Peer-reviewed veterinary case report
Metabolic changes after eating in overweight Labrador Retrievers
By Söder, Josefin et al.·Published in BMC veterinary research·2019·Department of Anatomy·View original on PubMed →
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Original publication title: Indication of metabolic inflexibility to food intake in spontaneously overweight Labrador Retriever dogs.
- Species:
- dog
Plain-English summary
A group of overweight Labrador Retrievers showed signs of metabolic issues related to food intake during a study. Researchers found that these dogs had lower levels of certain metabolites, like acetylcarnitine, which suggests they may struggle to properly process fats after eating. In contrast, lean dogs had a normal response to food, indicating that overweight dogs might have a problem with how their bodies handle fat. This could mean that if your dog is overweight, they might not be metabolizing food as effectively as they should.
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Abstract
BACKGROUND: Obesity in dogs is an increasing problem associated with morbidity, shortened life span and poor life quality. Overweight dogs exhibit postprandial hyperlipidaemia, highlighting the need to identify potential dysregulations in lipid metabolism. This study investigated metabolites related to lipid metabolism (i.e. acylcarnitines and taurine) and phospholipids in a feed-challenge test and aimed to identify metabolic variations in spontaneously overweight dogs. Twenty-eight healthy male Labrador Retriever dogs were included, 12 of which were classified as lean (body condition score (BCS) 4-5 on a 9-point scale) and 16 as overweight (BCS 6-8). After overnight fasting (14-17 h), fasting blood samples were collected and dogs were fed a high-fat meal followed by postprandial blood sample collection hourly for 4 h. Liquid chromatography-time of flight mass spectrometry (LC-TOFMS) was used to identify plasma metabolites and phospholipids. Multivariate models, mixed model repeated measures and linear regression analyses were used for data interpretation. RESULTS: In all dogs, propionylcarnitine, stearoylcarnitine and nine phospholipids increased in response to food intake, while vaccenylcarnitine decreased (P ≤ 0.005 for all). Overall, carnitine and acetylcarnitine signal areas in the feed-challenge test were lower in overweight dogs (P ≤ 0.004). Notably, fasting plasma acetylcarnitine was lower in overweight dogs than in lean dogs (P = 0.001) and it did not change in response to feeding. The latter finding was in contrast to the decreased acetylcarnitine signal area found in lean dogs at one hour postprandially (P < 0.0001). One fasting phosphatidylcholine (PCaa C38:4) was higher in prominently overweight dogs (BCS > 6) than in lean dogs (P < 0.05). CONCLUSIONS: Plasma carnitine status was overall lower in spontaneously overweight dogs than in lean dogs in this cohort of healthy Labrador Retriever dogs, indicating a potential carnitine insufficiency in the overweight group. The acetylcarnitine response in overweight dogs indicated decreased fatty acid oxidation at fasting and metabolic inflexibility to food intake. Further studies on metabolic inflexibility and its potential role in the metabolism of overweight dogs are warranted.
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Search related cases →Original publication on PubMed: https://pubmed.ncbi.nlm.nih.gov/30894172/