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Diabetes Mellitus in Dogs and Cats

Jacquie S. Rand, BVsc, DVSc, MANZVS, DACVIM (SAIM)
School of Veterinary Science, University of Queensland, Gatton, Queensland, Australia; Australian Pet Welfare Foundation, Kenmore, Queensland, Australia

Etiology/Pathophysiology secondary to glucocorticoid administration or obesity,
and diseases which antagonize insulin’s actions would
Glucose is the primary source of energy in the body. be expected to hasten onset of clinical signs when
Blood glucose concentrations are tightly controlled by a superimposed on a reduced capacity to secrete insulin
feedback system of endocrine hormones. Insulin is pro- as a result of immune‐mediated beta‐cell destruction.
duced by the pancreatic beta‐cells in response to ● Type 2 diabetes is characterized by insulin resistance
increased blood glucose, and promotes storage of glu- with concomitant beta-cell dysfunction. In developed
cose, fatty acids, and amino acids as glycogen, fat, and countries, the majority of feline diabetics are type 2.
protein. Insulin promotes uptake of glucose into most Insulin resistance is multifactorial and associated with
body cells for use, promotes storage of glucose as glycogen genetic factors, obesity, physical inactivity, male gen-
in liver and muscle, and inhibits gluconeogenesis. der, and glucocorticoid steroids. Beta‐cell destruction
Cortisol, glucagon, epinephrine, and growth hormone is initiated and propagated by a variety of factors, not
oppose the actions of insulin, promoting catabolism of yet fully understood, that lead to a decline in insulin
stored carbohydrate into glucose, stored triglycerides secretory capacity. When the increased demand to
into free fatty acids and ketone bodies, and stored protein produce insulin as a result of insulin resistance is
into amino acids. Because they oppose insulin’s effects, superimposed on beta‐cell dysfunction, chronic
these four hormones are called “counterregulatory hor- hyperglycemia ensues. Chronic hyperglycemia is toxic
mones” (Table 12.1). to beta‐cells and in turn causes injury and death of the
Diabetes mellitus is a disease characterized by hyper- beta‐cells, reducing insulin production even further.
glycemia and associated clinical signs. It is classified into ● “Other specific types of diabetes” includes most other
four broad types in human and veterinary medicine. forms in companion animals, including drug‐induced
diabetes (usually steroid use), endocrinopathies that
Type 1 diabetes is a result of immune‐mediated beta‐ antagonize insulin action (acromegaly, hyperadreno-
●
cell destruction, usually leading to an absolute insulin corticism), or exocrine pancreatic disease. Chronic
deficiency. The majority of neutered diabetic dogs have pancreatitis is the most common cause of canine dia-
type 1 diabetes, but this form appears to be very rare in betes in this category, accounting for approximately
cats. The etiology of type 1 diabetes in dogs is multifac- 30% of cases. Approximately 25–30% of poorly con-
torial, and likely involves genetic factors and poorly trolled diabetic cats have acromegaly.
understood environmental factors, which trigger beta‐ ● Gestational diabetes is not a significant cause of diabe-
cell injury and inflammation. In type 1 diabetes, follow- tes in companion animals in the US, as most compan-
ing nonspecific beta‐cell injury, autoimmunity then ion animals are desexed. Pregnancy and diestrus are
propagates continued destruction of beta‐cells, pre- associated with increased progesterone concentrations,
venting regeneration after injury. Factors which trigger which uniquely in the bitch stimulate the mammary
the gastrointestinal immune system are implicated in glands to produce growth hormone. Both hormones
human type 1 diabetes, and in dogs, pancreatitis is a oppose insulin’s glucose lowering effects, leading to
potential triggering factor. As in humans, there is a sea- periodic insulin resistance in intact female dogs, and
sonal influence, with the incidence peaking in winter. diestrus‐associated diabetes. Concurrent obesity would
Environmental factors such as chronic insulin resistance be expected to exacerbate this insulin resistance.

Clinical Small Animal Internal Medicine Volume I, First Edition. Edited by David S. Bruyette.
© 2020 John Wiley & Sons, Inc. Published 2020 by John Wiley & Sons, Inc.
Companion website: www.wiley.com/go/bruyette/clinical