Sexual dimorphisms in genetic loci linked to body fat distribution.

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diabetes mellitus 9540 individuals, but younger ones as well. As an example, obesity is a primary risk factor for gestational diabetes mellitus (GDM) [[24]], which increases the risk of death for the mother and the child, increases risk of cardiometabolic
obesity 687 well-established predictor of adverse metabolic outcomes. Body fat distribution is distinct from overall obesity in measurement, but studies of body fat distribution can yield insights into the risk factors for and
obesity 815 studies of body fat distribution can yield insights into the risk factors for and causes of overall obesity . Sexual dimorphism in body fat distribution is present throughout life. Though sexual dimorphism is
obesity 1496 genetic regulation of fat distribution traits. Importantly, sexual dimorphism is not observed for overall obesity (as assessed by body mass index or total fat percentage). Notably, the genetic loci associated with
obesity 2014 dimorphism in fat distribution can provide novel insights into human physiology and into the development of obesity and its comorbidities, as well as yield biological clues that will aid in the improvement of disease
obesity 6160 denoted as simply “HIP”). Many of these traits are closely linked. For example, BMI or overall obesity is significantly correlated with body fat distribution (Pearon's r~0.60) [[13]]. Both WC and WHR are
obesity 7935 are the key for genetic association studies looking to further elucidate the genetic architecture of obesity in humans.Figure 1Sexual dimorphism in body shape and fat distribution over a human lifespanSexual dimorphism
obesity 8960 for adverse cardiometabolic outcomes, a risk that is in fact distinct from the effect that overall obesity has on disease [[22]]. Epidemiological studies of body fat distribution (measured proximally by WHR
obesity 9268 cardiovascular disease, T2D, stroke, hypertension and a host of other common diseases [[19],[23]]. The worsening obesity epidemic in the United States and around the globe has dramatically increased the incidence of these
obesity 9491 of these diseases affects not only adult-age individuals, but younger ones as well. As an example, obesity is a primary risk factor for gestational diabetes mellitus (GDM) [[24]], which increases the risk of
obesity 9708 for the mother and the child, increases risk of cardiometabolic diseases as well as increased risk of obesity later in life [[25]]. In addition to increasing risk of disease, obesity can also adversely affect fertility
obesity 9781 well as increased risk of obesity later in life [[25]]. In addition to increasing risk of disease, obesity can also adversely affect fertility and reproduction. Obesity can increase the risk of infertility,
obesity 10012 complications during pregnancy [[26],[27]]. Notably, infertility in particular is associated not only with obesity , but also with being underweight. This “U-shaped” risk curve is observable in both males and females
obesity 10913 “organogenesis” and “embryonic development” [[31]]) are likely to contribute to the underpinnings of obesity and fat distribution [[31]]. In a study of mice kept on a high-fat diet for 12 weeks, microarray analysis
obesity 16634 The sexual dimorphism in these heritabilities also indicates that risk for diseases associated with obesity or fat distribution may also have biological drivers that are specific or differentially regulated in
obesity 20066 [[13],[14],[20],[21]]. A number of large-scale GWAS have sought to identify common SNPs influencing overall obesity through BMI [[49]], the largest and most recent of which analysed more than 339,000 individuals and
obesity 20923 revealed potential overlapping genetic architectures between monogenic and population-level forms of obesity . Although mutations in the MC4R gene, for example, are the leading cause of monogenic obesity in humans,
obesity 21017 forms of obesity. Although mutations in the MC4R gene, for example, are the leading cause of monogenic obesity in humans, this locus has also revealed through GWAS to contain common, BMI-increasing polymorphisms
obesity 23947 diseases [[56]]. Animal models have added additional empirical evidence for the potential role of GRB14 in obesity : specifically, an analysis of GRB14 expression in adipose tissue found a negative correlation between
obesity 24472 biological role of GRB14 may yield insights into potential therapeutics used to treat the rapidly growing obesity epidemic.In addition, the gene ADAMTS9, which lies in a locus discovered through GWAS of WHRadjBMI,
obesity 25578 [[14],[61]].The lack of sexually dimorphic loci in body fat percentage and BMISome GWAS of overall obesity have revealed a notable lack of sexual dimorphism. For example, of the four loci discovered by the recently
obesity 25804 GWAS in BF% (in or near COBLL1/GRB14, IGF2BP1, PLA2G6, CRTC1) [[52]] and in the most recent GWAS of obesity as measured by BMI [[21]] only a very small number of these overall obesity loci exhibited sexual dimorphism
obesity 25880 the most recent GWAS of obesity as measured by BMI [[21]] only a very small number of these overall obesity loci exhibited sexual dimorphism (approximately 3–5%) [[21],[52]]. There are several potential explanations
obesity 26578 adipocytes [[20],[21]]. These findings again point to a striking difference across the many facets of obesity and raise the possibility that different organs are differentially susceptible for sexually dimorphic
obesity 27225 may help reveal therapeutic targets or diagnostically relevant mechanisms used to predict or treat obesity in men or women specifically. One such example is PPARG, a gene found to be associated with T2D and
obesity 27360 women specifically. One such example is PPARG, a gene found to be associated with T2D and monogenic forms of severe obesity and severe digenic insulin resistance [[62],[63]]. An SNP in PPARG associated with WHRadjBMI exhibits
obesity 28001 through ongoing functional work, may help in our movement towards precision medicine. Clinical trials for obesity treatments or treatments of obesity-related disease, for example, may be improved by stratifying on
obesity 28037 in our movement towards precision medicine. Clinical trials for obesity treatments or treatments of obesity -related disease, for example, may be improved by stratifying on sex.Very few GWAS (or large-scale epidemiologic
obesity 29056 analysing both sexes jointly, this amassing of samples now enables us to investigate sexual dimorphism in obesity and related traits in samples numbering in tens or hundreds of thousands. Such studies may reveal additional
obesity 29227 thousands. Such studies may reveal additional sexually dimorphic risk loci associated with not only obesity , but to an array of obesity-related traits and diseases such as cardiovascular disease [[22]], metabolic
obesity 29255 reveal additional sexually dimorphic risk loci associated with not only obesity, but to an array of obesity -related traits and diseases such as cardiovascular disease [[22]], metabolic diseases [[17]], schizophrenia
obesity 30884 us to understand disease severity in cell, tissue and developmental stage specific settings.As the obesity epidemic has now reached global proportions, fat distribution and obesity are worthy of scientific study
obesity 30958 specific settings.As the obesity epidemic has now reached global proportions, fat distribution and obesity are worthy of scientific study more than ever. The epidemic brings with it an increased prevalence of
obesity 31131 brings with it an increased prevalence of diseases that are epidemiologically and biologically linked to obesity , such as cardiovascular and metabolic diseases; these diseases are often chronic, can be fatal, and
obesity 31535 in the United States and elsewhere [[81],[82]]. Due to the environmental components that influence obesity , such as diet and exercise, information on how to curb the epidemic is often drawn from a wide range
obesity 31949 examining male participants; this bias greatly limits our understanding of the effect of exercise on obesity in women [[83]], even though women are equally affected by the epidemic [[84]]. Given the various sources
obesity 32085 women are equally affected by the epidemic [[84]]. Given the various sources of information around obesity and its treatment and the increasing number of individuals affected by the disease, obesity deseves
obesity 32177 around obesity and its treatment and the increasing number of individuals affected by the disease, obesity deseves not only our attention but the utmost scientific rigor as well. Sexual dimorphism and its role
obesity 32423 epidemiologic and genetic studies, will be a key part of unravelling the biological risk factors of obesity in a rigorous and complete manner. In particular, further disentangling the sexual dimorphism at loci
obesity 32599 disentangling the sexual dimorphism at loci associated with fat distribution, as well as designing studies of obesity that explicitly focus on females or males only, will yield insights into the biological signatures of
obesity 32896 sex-stratified clinical trials, and help in moving us towards treating and ultimately stemming the obesity epidemic worldwide

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