Growth hormone (GH) is produced in the anterior pituitary gland and is normally under the control of the hypothalamus via gonadotrophin-releasing hormone (GnRH). Growth hormone is challenging to measure directly for several reasons, both physiologically and from a laboratory perspective. Growth hormone is produced in a pulsatile fashion, is highly influenced by various physiological states, and has a short half-life in the blood stream. In addition, growth hormone is not well conserved among species making assay availability problematic.

Insulin-like growth factor 1 (IGF-1) is produced primarily in the liver in response to growth hormone stimulation. IGF-1 has a much longer half-life compared to growth hormone, is produced in a non-pulsatile manner, is stable in serum, and is well-conserved between species. These features make IGF-1 a suitable substitute for direct measurement of growth hormone, and IGF-1 results can be expected to reflect growth hormone production in dogs and cats. Serum or plasma may be submitted for IGF-1 testing (20005).

Hypersomatotropism (HST) in aging cats is usually associated with a benign tumor of the pituitary gland that autonomously secretes growth hormone in excess. Catabolic effects of excess growth hormone include peripheral and hepatic insulin resistance, resulting in both reduced cellular uptake of glucose and decreased ability to suppress glucose production in the liver. These actions culminate in insulin resistance, marked hyperglycemia, and very often diabetes mellitus which can be difficult to control even with high doses of insulin.

Anabolic effects of growth hormone, mediated in large part via IGF-1, include bone, cartilage and muscle growth, which account for the syndrome of physical changes known as acromegaly. Cats with acromegaly may present with polyphagia, prognathia inferior, “clubbed” paws, cardiomyopathy +/- heart murmur, respiratory stridor from growth of oropharyngeal/lingual tissue, unexpected weight gain, and generalized organomegaly (particularly kidneys and liver).

Hypersomatotropism and acromegaly are not synonymous, and individual cats may present on a continuum. For example, some cats may present with significant insulin resistance but lack the stereotypical physical changes of acromegaly. Conversely, there is a small percentage of cats wherein physical changes of musculoskeletal growth, organomegaly, and cardiac muscle disease predominate, and diabetes mellitus may be absent.

In cats with diabetes mellitus, IGF-1 concentration in excess of 1,000 ng/mL have been associated with a high probability of hypersomatotropism. IGF-1 results of 800 – 1000 ng/mL have been considered equivocal for the presence of hypersomatotropism in some studies, while others consider this gray zone to extend lower to 500 – 1000 ng/mL in the presence of a compatible clinical presentation. Cats evaluated early in course of diagnosis and treatment of diabetes mellitus may have lowered IGF-1 concentration due to impairment of hepatic IGF-1 production in insulin deficient states. Repeat analysis of IGF-1 in 2 to 6 months may be warranted if suspicion for hypersomatotropism remains in cats with equivocal results.

Pituitary dwarfism is rare in cats. A low IGF-1 concentration in a kitten does not exclude the possibility for growth hormone insufficiency but interpretation of results must consider the clinical presentation and other diagnostic measurements. IGF-1 concentrations may decrease as a metabolic consequence of negative energy balance and alterations in hepatic function. Additionally, low concentrations of IGF-1 have been observed in kittens with congenital primary hypothyroidism, with some kittens exhibiting increases in serum IGF-1 in response to thyroid supplementation.