• counter-regulatory hormones;
  • feline;
  • insulin resistance;
  • stress hyperglycemia


Objective: To characterize the alterations in carbohydrate metabolism as they relate to the development of hyperglycemia in critically ill cats.

Design: Prospective, observational, controlled study.

Setting: Intensive care unit at a university veterinary teaching hospital.

Animals: Twenty-six non-diabetic cats admitted into the intensive care unit for a variety of diseases and 21 healthy control cats.


Blood samples were obtained from critically ill cats upon admission to the intensive care unit. Blood was similarly obtained from control cats.

Measurements and main results: For all cats, venous blood glucose, lactate, cortisol, insulin, glucagon, epinephrine, norepinephrine, and non-esterified fatty acid concentrations were determined and compared between the 2 groups of cats. Compared with controls, critically ill cats had significantly higher median concentrations of glucose [183 (range 51–321) mg/dL versus 110 (91–165) mg/dL; P<0.001], lactate [2.5 (0.6–11.1) mmol/L versus 1.8 (0.4–4.1) mmol/L; P=0.01], cortisol [7.8 (0.3–53.7) μg/dL versus 4.4 (1.5–8.3) μg/dL; P=0.005], glucagon [186 (46–3128) pg/mL versus 97 (30–252) pg/mL; P=0.001], and norepinephrine [1.5 (0.2–16.4) pg/mL versus 0.63 (0.21–3.61) pg/mL; P=0.003]. Compared with controls, critically ill cats also had a significantly lower median plasma insulin concentration [9 (2–52) μU/mL versus 17 (3–35) μU/mL; P=0.04]. The presence or degree of hyperglycemia in critically ill cats was not related to any single measured variable.

Conclusions: Similar to critically ill human patients, alterations in carbohydrate metabolism are present in critically ill cats and likely contribute to the hyperglycemia commonly observed in this population.