Monk has just stolen 7 of my posts from here and posted them in his MRB.

He hasn't changed - he can't find his own content so takes mine.

Monk is the worst plagiarist on Ozpolitic.

The mutation is in a gene called POMC, which plays a critical role in hunger and energy use. Around 25% of Labradors and 66% of flatcoated retriever dogs have the POMC mutation, which researchers previously showed causes increased interest in food and risk of obesity.6 Mar 2024
Genetic mutation in a quarter of all Labradors hard-wires them ...

Summary
Sequencing of candidate genes for obesity in Labrador retriever dogs identified a 14 bp deletion in pro-opiomelanocortin (POMC) with an allele frequency of 12%. The deletion disrupts the β-MSH and β-endorphin coding sequences and is associated with body weight (per allele effect of 0.33 SD), adiposity, and greater food motivation. Among other dog breeds, the deletion was only found in the closely related flat-coat retriever (FCR), where it is similarly associated with body weight and food motivation. The mutation is significantly more common in Labrador retrievers selected to become assistance dogs than pets. In conclusion, the deletion in POMC is a significant modifier of weight and appetite in Labrador retrievers and FCRs and may influence other behavioral traits.


Introduction

In developed countries, the prevalence of canine obesity ranges between 34% and 59% [. . .] Obesity in dogs is associated with reduced lifespan and several specific morbidities similar to those seen in human obesity [. . .]

Recent changes in the prevalence of obesity in dogs mirror increases in the prevalence of the human condition, and similar environmental factors such as reduced exercise and ready access to high-calorie food are implicated. However, despite the fact that dog owners control their pets’ diet and exercise, susceptibility to obesity varies between dog breeds, which suggests the influence of genetic factors.

Over the past 20 years, insights from human and mouse genetics have illuminated multiple pathways within the brain that play a key role in the control of food intake (Yeo and Heisler, 2012). In particular, we now know that the hypothalamic leptin melanocortin signaling pathway is crucial for the appropriate control of food intake, with genetic disruption of most components of the pathway resulting in severe obesity in both mouse and man (Yeo and Heisler, 2012). However, the majority of common obesity in humans is polygenic, with the most reproducible finding from genome-wide association studies, an association at the fat mass and obesity (FTO) locus, explaining only a small component of obesity risk (Tung et al., 2014).
Of all dog breeds for which data have been reported, Labrador retrievers have the greatest documented obesity prevalence (Edney and Smith, 1986; Lund et al., 2006; Mason, 1970; O Neill et al., 2014) and have been shown to be more food motivated than other breeds (Raffan et al., 2015). The fact that most modern dog breeds originated relatively recently from a small number of founder animals makes the genetic basis of canine traits particularly amenable to dissection (Sutter and Ostrander, 2004).

In order to begin exploiting the power of canine genetics to identify alleles predisposing to obesity, we studied a cohort of companion and assistance Labrador retriever dogs. Here, we report that a 14 bp deletion in the pro-opiomelanocortin (POMC) gene, which results in the disruption of β-MSH (melanocyte-stimulating hormone) and β-endorphin, is associated with increased body weight, adiposity, and food motivation in both Labrador retrievers and the closely related flat-coat retrievers (FCRs). We also find that the mutation is significantly more common in Labradors selected to become assistance dog breeding stock than those selected to be companions.


Results

Identification of a POMC Deletion in Obese Labrador Retrievers
We recruited a cohort of 310 pet and assistance dog Labrador retrievers. Dogs were weighed, and their body condition score (a validated measure of adiposity that accounts for variation in body morphology within and across breeds; Laflamme, 1997; Mawby et al., 2004) was assessed by independent veterinary professionals.

Initially, the coding sequence of three candidate obesity genes, melanocortin-4 receptor (MC4R), agouti-related peptide (AGRP), and POMC, all part of the hypothalamic melanocortin pathway, was examined in 15 obese and 18 lean Labrador retrievers. No variants from the reference sequence were identified in AGRP. In MC4R, four novel variants were identified, but there was no significant difference in distribution of the variants between lean and obese groups (Table S1, available online).

41,170 views  3 Jan 2010