Obesity-related metabolic dysfunction in dogs: a comparison with human metabolic syndrome
1 Department of Animal Medicine and Surgery, Veterinary School, Regional Campus of International Excellence "Campus Mare Nostrum", University of Murcia, 30100, Murcia, Spain
2 Department of Obesity and Endocrinology, University of Liverpool, Leahurst Campus, Chester High Road, Neston, Wirral, CH64 7TE, United Kingdom
3 Department of Obesity and Endocrinology, University of Liverpool, University Hospital Aintree, Longmoor Lane, Fazakerley, Liverpool, L9 7AL, United Kingdom
4 Royal Canin Research Center, B.P.4 – 650 Avenue de la Petite Camargue, 30470, Aimargues, France
5 The WALTHAM Centre for Pet Nutrition, Freeby Lane, Waltham-on-the-Wolds, Melton Mowbray, LE14 4RT, UK
Citation and License
BMC Veterinary Research 2012, 8:147 doi:10.1186/1746-6148-8-147Published: 28 August 2012
Recently, metabolic syndrome (MS) has gained attention in human metabolic medicine given its associations with development of type 2 diabetes mellitus and cardiovascular disease. Canine obesity is associated with the development of insulin resistance, dyslipidaemia, and mild hypertension, but the authors are not aware of any existing studies examining the existence or prevalence of MS in obese dogs.
Thirty-five obese dogs were assessed before and after weight loss (median percentage loss 29%, range 10-44%). The diagnostic criteria of the International Diabetes Federation were modified in order to define canine obesity-related metabolic dysfunction (ORMD), which included a measure of adiposity (using a 9-point body condition score [BCS]), systolic blood pressure, fasting plasma cholesterol, plasma triglyceride, and fasting plasma glucose. By way of comparison, total body fat mass was measured by dual-energy X-ray absorptiometry, whilst total adiponectin, fasting insulin, and high-sensitivity C-reactive protein (hsCRP) were measured using validated assays.
Systolic blood pressure (P = 0.008), cholesterol (P = 0.003), triglyceride (P = 0.018), and fasting insulin (P < 0.001) all decreased after weight loss, whilst plasma total adiponectin increased (P = 0.001). However, hsCRP did not change with weight loss. Prior to weight loss, 7 dogs were defined as having ORMD, and there was no difference in total fat mass between these dogs and those who did not meet the criteria for ORMD. However, plasma adiponectin concentration was less (P = 0.031), and plasma insulin concentration was greater (P = 0.030) in ORMD dogs.
In this study, approximately 20% of obese dogs suffer from ORMD, and this is characterized by hypoadiponectinaemia and hyperinsulinaemia. These studies can form the basis of further investigations to determine path genetic mechanisms and the health significance for dogs, in terms of disease associations and outcomes of weight loss.