Peer-reviewed veterinary case report
Obese dogs have higher blood sugar and fat after eating than lean dogs
By Verkest, K R et al.·Published in Domestic animal endocrinology·2012·School of Veterinary Science, Australia·View original on PubMed →
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Original publication title: Spontaneously obese dogs exhibit greater postprandial glucose, triglyceride, and insulin concentrations than lean dogs.
- Species:
- dog
Plain-English summary
A group of obese dogs was studied to see how their blood sugar and fat levels compared to lean dogs after eating. The researchers found that the obese dogs had higher levels of glucose and insulin after meals, but none of the dogs showed signs of diabetes over the following years. This suggests that, unlike in some other animals, obesity in dogs may not lead to diabetes. The findings indicate that dogs' pancreatic cells might not be affected by mild high blood sugar levels in the same way as other species.
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Abstract
Dogs do not appear to progress from obesity-induced insulin resistance to type 2 diabetes mellitus. Both postprandial hyperglycemia and postprandial hypertriglyceridemia have been proposed to cause or maintain beta cell failure and progression to type 2 diabetes mellitus in other species. Postprandial glucose, triglyceride, and insulin concentrations have not been compared in lean and obese dogs. We measured serum glucose, triglyceride, and insulin concentrations in nine naturally occurring obese and nine age- and gender-matched lean dogs. After a 24-h fast, dogs were fed half their calculated daily energy requirement of a standardized diet that provided 37% and 40% of metabolizable energy as carbohydrate and fat, respectively. Fasting and postprandial glucose and triglyceride concentrations were greater in the obese dogs (P < 0.001), although the mean insulin concentration for this group was five times greater than that of the lean group (P < 0.001). Most of the 0.6 mM (11 mg/dL) difference in mean postprandial glucose concentrations between lean and obese dogs was attributable to a subset of persistently hyperglycemic obese dogs with mean postprandial glucose concentrations 1.0 mM (18 mg/dL) greater than that in lean dogs. Persistently hyperglycemic obese dogs had lower triglyceride (P = 0.02 to 0.04) and insulin (P < 0.02) concentrations than other obese dogs. None of the dogs developed clinical signs of diabetes mellitus during follow-up for a median of 2.6 yr. We conclude that pancreatic beta cells in dogs are either not sensitive to toxicity because of mild hyperglycemia or lack another component of the pathophysiology of beta cell failure in type 2 diabetes mellitus.
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Search related cases →Original publication on PubMed: https://pubmed.ncbi.nlm.nih.gov/22130330/