Felis ISSN 2398-2950


Contributor(s): David Bruyette, Dr Linda Fleeman


  • Plasma glucose less than 3.0 mmol/L (55 mg/dL) is significant.
  • In animals that have chronic low blood glucose concentrations may have to drop very low (less than 2.0 mmol/L (35 mg/dL)) before clinical signs are exhibited.
  • Signs: ataxia, weakness, disorientation, seizures.
  • Diagnosis: blood or plasma glucose concentration.
  • Treatment: glucose (oral or intravenous), and correct underlying cause. Note that consumption of food will not reliably increase blood glucose in cats.




  • Neonatal hypoglycemia - dystocia, hypothermia, hypoxia, failure to feed/maternal rejection/maternal agalactia, dehydration, diarrhea may be contributing causes.
  • Anorexia/malnourishment - especially in neonate/juvenile cats.

Primary disease

Exogenous agents

Predisposing factors


  • Neonatal/juvenile animals have immature mechanisms for regulating blood glucose.


  • Decrease of blood glucose towards the lower end of the physiological range stimulates secretion of counter-regulatory hormones (glucagon, adrenaline, noradrenaline, cortisol and growth hormone), which increase glycogenolysis and gluconeogenesis and so increase blood glucose concentration.
  • Hypoglycemia results from failure of these mechanisms due to excess insulin, deficiency of counter-regulatory hormones, and/or inadequate glucose production.
  • Hypoglycemia also → an increased appetite.
  • If these protective counter-regulatory mechanisms are overwhelmed, hypoglycemia → reduced glucose availability to central and peripheral nervous system → lethargy, weakness, ataxia, disorientation, seizures.
  • Prolonged severe hypoglycemia → reversible or irreversible brain damage, and rarely death.


  • Neonatal hypoglycemia - gluconeogenesis limited in neonate and limited glycogen stores rapidly deplete - relies upon regular feeding - may develop hypoglycemia after only 12 hour fast.
  • Starvation - severe malnutrition  →  decreased hepatic glycogen, decreased fat stores  →  decreased gluconeogenesis  →  hypoglycemia.
  • Exogenous agents: direct drug action  →  hypoglycemia.
  • Bacterial shock  →  depletion of glycogen stores, increased peripheral use of glucose, decreased gluconeogenesis + ?circulatory factors  →  hypoglycemia.
  • Extra-pancreatic tumors:
    • Secretion of Insulin/insulin-like/insulin precursor.
    • Accelerated glucose utilization.
    • Inhibited glucose release from liver  →  hypoglycemia.
  • Functional islet cell tumor or non-neoplastic beta cell hyperplasia →  insulin secretion →  hypoglycemia.
  • Insulin overdose, inappetence/starvation, and/or concurrent illness during treatment with insulin may →  hypoglycemia.


This article is available in full to registered subscribers

Sign up now to purchase a 30 day trial, or Login


This article is available in full to registered subscribers

Sign up now to purchase a 30 day trial, or Login


This article is available in full to registered subscribers

Sign up now to purchase a 30 day trial, or Login

Further Reading


Refereed papers

  • Recent references from PubMed and VetMedResource.
  • Behrend E, Holford A, Lathan P et al (2018) 2018 AAHA Diabetes Management Guidelines for Dogs and Cats. JAAHA 54 (1), 1-21 PubMed.
  • Viebrock K A, Dennis J (2017) Hypoglycemia episodes in cats with diabetes mellitus: 30 cases (2013-2015). J Feline Med Surg 20 (6), 563-70 PubMed.
  • Hambrook L E, Ciavarella A A, Nimmo J S et al (2016) Hyperinsulinaemic, hypoglycaemic syndrome due to acquired nesidioblastosis in a cat. JSFM Open Rep (2), 2055116916657846 PubMed.
  • Greene S N, Bright R M (2008) Insulinoma in a cat. JSAP 49 (1), 38-40 PubMed.
  • Münnich A (2008) The pathological newborn in small animals: the neonate is not a small adult. Vet Res Commun 32 (Suppl 1), S81-5 PubMed.
  • Gabor L J, Canfield P J, Malik R (2000) Haematological and biochemical findings in cats in Austrlia with lymphosaroma. Aust Vet J 78 (7), 456-461 PubMed.