Glucose

Glucose is a cellular energy source. Blood glucose levels are strictly controlled by hormones (eg insulin, glucagon). The most common cause of elevated blood glucose levels is diabetes mellitus. Blood glucose is reliably measured only from fasting samples, as eating can increase glucose levels. Hypoglycaemia may be caused, for example, by insulinoma or problems with insulin adminstration in diabetic patients. Also delayed separation of red blood cells from the sample causes decreased glucose levels.

 

Increased concentrations

– Diabetes mellitus
– Pancreatitis
– Cushing’s disease
– Hyperpituitarism
– Pheochromocytoma
– Acromegaly
– Stress
– Drugs: e.g. glucocorticoids, detomidine, xylazine, propanolol, thyroxine, progestins, morphine
– Progesterone effect
– Eating before blood sampling

Decreased concentrations

– Liver failure
– Addison’s disease
– Sepsis
– Pregnancy hypoglycaemia
– Intense physical activity
– Renal glucosuria
– Hypopituitarism
– Insulinoma
– Glycogen storage disorders and familial hypoglycemia
– Paraneoplastic syndrome
– Certain drugs and toxins: xylitol, insulin, sulfonylurea
– Severe malnutrition
– Neonatal/juvenile
– Delayed plasma/serum separation

Additional information

Thrall, M. A., Weiser, G., Allison, R. W. & Campbell, T. W. Veterinary Hematology and Clinical Chemistry. (Wiley-Blackwell, 2012).
Thompson, M. F., Fleeman, L. M., Kessell, A. E., Steenhard, L. A. & Foster, S. F. Acquired proximal renal tubulopathy in dogs exposed to a common dried chicken treat: retrospective study of 108 cases (2007-2009). Aust. Vet. J. 91, 368–373 (2013).

 

Lactate

Lactate is formed when cells use anaerobic glycolysis for energy production. Lactate accumulates in the bloodstream either as a result of increased anaerobic glycolysis (e.g. in circulatory disorders) or in conditions where the removal of lactate from the circulation is disturbed. Monitoring of lactate levels is used to assess the prognosis of some diseases, and the high concentration in these diseases is associated with higher mortality. Intense physical exercise also raises lactate levels. In sporting dogs, lactate levels can be used to monitor circulatory capacity. It must be noted, that delayed separation of red blood cells from the sample causes an increased lactate concentrations.

 

Increased concentrations

– Ischemia/hypoxia
– Sepsis
– Hypovolemia
– Severe anemia
– Cardiogenic shock
– Seizures
– Intense physical exercise
– Renal failure
– Diabetes mellitus
– Neoplasia
– Certain drugs/toxins: e.g. ethylene glycol, catecholamines, cyanide, salicylates, strychnine, nitroprusside, bicarbonate, paracetamol, terbutaline, activated charcoal
– Delayed plasma/serum separation
– Prolonged venous stasis when blood sampling

Additional information

Allen, S. E. & Holm, J. L. Lactate: physiology and clinical utility. J. Vet. Emerg. Crit. Care 18, 123–132 (2008).
Pang, D. S. & Boysen, S. Lactate in veterinary critical care: pathophysiology and management. J. Am. Anim. Hosp. Assoc. 43, 270–279 (2007).
Mooney, E., Raw, C. & Hughes, D. Plasma lactate concentration as a prognostic biomarker in dogs with gastric dilation and volvulus. Top. Companion Anim. Med. 29, 71–76 (2014).
Cortellini, S., Seth, M. & Kellett-Gregory, L. M. Plasma lactate concentrations in septic peritonitis: A retrospective study of 83  dogs (2007-2012). J. Vet. Emerg. Crit. Care (San Antonio). 25, 388–395 (2015).
Holahan, M. L., Brown, A. J. & Drobatz, K. J. The association of blood lactate concentration with outcome in dogs with idiopathic immune-mediated hemolytic anemia: 173 cases (2003-2006). J. Vet. Emerg. Crit. Care (San Antonio). 20, 413–420 (2010).

 

Citrate

Citrate is an intermediate metabolite in an important metabolic pathway, the citric acid cycle. The metabolism of citrate occurs mainly in the liver but also partly in the kidneys and muscles. Higher levels of citrate have been reported in humans in both hepatic and renal failure and after intense physical exercise. Citrate metabolism has mainly been studied in other species than dogs.

 

Additional information

Record, C. O. et al. Plasma and brain amino acids in fulminant hepatic failure and their relationship  to hepatic encephalopathy. Eur. J. Clin. Invest. 6, 387–394 (1976).
Kramer, L. et al. Citrate pharmacokinetics and metabolism in cirrhotic and noncirrhotic critically ill patients. Crit. Care Med. 31, 2450–2455 (2003).
Klingele, M. et al. Long-term continuous renal replacement therapy and anticoagulation with citrate in critically ill patients with severe liver dysfunction. Crit. Care 21, 294 (2017).
Gamble, L.-J. et al. Serum metabolomics of Alaskan sled dogs during endurance racing. Comp. Exerc. Physiol. 14, 1–12 (2018).