Polygenic Obesity

Giuranna, Johanna

doi:10.1007/978-3-319-68192-4_10

Cited by 5 publications

(4 citation statements)

References 77 publications

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“…Common polygenic obesity-a common form of obesity, resulting from hundreds of genetic variations in or near many genes, each having a small effect on the risk of obesity development. Polygenic obesity is characterized by late-onset obesity, with a profound environmental influence [173].…”

Section: The Genetic Contribution To Obesitymentioning

confidence: 99%

Adipose Tissue Hyperplasia and Hypertrophy in Common and Syndromic Obesity—The Case of BBS Obesity

Horwitz

Birk

2023

Nutrients

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Obesity is a metabolic state generated by the expansion of adipose tissue. Adipose tissue expansion depends on the interplay between hyperplasia and hypertrophy, and is mainly regulated by a complex interaction between genetics and excess energy intake. However, the genetic regulation of adipose tissue expansion is yet to be fully understood. Obesity can be divided into common multifactorial/polygenic obesity and monogenic obesity, non-syndromic and syndromic. Several genes related to obesity were found through studies of monogenic non-syndromic obesity models. However, syndromic obesity, characterized by additional features other than obesity, suggesting a more global role of the mutant genes related to the syndrome and, thus, an additional peripheral influence on the development of obesity, were hardly studied to date in this regard. This review summarizes present knowledge regarding the hyperplasia and hypertrophy of adipocytes in common obesity. Additionally, we highlight the scarce research on syndromic obesity as a model for studying adipocyte hyperplasia and hypertrophy, focusing on Bardet–Biedl syndrome (BBS). BBS obesity involves central and peripheral mechanisms, with molecular and mechanistic alternation in adipocyte hyperplasia and hypertrophy. Thus, we argue that using syndromic obesity models, such as BBS, can further advance our knowledge regarding peripheral adipocyte regulation in obesity.

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Section: The Genetic Contribution To Obesitymentioning

confidence: 99%

Adipose Tissue Hyperplasia and Hypertrophy in Common and Syndromic Obesity—The Case of BBS Obesity

Horwitz

Birk

2023

Nutrients

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“…Using in vitro analysis, the authors further demonstrated that variants in the nuclear PHIP suppressed the transcription of the POMC gene, which may contribute to hyperphagia [ 49 ]. On the other hand, polygenic obesity is characterized by multiple-gene dysfunction that results in obesity due to their interaction with the environment [ 50 ]. Importantly, polygenes enclose one allele that is susceptible to higher and another to lower body weight.…”

Section: Adipose Tissue Developmentmentioning

confidence: 99%

Adipose Tissue Development and Expansion from the Womb to Adolescence: An Overview

et al. 2020

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Prevalence rates of pediatric obesity continue to rise worldwide. Adipose tissue (AT) development and expansion initiate in the fetus and extend throughout the lifespan. This paper presents an overview of the AT developmental trajectories from the intrauterine period to adolescence; factors determining adiposity expansion are also discussed. The greatest fetal increases in AT were observed in the third pregnancy trimester, with growing evidence suggesting that maternal health and nutrition, toxin exposure, and genetic defects impact AT development. From birth up to six months, healthy term newborns experience steep increases in AT; but a subsequent reduction in AT is observed during infancy. Important determinants of AT in infancy identified in this review included feeding practices and factors shaping the gut microbiome. Low AT accrual rates are maintained up to puberty onset, at which time, the pattern of adiposity expansion becomes sex dependent. As girls experience rapid increases and boys experience decreases in AT, sexual dimorphism in hormone secretion can be considered the main contributor for changes. Eating patterns/behaviors and interactions between dietary components, gut microbiome, and immune cells also influence AT expansion. Despite the plasticity of this tissue, substantial evidence supports that adiposity at birth and infancy highly influences its levels across subsequent life stages. Thus, a unique window of opportunity for the prevention and/or slowing down of the predisposition toward obesity, exists from pregnancy through childhood.

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“…Polygenic obesity. More than an hundred polygenic loci harboring genetic variants associated with overweight and obesity have been identified [96][97][98]. Polygenic obesity is caused by the cumulative effect of obesogenic environment and weight-gain promoting genes.…”

Section: Pseudohypoparathyroidism (Php)mentioning

confidence: 99%

The Multiple Causes of Obesity

Saxena¹,

Suman²,

Kaur³

et al. 2021

Role of Obesity in Human Health and Disease

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Obesity is known to cause physical and metabolic diseases. It is often assumed by people (including the healthcare workers) that the person with obesity lacks self-control in matters of diet and physical exercise, and is therefore responsible for his or her weight. Persons with obesity have to face sarcasm, barbs, and discrimination due to their condition. They often have difficulty in getting jobs or have to accept lower than standard pay for their work. Although weight gain requires calorie intake in excess of calorie expenditure, it is sometimes not easy for the person to restrict calories due to the underlying causes of obesity. The body resists losing weight, and attempts to hoard calories by reducing the metabolic rate. In this chapter we have explained and classified the causes of obesity into endogenous and exogenous. The endogenous causes include genetic and epigenetic causes, maternal factors, and hormonal causes, while exogenous causes include obesogenic environment, lifestyle, and weight-gain promoting medicines. It must be realized that losing weight and keeping it off is not easy for a person with obesity.

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Polygenic Obesity

Cited by 5 publications

References 77 publications

Adipose Tissue Hyperplasia and Hypertrophy in Common and Syndromic Obesity—The Case of BBS Obesity

Adipose Tissue Hyperplasia and Hypertrophy in Common and Syndromic Obesity—The Case of BBS Obesity

Adipose Tissue Development and Expansion from the Womb to Adolescence: An Overview

The Multiple Causes of Obesity

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