 258 mothers participated in the study (126 mothers of children with obesity and 132 mothers of children without obesity). Weight and height were measured and the body mass index was calculated. The Minnesota Multiphasic Personality Inventory second edition (MMPI-2), evaluating personality and psychological disorders, was used to evaluate the personality profile. The results suggested that mothers of children with obesity score higher than the mothers of children without obesity in all MMPI-2 subscales. In most of these subscales, the differences between the two groups of mothers were statistically significant and with a medium to high effect size. These data suggest a new perspective on childhood obesity, identifying it as a multifactorial pathology that requires a multimodal and multidisciplinary approach that also takes care of caregivers to ensure optimal therapeutic efficacy.
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Kadykova, O. I. "GENETIC ASPECTS OF DEVELOPMENT AND PROGRESSION OF CONGESTIVE HEART FAILURE IN PATIENTS WITH ISCHEMIC HEART DISEASE AND OBESITY∗." Problems of Endocrine Pathology 57, no. 3 (August 23, 2016): 17–21. http://dx.doi.org/10.21856/j-pep.2016.3.02.
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In this article elucidated the influence of allelic polymorphism of Gln27Glu of β2-adrenoceptors gene on patients that have coronary heart disease and obesity on the expansion and progression of congestive heart failure and left ventricular systolic dysfunction by surveying 222 patients. Presence of C allel of polymorphous locus Gln27Glu of β2-adrenoreceptors gene in patients with ischemic heart disease and concomitant obesity was associated with decreased risk of development of congestive heart failure (p < 0.05). The obtained data shown the absence of influence of polymorphous variants of β2-adrenoreceptors gene on progression of congestive heart failure in patients with ischemic heart disease and obesity (p > 0.05).
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STĂNESCU, Ana Maria Alexandra, Ioana Veronica GRĂJDEANU, Anca Angela SIMIONESCU, and Mira FLOREA. "Essential clinical and diagnostic aspects in pediatric psoriasis." Romanian Journal of Medical Practice 16, S4 (August 15, 2021): 50–53. http://dx.doi.org/10.37897/rjmp.2021.s4.11.
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Psoriasis is a chronic, immune-mediated, inflammatory disease of the skin. The quality of life is significantly affected, being characterized by relapses, remissions and the presence of comorbidities associated with psoriasis. Several factors are implicated in the onset of psoriasis in children, including: genetic factors, environmental factors, psychosocial stress, obesity, trauma, skin irritation, use of certain drugs such as lithium, β-adrenergic antagonists and necrosis factor inhibitors. (TNF), the presence of Crohn's disease or juvenile rheumatoid arthritis. Psoriasis is a burden for the patient in the case of the adult, being even more difficult in the case of children. Atypical manifestations in pediatric psoriasis can be difficult to diagnose.
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Genovesi, Simonetta, and Gianfranco Parati. "Cardiovascular Risk in Children: Focus on Pathophysiological Aspects." International Journal of Molecular Sciences 21, no. 18 (September 10, 2020): 6612. http://dx.doi.org/10.3390/ijms21186612.
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Cardiovascular diseases are the leading cause of death, disability, and health care costs in industrialized countries. In general, cardiovascular diseases occur in adulthood, but cardiovascular damage, including stiffening of the arteries, begins very early. Already in the first decade of life, alterations that will favor the formation of atherosclerotic plaques may be present. Cardiovascular risk factors, associated with genetic predisposition, may trigger a sequence of pathophysiological changes which are associated with the progression of the atherosclerosis process. In this frame, the role of obesity has been increasingly emphasized. Different mechanisms linking obesity to cardiovascular disease have been postulated. Endothelial dysfunction and subclinical inflammation seem to be related to the worsening of cardiovascular risk factors in obese subjects and might have an essential role in the development of insulin resistance and the initiation and progression of atherosclerotic lesions. Excess weight, and in particular visceral adiposity, are associated with hypertrophy and hyperplasia of the adipocytes, increased secretion of adipokines and inflammatory cytokines and increase in serum uric acid levels. The list of obesity-related biomarkers associated with cardiovascular damage is rapidly expanding and their importance has already been described in children as well. Pathophysiological changes involved in determining early cardiovascular damage starting from childhood are discussed in this Special Issue.
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Denou, Emmanuel, Katarina Marcinko, Michael G. Surette, Gregory R. Steinberg, and Jonathan D. Schertzer. "High-intensity exercise training increases the diversity and metabolic capacity of the mouse distal gut microbiota during diet-induced obesity." American Journal of Physiology-Endocrinology and Metabolism 310, no. 11 (June 1, 2016): E982—E993. http://dx.doi.org/10.1152/ajpendo.00537.2015.
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Diet and exercise underpin the risk of obesity-related metabolic disease. Diet alters the gut microbiota, which contributes to aspects of metabolic disease during obesity. Repeated exercise provides metabolic benefits during obesity. We assessed whether exercise could oppose changes in the taxonomic and predicted metagenomic characteristics of the gut microbiota during diet-induced obesity. We hypothesized that high-intensity interval training (HIIT) would counteract high-fat diet (HFD)-induced changes in the microbiota without altering obesity in mice. Compared with chow-fed mice, an obesity-causing HFD decreased the Bacteroidetes-to-Firmicutes ratio and decreased the genetic capacity in the fecal microbiota for metabolic pathways such as the tricarboxylic acid (TCA) cycle. After HFD-induced obesity was established, a subset of mice were HIIT for 6 wk, which increased host aerobic capacity but did not alter body or adipose tissue mass. The effects of exercise training on the microbiota were gut segment dependent and more extensive in the distal gut. HIIT increased the alpha diversity and Bacteroidetes/Firmicutes ratio of the distal gut and fecal microbiota during diet-induced obesity. Exercise training increased the predicted genetic capacity related to the TCA cycle among other aspects of metabolism. Strikingly, the same microbial metabolism indexes that were increased by exercise were all decreased in HFD-fed vs. chow diet-fed mice. Therefore, exercise training directly opposed some of the obesity-related changes in gut microbiota, including lower metagenomic indexes of metabolism. Some host and microbial pathways appeared similarly affected by exercise. These exercise- and diet-induced microbiota interactions can be captured in feces.
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Owen, J. B. "Genetic aspects of appetite and feed choice in animals." Journal of Agricultural Science 119, no. 2 (October 1992): 151–55. http://dx.doi.org/10.1017/s0021859600014052.
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Body composition in wild animals is regulated within a band that encompasses variations due to seasonal food supply and physiological state (e.g. that of the reproducing, lactating female and the growing juvenile). This body composition is characteristic of the genotype and is notable for the avoidance of obesity (Pitts & Bullard 1968). Urgent behavioural responses are also invoked to minimize weight loss. Figure 1 illustrates this homeostasis diagrammatically for the non-lactating, mature animal.In this integrated complex, both food intake (quantity) and diet choice (quality) play a major role in achieving the required balance between food-energy intake and ‘net output’ of energy in its various forms such as activity, growth, lactation and change in body reserves. The development of such a system, through evolution, to achieve optimum reproductive fitness in a given environment, is consistent with the theory of optimal foraging which is characteristic of many animals in the wild. Newman (1991) has used such an approach in modelling diet selection by sheep.Domesticated animals have inherited the complex genome of their progenitors, albeit modified in certain respects through natural and artificial selection, in their new circumstances. Many aspects of the physiology and behaviour of the domesticated animal still relate to the environment in which they evolved. For example Jensen & Redbo (1987) have demonstrated the complex nesting behaviour retained by the modern domestic pig, under free ranging conditions similar to those of its wild progenitor.Two major non-genetic factors have emerged as major influences on the appetite of domesticated animals and man in modern times.
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Suter, Paolo M. "Alcohol, nutrition and health maintenance: selected aspects." Proceedings of the Nutrition Society 63, no. 1 (February 2004): 81–88. http://dx.doi.org/10.1079/pns2003326.
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In view of the developments in health care relating to the increased prevalence and incidence of chronic diseases and the continuing increase in health-care expenditure, more attention should be paid to health maintenance and disease prevention. Any strategy that can influence health maintenance is of interest, especially lifestyle factors such as nutrition, exercise or stress control. Alcohol has an important place in the daily life of many healthy as well as sick individuals. Alcohol has three major characteristics; it is a nutrient (energy source), a psycho-active drug and a toxin. Each consumer has the choice of which of the characteristics of alcohol he/she wants to utilise. Thus, alcohol represents one of the most important self-implemented disease modifiers in our modern society. The major determinants of the health effects of alcohol are the absolute amount consumed, the consumption frequency, associated lifestyle factors (e.g. smoking, nutrient intake, substrate composition, physical activity pattern) and last, but not least, the genetic background. There are few known disease conditions that have not already been associated positively or negatively with alcohol consumption. The list of diseases includes atherosclerosis, dementia, diabetes, obesity and conditions relating to Zn metabolism. Obesity represents the most important disease modifier in the world and the prevalence rates are increasing rapidly. Evidence suggests that alcohol represents a risk factor for overweight and obesity as a result of specific effects on energy metabolism and substrate metabolism. The potential role of alcohol as an important modulator for the postprandial lipidaemia and its role in the pathogenesis of modern diseases will be discussed.
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Rand Abdulateef Abdullah. "Review of literature: Etiology of obesity, risk factors, and the role of genetics." GSC Biological and Pharmaceutical Sciences 21, no. 2 (November 30, 2022): 197–201. http://dx.doi.org/10.30574/gscbps.2022.21.2.0443.
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Obesity is considered one of the global most significant public problem as it has been associated with different diseases and even death. It is an excess accumulation of fat in the body as a result of increase calorie intake compared to energy expenditure. It is considered as multifactorial condition as many factors play role in its occurrence including genetic susceptibility, external environmental factors, individual attitude. The exact etiology of obesity is intermingled with different factors and nowadays because of development of different aspects of life, sedentary life style dominates the social communities, reduced physical activities, all these factors can enhance the risk of obesity. Furthermore, disturbances of the endocrine system like Cushing’s syndrome, hypothyroidism, diabetes type II. The genetic obesity it will be divided into two groups: 1) The monogenic type, the Poly genic type, syndrome associated obesity. Many individuals are suffering from obesity because of different genes that they already have which encourage them to high calorie diet with more food consumption, unlimited and uncontrolled food intake together with reduced physical activity. In conclusion the etiology, risk factors, as well as genetic susceptibility all are combined and correlated to each other as they may act separately or together to induce onset of obesity. The physical exercise and energy expenditure are having the key role., in addition to endocrine hormonal disturbances.
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Hedström, Anna Karin, Nicole Brenner, Julia Butt, Jan Hillert, Tim Waterboer, Tomas Olsson, and Lars Alfredsson. "Overweight/obesity in young adulthood interacts with aspects of EBV infection in MS etiology." Neurology - Neuroimmunology Neuroinflammation 8, no. 1 (December 15, 2020): e912. http://dx.doi.org/10.1212/nxi.0000000000000912.
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ObjectiveBecause obesity affects the cellular immune response to infections, we aimed to investigate whether high body mass index (BMI) in young adulthood and high Epstein-Barr nuclear antigen 1 (EBNA-1) antibody levels interact with regard to MS risk. We also aimed at exploring potential 3-way interactions between BMI at age 20 years, aspects of Epstein-Barr virus (EBV) infection (high EBNA-1 antibody levels and infectious mononucleosis [IM] history, respectively) and the human leukocyte antigen (HLA)-DRB1*15:01 allele.MethodsUsing Swedish population-based case-control studies (5,460 cases and 7,275 controls), we assessed MS risk in relation to interactions between overweight/obesity at age 20 years, IM history, EBNA-1 levels, and HLA-DRB1*15:01 status by calculating ORs with 95% CIs using logistic regression. Potential interactions were evaluated on the additive scale.ResultsOverweight/obesity, compared with normal weight, interacted significantly with high (>50th percentile) EBNA-1 antibody levels (attributable proportion due to interaction 0.2, 95% CI 0.1–0.4). The strength of the interaction increased with higher category of EBNA-1 antibody levels. Furthermore, 3-way interactions were present between HLA-DRB1*15:01, overweight/obesity at age 20 years, and each aspect of EBV infection.ConclusionsWith regard to MS risk, overweight/obesity in young adulthood acts synergistically with both aspects of EBV infection, predominantly among those with a genetic susceptibility to the disease. The obese state both induces a chronic immune-mediated inflammation and affects the cellular immune response to infections, which may contribute to explain our findings.
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Elena, Grechi, Cammarata Bruna, Mariani Benedetta, Di Candia Stefania, and Chiumello Giuseppe. "Prader-Willi Syndrome: Clinical Aspects." Journal of Obesity 2012 (2012): 1–13. http://dx.doi.org/10.1155/2012/473941.
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Prader-Willi Syndrome (PWS) is a complex multisystem genetic disorder that shows great variability, with changing clinical features during a patient’s life. The syndrome is due to the loss of expression of several genes encoded on the proximal long arm of chromosome 15 (15q11.2–q13). The complex phenotype is most probably caused by a hypothalamic dysfunction that is responsible for hormonal dysfunctions and for absence of the sense of satiety. For this reason a Prader-Willi (PW) child develops hyperphagia during the initial stage of infancy that can lead to obesity and its complications. During infancy many PW child display a range of behavioural problems that become more noticeable in adolescence and adulthood and interfere mostly with quality of life. Early diagnosis of PWS is important for effective long-term management, and a precocious multidisciplinary approach is fundamental to improve quality of life, prevent complications, and prolong life expectancy.
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Mikhailova, Svetlana V., and Dinara E. Ivanoshchuk. "Innate-Immunity Genes in Obesity." Journal of Personalized Medicine 11, no. 11 (November 14, 2021): 1201. http://dx.doi.org/10.3390/jpm11111201.
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The main functions of adipose tissue are thought to be storage and mobilization of the body’s energy reserves, active and passive thermoregulation, participation in the spatial organization of internal organs, protection of the body from lipotoxicity, and ectopic lipid deposition. After the discovery of adipokines, the endocrine function was added to the above list, and after the identification of crosstalk between adipocytes and immune cells, an immune function was suggested. Nonetheless, it turned out that the mechanisms underlying mutual regulatory relations of adipocytes, preadipocytes, immune cells, and their microenvironment are complex and redundant at many levels. One possible way to elucidate the picture of adipose-tissue regulation is to determine genetic variants correlating with obesity. In this review, we examine various aspects of adipose-tissue involvement in innate immune responses as well as variants of immune-response genes associated with obesity.
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Darmawan, Arif, Sih Ageng Lumadi, and Achmad Dafir Firdaus. "LITERATURE REVIEW : FAKTOR - FAKTOR YANG BERHUBUNGAN DENGAN KEJADIAN OBESITAS PADA REMAJA LITERATURE REVIEW : FACTORS ASSOCIATED WITH OBESITY IN TEENAGER." Journal of Nursing Care and Biomoleculer 7, no. 1 (June 29, 2022): 52–60. http://dx.doi.org/10.32700/jnc.v7i1.258.
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Obesity is defined as abnormal or excessive fat accumulation that poses a risk to health. Obesity will have a negative impact on adolescent growth and development, especially in organic and psychosocial aspects. Because obesity in adolescents has a high risk of becoming obese in adulthood and has the potential to experience various causes of disease and death. This study uses a Literature Review method obtained from four data bases (Proquest, Pubmed, Google Scholar, and Garuda Portal) with the keywords Obesitas AND Remaja, Obesity AND Adolescent published in the 2015 – 2020 timeframe Indonesian and English language. There were 10 journals that met the inclusion and exclusion criteria. Proquest 3, Pubmed 2, Google Scholar 3, Portal Garuda 2 journal. From the discussion, the results obtained 6 factors that influence the incidence of obesity in adolescents, namely socio-economic factors, sleep pattern factors, dietary factors, physical activity factors, parental stressor factors, and genetic factors. Suggestions that need to be investigated further about obesity in children. Along with the times, various advertisements appear that attract various fast foods that are high in calories, which make children choose the wrong snacks, and less time to play outside the home because technological advances make children tend to play with gadgets or in front of television.
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Muscogiuri, G., L. Barrea, F. Faggiano, M. I. Maiorino, M. Parrillo, G. Pugliese, R. M. Ruggeri, E. Scarano, S. Savastano, and A. Colao. "Obesity in Prader–Willi syndrome: physiopathological mechanisms, nutritional and pharmacological approaches." Journal of Endocrinological Investigation 44, no. 10 (April 23, 2021): 2057–70. http://dx.doi.org/10.1007/s40618-021-01574-9.
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AbstractPrader–Willi syndrome (PWS) is a genetic disorder caused by the lack of expression of genes on the paternally inherited chromosome 15q11.2-q13 region. The three main genetic subtypes are represented by paternal 15q11-q13 deletion, maternal uniparental disomy 15, and imprinting defect. Clinical picture of PWS changes across life stages. The main clinical characteristics are represented by short stature, developmental delay, cognitive disability and behavioral diseases. Hypotonia and poor suck resulting in failure to thrive are typical of infancy. As the subjects with PWS age, clinical manifestations such as hyperphagia, temperature instability, high pain threshold, hypersomnia and multiple endocrine abnormalities including growth hormone and thyroid-stimulating hormone deficiencies, hypogonadism and central adrenal insufficiency due to hypothalamic dysfunction occur. Obesity and its complications are the most common causes of morbidity and mortality in PWS. Several mechanisms for the aetiology of obesity in PWS have been hypothesized, which include aberration in hypothalamic pathways of satiety control resulting in hyperphagia, disruption in hormones regulating appetite and satiety and reduced energy expenditure. However, despite the advancement in the research field of the genetic basis of obesity in PWS, there are contradictory data on the management. Although it is mandatory to adopt obesity strategy prevention from infancy, there is promising evidence regarding the management of obesity in adulthood with current obesity drugs along with lifestyle interventions, although the data are limited. Therefore, the current manuscript provides a review of the current evidence on obesity and PWS, covering physiopathological aspects, obesity-related complications and conservative management.
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Jańczuk, Anna, Aneta Brodziak, Tomasz Czernecki, and Jolanta Król. "Lactoferrin—The Health-Promoting Properties and Contemporary Application with Genetic Aspects." Foods 12, no. 1 (December 23, 2022): 70. http://dx.doi.org/10.3390/foods12010070.
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The aim of the study is to present a review of literature data on lactoferrin’s characteristics, applications, and multiple health-promoting properties, with special regard to nutrigenomics and nutrigenetics. The article presents a new approach to food ingredients. Nowadays, lactoferrin is used as an ingredient in food but mainly in pharmaceuticals and cosmetics. In the European Union, bovine lactoferrin has been legally approved for use as a food ingredient since 2012. However, as our research shows, it is not widely used in food production. The major producers of lactoferrin and the few available food products containing it are listed in the article. Due to anti-inflammatory, antibacterial, antiviral, immunomodulatory, antioxidant, and anti-tumour activity, the possibility of lactoferrin use in disease prevention (as a supportive treatment in obesity, diabetes, as well as cardiovascular diseases, including iron deficiency and anaemia) is reported. The possibility of targeted use of lactoferrin is also presented. The use of nutrition genomics, based on the identification of single nucleotide polymorphisms in genes, for example, FTO, PLIN1, TRAP2B, BDNF, SOD2, SLC23A1, LPL, and MTHFR, allows for the effective stratification of people and the selection of the most optimal bioactive nutrients, including lactoferrin, whose bioactive potential cannot be considered without taking into account the group to which they will be given.
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Samad, Fahumiya, and Wolfram Ruf. "Inflammation, obesity, and thrombosis." Blood 122, no. 20 (November 14, 2013): 3415–22. http://dx.doi.org/10.1182/blood-2013-05-427708.
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Abstract Clinical and epidemiological studies support a connection between obesity and thrombosis, involving elevated expression of the prothrombotic molecules plasminogen activator inhibitor-1 and tissue factor (TF) and increased platelet activation. Cardiovascular diseases and metabolic syndrome–associated disorders, including obesity, insulin resistance, type 2 diabetes, and hepatic steatosis, involve inflammation elicited by infiltration and activation of immune cells, particularly macrophages, into adipose tissue. Although TF has been clearly linked to a procoagulant state in obesity, emerging genetic and pharmacologic evidence indicate that TF signaling via G protein-coupled protease-activated receptors (PAR2, PAR1) additionally drives multiple aspects of the metabolic syndrome. TF–PAR2 signaling in adipocytes contributes to diet-induced obesity by decreasing metabolism and energy expenditure, whereas TF–PAR2 signaling in hematopoietic and myeloid cells drives adipose tissue inflammation, hepatic steatosis, and insulin resistance. TF-initiated coagulation leading to thrombin–PAR1 signaling also contributes to diet-induced hepatic steatosis and inflammation in certain models. Thus, in obese patients, clinical markers of a prothrombotic state may indicate a risk for the development of complications of the metabolic syndrome. Furthermore, TF-induced signaling could provide new therapeutic targets for drug development at the intersection between obesity, inflammation, and thrombosis.
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Kupczak-Wiśniowska, Bogusława, Jolanta Borgosz, Beata Podsiadło, Bogusława Serzysko, and Elżbieta Jędrkiewicz. "Obesity in children - a problem of the contemporary civilization." Pielegniarstwo XXI wieku / Nursing in the 21st Century 16, no. 1 (March 1, 2017): 44–50. http://dx.doi.org/10.1515/pielxxiw-2017-0007.
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AbstractIntroduction. In the recent thirty years obesity has become one of the most serious and still increasing health problems among children and adults in the world. Scientific magazines inform about world obesity epidemic. Lack of physical activity, excessive energy supply compared to needs of organism, as well as bad eating habits, have made obesity a civilization disease. Excess weight and obesity lead to premature atherosclerosis development and consequently, to other cardiovascular diseases such as arterial hypertension, thrombosis, cardiac insufficiency, hyperlipemia.Aim. The aim of the thesis is to present, on the basis of literature, the most important factors which can lead to obesity in children.Conclusions.Among the most important aspects which can lead to obesity in children the following factors can be mentioned: genetic factors - it is probable that mutations within many genes connected with energy efficiency regulation of an organism are responsible for the genetic tendency to being obeseenvironmental factors - there is another fact that together with technological development, the level of physical activity has decreasedpsychological factors, like stress, fear, failures at school, family and peer conflicts have become the reasons for compulsive behaviour which lead to excessive consumption of highly processed foodsObesity results in lowering the quality of life in a significant way.
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Motevalli, Mohamad, Clemens Drenowatz, Derrick R. Tanous, Naim Akhtar Khan, and Katharina Wirnitzer. "Management of Childhood Obesity—Time to Shift from Generalized to Personalized Intervention Strategies." Nutrients 13, no. 4 (April 6, 2021): 1200. http://dx.doi.org/10.3390/nu13041200.
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As a major public health concern, childhood obesity is a multifaceted and multilevel metabolic disorder influenced by genetic and behavioral aspects. While genetic risk factors contribute to and interact with the onset and development of excess body weight, available evidence indicates that several modifiable obesogenic behaviors play a crucial role in the etiology of childhood obesity. Although a variety of systematic reviews and meta-analyses have reported the effectiveness of several interventions in community-based, school-based, and home-based programs regarding childhood obesity, the prevalence of children with excess body weight remains high. Additionally, researchers and pediatric clinicians are often encountering several challenges and the characteristics of an optimal weight management strategy remain controversial. Strategies involving a combination of physical activity, nutritional, and educational interventions are likely to yield better outcomes compared to single-component strategies but various prohibitory limitations have been reported in practice. This review seeks to (i) provide a brief overview of the current preventative and therapeutic approaches towards childhood obesity, (ii) discuss the complexity and limitations of research in the childhood obesity area, and (iii) suggest an Etiology-Based Personalized Intervention Strategy Targeting Childhood Obesity (EPISTCO). This purposeful approach includes prioritized nutritional, educational, behavioral, and physical activity intervention strategies directly based on the etiology of obesity and interpretation of individual characteristics.
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Boulet, Louis-Philippe, and Qutayba Hamid. "Symposium on Obesity and Asthma –November 2, 2006." Canadian Respiratory Journal 14, no. 4 (2007): 201–8. http://dx.doi.org/10.1155/2007/342618.
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Asthma and obesity are frequently associated, and obesity has been considered a factor contributing to both an increase in severity of asthma and to its development. The present document summarizes the proceedings of a symposium held in Montreal, Quebec, on November 2, 2006, under the auspices of the Réseau en santé respiratoire du Fonds de la recherche en santé du Québec in collaboration with the McGill University – Strauss Severe Asthma Program, Université Laval (Quebec City) and Université de Montréal. It includes an overview of the various aspects of the relationships between asthma and obesity with regard to animal models; genetic, hormonal and physiological determinants; influence of comorbidities (eg, sleep apnea syndrome); epidemiology; clinical and psychological features; and management of asthma in the obese population.
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Yajnik, C. S. "Obesity epidemic in India: intrauterine origins?" Proceedings of the Nutrition Society 63, no. 3 (August 2004): 387–96. http://dx.doi.org/10.1079/pns2004365.
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The epidemic of ‘obesity’ in India is not appreciated because BMI underestimates the adiposity of Indians. Specific adiposity measurements are necessary for recognition of the adiposity of ‘thin’ Indians. The origin of this adiposity is only beginning to be understood. In addition to a possible genetic predisposition, intrauterine ‘programming’ might be responsible, although in the ‘thrifty phenotype’ hypothesis the adiposity of the ‘thin’ fetus has not been appreciated. Dutch men who faced ‘winter hunger’ during the first trimester of their in utero life have become more obese as adults. Low birth weight predicts central obesity in some studies, including studies in urban children. It has also been shown that small and thin Indian newborns (weight 2·7?kg and ponderal index 2·4?kg\m3) have poor muscle and visceral mass but higher adiposity for a given weight compared with white Caucasian babies. This body composition is influenced by maternal adiposity before pregnancy and by aspects of maternal nutritional intake and circulating nutrient concentrations during pregnancy. There are no strong paternal determinants of adiposity at birth. Adiposity may be an integral part of the orchestrated adjustments made to support ‘brain preservation’ during intrauterine growth, because brain tissue is predominantly fat. Increased nutrition in the face of a genetic predisposition or multigenerational undernutrition increases maternal insulin resistance in late pregnancy and promotes fetal adiposity even in absence of marked hyperglycaemia. Further research is necessary to define the role of specific nutrients and metabolites in the intrauterine processes promoting adiposity before maternal interventions to curtail the epidemic of obesity and diabetes are planned.
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Valenti, Maria Teresa, Angelo Pietrobelli, Maria Grazia Romanelli, Elia Franzolin, Giovanni Malerba, Donato Zipeto, Monica Mottes, and Luca Dalle Carbonare. "Molecular and Lifestyle Factors Modulating Obesity Disease." Biomedicines 8, no. 3 (March 1, 2020): 46. http://dx.doi.org/10.3390/biomedicines8030046.
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Obesity adversely affects bone health by means of multiple mechanisms, e.g., alterations in bone-regulating hormones, inflammation, and oxidative stress. Substantial evidence supports the relationship between adiposity and bone disorders in overweight/obese individuals. It is well known that the balance between mutually exclusive differentiation of progenitor cells into osteoblasts or adipocytes is controlled by different agents, including growth factors, hormones, genetic and epigenetic factors. Furthermore, an association between vitamin D deficiency and obesity has been reported. On the other hand, regular physical activity plays a key role in weight control, in the reduction of obesity-associated risks and promotes osteogenesis. The aim of this review is to highlight relevant cellular and molecular aspects for over-weight containment. In this context, the modulation of progenitor cells during differentiation as well as the role of epigenetics and microbiota in obesity disease will be discussed. Furthermore, lifestyle changes including an optimized diet as well as targeted physical activity will be suggested as strategies for the treatment of obesity disease.
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Matys, Tomasz, Anna Szymańska-Chabowska, Rafał Poręba, Grzegorz Mazur, and Paweł Gać. "Genetic aspects of obesity and metabolic syndrome in people occupationally exposed to arsenic and certain heavy metals." Environmental Medicine 22, no. 1-2 (June 24, 2020): 29–32. http://dx.doi.org/10.26444/ms/122202.
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Kumar, Rakesh, S. Minerva, Ruchi Shah, Amrita Bhat, Sonali Verma, Gresh Chander, Gh Rasool Bhat, et al. "Role of genetic, environmental, and hormonal factors in the progression of PCOS: A review." Journal of Reproductive Healthcare and Medicine 3 (June 28, 2022): 3. http://dx.doi.org/10.25259/jrhm_16_2021.
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Polycystic ovary syndrome (PCOS) can be mainly defined as a gynecological problem accompanied by an endocrine disturbance in females and can be seen mainly during their menstruation age. Worldwide PCOS prevalence ranges between 6% and 10%. Many of the risk factors are responsible for the pathogenesis of PCOS. Environmental factors such as environmental toxins and obesity play a major role in the occurrence of PCOS, followed by the hormonal disturbance in androgen levels, that is, hyperandrogenism, and insulin levels, that is, hyperinsulinemia. The previous studies have suggested that there is a major contribution of genetics in the etiology of PCOS. However, there is no strong evidence about the mode of inheritance of PCOS. It has been seen that there is a strong correlation between environmental, hormonal, and genetic factors which follow a vicious cycle in the development of PCOS that leads to ovarian dysfunction, metabolic syndrome, that is, metabolic abnormalities include insulin resistance, obesity, hypertension, dyslipidemia, and abnormal cholesterol level. The detailed study of PCOS is one of the most central topics in female reproductive endocrinology. On the other hand, the syndrome has been extensively investigated; however, its definition and pathophysiological aspects are still not very clear. The idea behind the current review was to make a non-systematic review of already published literature through PubMed and Google Scholar search. The keywords searched and publications were related to polycystic ovaries, including the incidence, environmental factors, genetics, hormones, as well as their association. The aim of the current review is to update the evidence regarding the pathogenesis of PCOS and emphasizes how genetic, non-genetic, and hormonal factors lead to the progression of PCOS.
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James, W. P. T., and A. Ralph. "New understanding in obesity research." Proceedings of the Nutrition Society 58, no. 2 (May 1999): 385–93. http://dx.doi.org/10.1017/s0029665199000506.
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A public-health approach considers the relevance of nutritional research in the prevention and management of obesity. Well-defined and internationally-agreed definitions based on BMI allow an assessment of the worldwide prevalence of overweight and obesity. There are about 250 million obese adults in the world, and many more overweight. Obesity is emerging in the Third World, first in urban middle-aged women. With economic developments, obesity then occurs in men and younger women. In the West childhood obesity is rapidly emerging, with concern that early-onset obesity is especially hazardous. In Asians the risks of excess visceral fat occur at lower body weights than in Caucasians. The propensity to visceral obesity in Asians may relate to malnourished mothers and low birth weight. The International Obesity Task Force is considering many issues, including the health economics of obesity. It has developed a strategy to define childhood obesity, which in children over 6 years is likely to predict long-term weight and health problems. While the search for genetic markers of obesity continues, with particular interest in the leptin gene, it is clear that societal change, with the decline in physical activity and the passive overconsumption of high-fat diets are major contributors to the global increase in obesity. The public-health aspects of obesity research are therefore challenging.
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Riha, Renata L. "Genetic Aspects of the Obstructive Sleep Apnoea/Hypopnoea Syndrome – Is There a Common Link with Obesity?" Respiration 78, no. 1 (2009): 5–17. http://dx.doi.org/10.1159/000221903.
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Pinto, Renata Machado, Cristiane Cominetti, and Aparecido Divino da Cruz. "Basic and Genetic Aspects of Food Intake Control and Obesity: Role of Dopamin Receptor D2 TaqIA Polymorphism." Obesity Research - Open Journal 2, no. 4 (March 28, 2016): 119–27. http://dx.doi.org/10.17140/oroj-2-119.
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Jeki, Andicha G., and Dwiko F. Rizki. "Tingkat Kegemukan dan Kebugaran Jasmani Siswa Sekolah Menengah Atas Berbasis Gender." Jurnal Ilmiah Universitas Batanghari Jambi 21, no. 1 (February 8, 2021): 327. http://dx.doi.org/10.33087/jiubj.v21i1.1315.
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Overweight and obesity are serious problems faced in the world, because it continues to increase in all countries. Riskesdas 2013 data shows that nationally, the problem of obesity in school-age children is quite high, namely adolescents at 10.8%. The main cause of obesity is a lack of physical activity which will have a direct impact on decreasing physical fitness. Physical education and sports in schools also aim to foster and develop children's potential in physical, mental, social, emotional, moral and even cognitive aspects. This study aims to see and analyze the level of obesity and physical fitness in high school students based on gender. The study was conducted in an observational manner with a cross sectional approach. The research location is Madrasah Aliah Negeri Cendikia Jambi. Respondents selected by purposive sampling of 56 respondents by comparing evenly, namely a number of 28:28 respondents based on obesity level and gender distribution. Data collected by filling questionnaires, anthropometric measurements, physical fitness tests. Data analyzed using chi square test with a significance value of p <0.05 at the 95% level of significance. The results showed 44:12 respondents in the study had a genetic history of obesity, 37 respondents aged <17 years and 19 respondents 17 years. The chi-square analysis results showed the p value = 0.00 (p <0.05) in men, which means there is relationship between obesity and physical fitness, and p value = 0.39 (p> 0.05) in women who means that there is no relationship between obesity and physical fitness. Strong relationships were simultaneously analyzed using binary logistic regression between variables, namely obesity, age, gender and genetic history, and it was found that obesity factors most influenced the dependent variable, namely physical fitness, indicated by the value of Exp. (B) 3, 60 and p value = 0.017.
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Parker, Victoria E. R., and Robert K. Semple. "GENETICS IN ENDOCRINOLOGY: Genetic forms of severe insulin resistance: what endocrinologists should know." European Journal of Endocrinology 169, no. 4 (October 2013): R71—R80. http://dx.doi.org/10.1530/eje-13-0327.
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‘Insulin resistance’ (IR) is a widely used clinical term. It is usually defined as a state characterised by reduced glucose-lowering activity of insulin, but it is also sometimes used as a shorthand label for a clinical syndrome encompassing major pathologies such as type 2 diabetes, polycystic ovary syndrome, fatty liver disease and atherosclerosis. Nevertheless, the precise cellular origins of IR, the causal links among these phenomena and the mechanisms underlying them remain poorly understood or contentious. Prevalent IR usually results from a genetic predisposition interacting with acquired obesity; however, even in some lean individuals, very severe degrees of IR can be observed. It is important to identify these people as they often harbour identifiable single-gene defects and they may benefit from molecular diagnosis, genetic counselling and sometimes tailored therapies. Observation of people with known single-gene defects also offers the opportunity to make inferences about the mechanistic links between IR and common pathologies. Herein, we summarise the currently known monogenic forms of severe IR, with an emphasis on the practical aspects of their recognition, diagnosis and management. In particular, we draw distinctions among the biochemical subphenotypes of IR that arise from primary adipose tissue dysfunction or from primary insulin signalling defects and discuss the implications of this dichotomy for management.
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Milano, Walter, Paola Ambrosio, Francesca Carizzone, Valeria De Biasio, Walter Di Munzio, Maria Gabriella Foia, and Anna Capasso. "Depression and Obesity: Analysis of Common Biomarkers." Diseases 8, no. 2 (June 14, 2020): 23. http://dx.doi.org/10.3390/diseases8020023.
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Depression and obesity are very common pathologies. Both cause significant problems of both morbidity and mortality and have decisive impacts not only on the health and well-being of patients, but also on socioeconomic and health expenditure aspects. Many epidemiological studies, clinical studies and meta-analyses support the association between mood disorders and obesity in relationships to different conditions such as the severity of depression, the severity of obesity, gender, socioeconomic status, genetic susceptibility, environmental influences and adverse experiences of childhood. Currently, both depression and obesity are considered pathologies with a high-inflammatory impact; it is believed that several overlapping factors, such as the activation of the cortico-adrenal axis, the exaggerated and prolonged response of the innate immune system and proinflammatory cytokines to stress factors and pathogens—as well as alterations of the intestinal microbiota which promote intestinal permeability—can favor the expression of an increasingly proinflammatory phenotype that can be considered a key and common phenomenon between these two widespread pathologies. The purpose of this literature review is to evaluate the common and interacting mechanisms between depression and obesity.
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Kolovou, Genovefa D., Gerald F. Watts, Dimitri P. Mikhailidis, Pablo Pérez-Martínez, Samia Mora, Helen Bilianou, George Panotopoulos, et al. "Postprandial Hypertriglyceridaemia Revisited in the Era of Non-Fasting Lipid Profile Testing: A 2019 Expert Panel Statement, Narrative Review." Current Vascular Pharmacology 17, no. 5 (August 1, 2019): 515–37. http://dx.doi.org/10.2174/1570161117666190503123911.
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Postprandial hypertriglyceridaemia, defined as an increase in plasma triglyceride-containing lipoproteins following a fat meal, is a potential risk predictor of atherosclerotic cardiovascular disease and other chronic diseases. Several non-modifiable factors (genetics, age, sex and menopausal status) and lifestyle factors (diet, physical activity, smoking status, obesity, alcohol and medication use) may influence postprandial hypertriglyceridaemia. This narrative review considers the studies published over the last decade that evaluated postprandial hypertriglyceridaemia. Additionally, the genetic determinants of postprandial plasma triglyceride levels, the types of meals for studying postprandial triglyceride response, and underlying conditions (e.g. familial dyslipidaemias, diabetes mellitus, metabolic syndrome, non-alcoholic fatty liver and chronic kidney disease) that are associated with postprandial hypertriglyceridaemia are reviewed; therapeutic aspects are also considered.
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O'Malley, Maureen A., and Karola Stotz. "Intervention, integration and translation in obesity research: Genetic, developmental and metaorganismal approaches." Philosophy, Ethics, and Humanities in Medicine 6, no. 1 (2011): 2. http://dx.doi.org/10.1186/1747-5341-6-2.
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Hart, Roger J. "Physiological Aspects of Female Fertility: Role of the Environment, Modern Lifestyle, and Genetics." Physiological Reviews 96, no. 3 (July 2016): 873–909. http://dx.doi.org/10.1152/physrev.00023.2015.
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Across the Western World there is an increasing trend to postpone childbearing. Consequently, the negative influence of age on oocyte quality may lead to a difficulty in conceiving for many couples. Furthermore, lifestyle factors may exacerbate a couple's difficulty in conceiving due mainly to the metabolic influence of obesity; however, the negative impacts of low peripheral body fat, excessive exercise, the increasing prevalence of sexually transmitted diseases, and smoking all have significant negative effects on fertility. Other factors that impede conception are the perceived increasing prevalence of the polycystic ovary syndrome, which is further exacerbated by obesity, and the presence of uterine fibroids and endometriosis (a progressive pelvic inflammatory disorder) which are more prevalent in older women. A tendency for an earlier sexual debut and to have more sexual partners has led to an increase in sexually transmitted diseases. In addition, there are several genetic influences that may limit the number of oocytes within the ovary; consequently, by postponing attempts at childbearing, a limitation of oocyte number may become evident, whereas in previous generations with earlier conception this potentially reduced reproductive life span did not manifest in infertility. Environmental influences on reproduction are under increasing scrutiny. Although firm evidence is lacking however, dioxin exposure may be linked to endometriosis, phthalate exposure may influence ovarian reserve, and bisphenol A may interfere with oocyte development and maturation. However, chemotherapy or radiotherapy is recognized to lead to ovarian damage and predispose the woman to ovarian failure.
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Diemieszczyk, Inna, Paulina Głuszyńska, Pawel Andrzej Wojciak, Jerzy Robert Ładny, and Hady Razak Hady. "METABOLIC SYNDROME. ETIOLOGY AND PATHOGENESIS." Wiadomości Lekarskie 74, no. 10 (2021): 2510–15. http://dx.doi.org/10.36740/wlek202110126.
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The aim of the study was to assess the impact of individual components of the metabolic syndrome on the human body, taking into account their etiology and pathogenesis. This article is analytical analysis of scientific and medical literature basing on aspects of the etiology and pathogenesis of the metabolic syndrome. The key role in the pathogenesis of the metabolic syndrome is played by insulin resistance, which may be a result of lifestyle conditions (low physical activity, overweight or obesity) or genetic background. A certain role in the pathogenesis of the metabolic syndrome is also attributed to disorders of the hypothalamic-pituitary-adrenal axis in the form of increased cortisol control, which may initiate the development of abdominal obesity, insulin resistance, hypertension and dyslipidemia. Aforementioned factors (environmental, hormonal and genetic) lead to excessive fat tissue gathering. The excess of abdominal fat tissue – abdominal obesity – leads to insulin resistance, the concentration of which causes body mass gain. Such mechanism is dangerous for our health and may lead to the occurrence of type 2 diabetes and premature development of atherosclerosis with all its consequences such as atherosclerotic cardiovascular diseases including coronary artery disease.
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I.K., Fedyainova. "LARON SYNDROME: DIFFERENT ASPECTS OF INSULIN-LIKE GROWTH FACTOR-1 DEFICIENCY." Natural resources of the Earth and environmental protection 3, no. 1 (April 20, 2022): 34–38. http://dx.doi.org/10.26787/nydha-2713-203x-2022-3-1-34-38.
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Annotation: Laron syndrome (Laron-type dwarfism) is a rare endocrine genetic disorder with an autosomal recessive inheritance pattern caused by a variety of mutations in the growth hormone receptor. Typical manifestations include dwarfism, «doll» face and obesity. Currently, the number of patients in the world is about 350. It is noteworthy that these people almost never suffer from cancer, show a delayed age-related decline in cognitive abilities and some of them are quite resistant to type 2 diabetes. Moreover, animals with artificially induced «Laron syndrome» have a markedly increased lifespan. All these phenomena are explained by the fact that with this disease in the blood there is a very low level of insulin-like growth factor-1 — a compound that is normally secreted by cells in response to the effect of growth hormone and mediates its action in tissues. These observations suggest that the study of Laron syndrome may allow one to get closer to understanding the endocrine mechanisms of cancer and a number of other pathological processes, and, in addition, throw light on some of the molecular genetic foundations of aging and longevity. This article provides information on some of the already discovered interesting consequences of congenital deficiency of insulin-like growth factor-1, further study of which seems to be very promising.