Polymorphism and methylation of the MC4R gene in obese and non-obese dogs

Mańkowska, M.; Nowacka‐Woszuk, Joanna; Graczyk, Aneta; Ciążyńska, Paulina; Stachowiak, Monika; Świtoński, M.

doi:10.1007/s11033-017-4114-3

Cited by 5 publications

(5 citation statements)

References 32 publications

(39 reference statements)

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“…We know that in some cases obesity is driven by recent mutations that have been introduced during the breeding and selection process. Mutations in the MC4R gene, for example, make beagles and other dogs susceptible to obesity [175,176]. Moreover, some Labrador dogs have a mutation in the POMC gene that makes them susceptible to over-eating and obesity [177].…”

Section: Problems With the Dual Intervention Point/ Drifty Gene Idea ...mentioning

confidence: 99%

Models of body weight and fatness regulation

Speakman,

Hall

2023

Phil. Trans. R. Soc. B

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Body weight and fatness appear to be regulated phenomena. Several different theoretical models are available to capture the essence of this idea. These include the set-point, dynamic equilibrium, adiposity force, control theory-settling point, Hall–Guo, operation point and dual intervention point (DIP) models. The set-point model posits a single reference point around which levels of fat are regulated. The dynamic equilibrium model suggests that the apparent regulation of body fat around a reference point is an illusion owing to the necessary impacts of weight change on energy expenditure. Control theory focuses on the importance of feedback gain and suggests set-point and dynamic equilibrium are ends of a continuum of feedback gain. Control theory models have also been called ‘settling point’ models. The Hall–Guo, operation point and DIP models also bring together the set-point and dynamic equilibrium ideas into a single framework. The DIP proposes a zone of indifference where dynamic equilibrium ‘regulation’ predominates, bounded by upper and lower intervention points beyond which physiological mechanisms are activated. The drifty gene hypothesis is an idea explaining where this individual variation in the upper intervention point might come from. We conclude that further experiments to test between the models are sorely required. This article is part of a discussion meeting issue ‘Causes of obesity: theories, conjectures and evidence (Part II)’.

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Section: Problems With the Dual Intervention Point/ Drifty Gene Idea ...mentioning

confidence: 99%

Models of body weight and fatness regulation

Speakman,

Hall

2023

Phil. Trans. R. Soc. B

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“…However, they misname this as N101T. Mankowska et al [ 136 ], in a subsequent review, note the mistake but further misname it c.301A>C (p.Asn101Thr). The authors’ (unpublished) capillary sequencing data means we can confirm the correct annotation as c.302C>A, p.Asn101Thr.…”

Section: Canine Obesity Geneticsmentioning

confidence: 99%

“…Mankowska et al [ 136 ] investigated MC4R variants in 270 dogs of four breeds in which they identified six known polymorphic sites (c.637G>T, p.Val213Phe, rs852614811; c.777T>C, p.Ala259Ala, rs851987283; c.868C>T, p.Leu290Leu, rs851062983; c.*33C>G, rs851539399; c.*227C>T; and c.-435T>C, rs852471376). Of the 270 dogs, they had full phenotypic data for 164.…”

Section: Canine Obesity Geneticsmentioning

confidence: 99%

The Genetic Basis of Obesity and Related Metabolic Diseases in Humans and Companion Animals

Wallis

Raffan

2020

Genes

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Obesity is one of the most prevalent health conditions in humans and companion animals globally. It is associated with premature mortality, metabolic dysfunction, and multiple health conditions across species. Obesity is, therefore, of importance in the fields of medicine and veterinary medicine. The regulation of adiposity is a homeostatic process vulnerable to disruption by a multitude of genetic and environmental factors. It is well established that the heritability of obesity is high in humans and laboratory animals, with ample evidence that the same is true in companion animals. In this review, we provide an overview of how genes link to obesity in humans, drawing on a wealth of information from laboratory animal models, and summarise the mechanisms by which obesity causes related disease. Throughout, we focus on how large-scale human studies and niche investigations of rare mutations in severely affected patients have improved our understanding of obesity biology and can inform our ability to interpret results of animal studies. For dogs, cats, and horses, we compare the similarities in obesity pathophysiology to humans and review the genetic studies that have been previously reported in those species. Finally, we discuss how veterinary genetics may learn from humans about studying precise, nuanced phenotypes and implementing large-scale studies, but also how veterinary studies may be able to look past clinical findings to mechanistic ones and demonstrate translational benefits to human research.

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“…Mankowska et al [121] investigated MC4R variants 270 dogs of 4 breeds in which they identified six known polymorphic sites (c.637G>T; rs852614811, c.777T>C; rs851987283, c.868C>T; rs851062983, c.*33C>G; rs851539399, c.*227C>T and c.-435T>C; rs852471376). Of the 270 dogs they had full phenotypic data for 164.…”

Section: Mc4rmentioning

confidence: 99%

“…However, they misname this as N101T. Mankowska et al [121] M. Mankowska, J. Nowacka-Woszuk, A. Graczyk, P. Ciazynska, M. Stachowiak, and M. Switonski, "Polymorphism and methylation of the MC4R gene in obese and non-obese dogs," Mol Biol Rep, vol. 44, no.…”

Section: Mc4rmentioning

confidence: 99%

The Genetic Basis of Obesity and Related Metabolic Diseases in Humans and Companion Animals

Wallis

Raffan

2020

Preprint

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Obesity is one of the most prevalent health conditions in humans and companion animals across the world. Obesity is associated with multiple health conditions across species including premature mortality. It is therefore of importance across the fields of medicine and veterinary medicine. The regulation of body weight is a homeostatic process vulnerable to disruption by genetic and environmental factors. It is well established that the heritability of obesity is high in humans and laboratory animals, with ample evidence that the same is true in companion animals. In this review, we provide an overview of how genes link to obesity in humans, drawing on a wealth of information from laboratory animal models, and summarising the mechanisms by which obesity causes related disease. Throughout, we focus on how large-scale human studies and niche investigations of rare mutations in severely affected patients have improved our understanding of obesity biology and can inform our ability to interpret results of animal studies. For dogs, cats and horses, we review the similarities in obesity pathophysiology to humans and review those genetic studies that have been done to investigate them. Finally, we discuss how veterinary genetics may learn from humans about studying precise, nuanced phenotypes and implementing large-scale studies, but also how veterinary studies may be able to look past clinical findings to mechanistic ones and demonstrate translational benefits to human research.

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Polymorphism and methylation of the MC4R gene in obese and non-obese dogs

Cited by 5 publications

References 32 publications

Models of body weight and fatness regulation

Models of body weight and fatness regulation

The Genetic Basis of Obesity and Related Metabolic Diseases in Humans and Companion Animals

The Genetic Basis of Obesity and Related Metabolic Diseases in Humans and Companion Animals

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