The role of insulin in blood glucose abnormalities in canine babesiosis

Abstract

Abnormal carbohydrate metabolism is a commonly encountered feature of malaria in people, and similar derangements have been detected in veterinary patients with canine babesiosis. Glucose, the major metabolic fuel source, is a key resource in critically ill patients as they mount an immunological response to infection and inflammation. The ability of the individual to effectively mobilise, distribute and utilise glucose is a major determinant of morbidity and mortality. Hypoglycaemia has been identified as a life threatening metabolic complication in almost 20% of severely ill dogs suffering from babesiosis due to Babesia rossi infection. Insulin and glucagon are the primary hormones involved in glucose homeostasis. Insulin lowers blood glucose concentration by facilitating cellular uptake and utilisation of glucose. Hyperinsulinaemia as a result of inappropriate insulin secretion may precipitate hypoglycaemia, and has been identif ed as a cause of hypoglycaemia in human and murine malaria. A similar phenomenon may exist in canine babesiosis. This prospective, cross-sectional, observational study, including 94 dogs with naturally acquired virulent babesiosis, sought to investigate and characterise the relationship between blood glucose concentrations and insulin concentrations in cases of canine babesiosis. Pre-treatment jugular blood samples were collected for simultaneous determination of plasma glucose and insulin concentrations. Animals were retrospectively divided into three groups: hypoglycaemic (plasma glucose concentration < 3.3 mmol/L; n=16), normoglycaemic (3.3-5.5 mmol/L; n=62), and hyperglycaemic (> 5.5 mmol/L; n=16). The median plasma insulin concentrations (IQR in parentheses) for the hypoglycaemic, normoglycaemic and hyperglycaemic groups were 10.7 pmol/L (10.7-18.8 pmol/L), 10.7 pmol/L (10.7-29.53 pmol/L; i.e below the detection limit of the assay), and 21.7 pmol/L (10.7-45.74 pmol/L), respectively. Statistical analysis revealed no significant difference in insulin concentration between the three groups. These results suggest that insulin secretion was appropriately suppressed in these dogs. Only two dogs had elevated insulin concentrations, one of which was hypoglycaemic. The median time since last meal (available for 87 dogs) was 24 hours (IQR 2-4 days), constituting a significant period of illness-induced starvation. We conclude that hyperinsulinaemia is not a cause of hypoglycaemia in virulent canine babesiosis. It is speculated that prolonged fasting due to disease-induced anorexia, in addition to increased glucose consumption, depletion of hepatic glycogen stores, and hepatic dysfunction with impaired gluconeogenesis, may play important roles in the pathophysiology of hypoglycaemia in canine babesiosis.