Postprandial glycaemia in cats fed a moderate carbohydrate meal persists for a median of 12 hours--female cats have higher peak glucose concentrations.

The postprandial increase in glucose concentration is typically not considered in selecting diets to manage diabetic and pre-diabetic cats. This study describes increases in glucose and insulin concentrations in 24 clinically healthy, neutered adult cats following one meal (59 kcal/kg) of a moderate carbohydrate diet (25% of energy). Median time to return to baseline after feeding for glucose was 12.2 h (1.8-≥24 h) and for insulin was 12.3 h (1.5-≥24 h). Time to return to baseline for glucose was not different between male (10.2 h) and female (17.2 h) cats. There was evidence female cats had a longer return to baseline for insulin (18.9 h versus 9.8 h) and females had higher (0.9 mmol/l difference) peak glucose than males. This demonstrates that the duration of postprandial glycaemia in cats is markedly longer than in dogs and humans, and should be considered when managing diabetic and pre-diabetic cats.

Canine and feline diabetes mellitus: nature or nurture?

There is evidence for the role of genetic and environmental factors in feline and canine diabetes. Type 2 diabetes is the most common form of diabetes in cats. Evidence for genetic factors in feline diabetes includes the overrepresentation of Burmese cats with diabetes. Environmental risk factors in domestic or Burmese cats include advancing age, obesity, male gender, neutering, drug treatment, physical inactivity, and indoor confinement. High-carbohydrate diets increase blood glucose and insulin levels and may predispose cats to obesity and diabetes. Low-carbohydrate, high-protein diets may help prevent diabetes in cats at risk such as obese cats or lean cats with underlying low insulin sensitivity. Evidence exists for a genetic basis and altered immune response in the pathogenesis of canine diabetes. Seasonal effects on the incidence of diagnosis indicate that there are environmental influences on disease progression. At least 50% of diabetic dogs have type 1 diabetes based on present evidence of immune destruction of beta-cells. Epidemiological factors closely match those of the latent autoimmune diabetes of adults form of human type 1 diabetes. Extensive pancreatic damage, likely from chronic pancreatitis, causes approximately 28% of canine diabetes cases. Environmental factors such as feeding of high-fat diets are potentially associated with pancreatitis and likely play a role in the development of pancreatitis in diabetic dogs. There are no published data showing that overt type 2 diabetes occurs in dogs or that obesity is a risk factor for canine diabetes. Diabetes diagnosed in a bitch during either pregnancy or diestrus is comparable to human gestational diabetes.