Hypersomatotropism in Diabetic Cats: Recognition, Diagnosis, and Clinical Importance

Poor glycaemic control in a diabetic cat is not always the result of inadequate insulin dosing or caregiver-related challenges. Underlying disorders that increase insulin resistance can significantly influence treatment response, and among these, hypersomatotropism (HST) deserves particular attention. Once considered uncommon, HST is now recognised as one of the leading causes of clinically relevant insulin-resistant diabetes mellitus in cats, occurring in approximately one in three to one in five diabetic cats^1,2,3,4. Early recognition is important because identifying the underlying condition can influence therapeutic decisions, improve diabetic management, and expand treatment options beyond simply increasing insulin doses. 

Why Hypersomatotropism Matters in Diabetic Cats 

Hypersomatotropism results from excessive secretion of growth hormone, usually caused by hyperplasia or an adenoma of the pars distalis of the anterior pituitary, while carcinoma remains uncommon. Excess growth hormone stimulates increased insulin-like growth factor-1 (IGF-1) production, leading to insulin resistance and making diabetic control more challenging². 

Importantly, HST should not be viewed solely as a condition affecting cats requiring exceptionally high insulin doses. The guideline highlights that affected cats may present across a broad spectrum. Some develop severe insulin resistance requiring large insulin doses, whereas others have relatively well-controlled diabetes or may even experience temporary diabetic remission early in the disease process¹. This variability reinforces the importance of maintaining clinical suspicion even when diabetic control appears acceptable. 

Recognising the Clinical Presentation 

One of the greatest diagnostic challenges is that physical appearance alone is often misleading. Approximately 75% of cats with HST lack obvious phenotypic changes that distinguish them from other diabetic cats². Consequently, relying solely on classical acromegalic features risks missing many affected patients. 

Certain clinical findings should nevertheless prompt consideration of HST, including: 

• Weight gain despite suboptimal diabetic control 

• Extreme polyphagia 

• Recent onset of respiratory stridor 

• Cardiac abnormalities 

• Persistently difficult diabetic regulation despite appropriate management 

However, these findings are inconsistent, and their absence should not discourage further investigation¹. 

The guideline therefore recommends discussing HST screening with caregivers of all diabetic cats rather than reserving testing only for those with obvious insulin resistance. This recommendation has become increasingly relevant as non-insulin therapeutic options are now available, potentially masking the degree of insulin resistance that would otherwise trigger further investigation. 

Practical Diagnostic Approach 

Serum IGF-1 measurement remains the preferred screening test for HST. A concentration exceeding 1000 ng/ml is considered diagnostic, while values between 700 and 1000 ng/ml represent a grey zone requiring reassessment after an interval, such as two months^1,5. 

Timing of testing is equally important. Because insulin is necessary for normal hepatic production of IGF-1 in response to growth hormone stimulation, measurements performed immediately after diagnosis may underestimate disease. Testing after approximately 6–8 weeks of diabetes treatment, whether using insulin or an SGLT2 inhibitor, provides a more reliable assessment. 

Following confirmation of elevated IGF-1 concentrations, advanced imaging with contrast-enhanced CT or MRI may be considered to evaluate the pituitary gland. Nevertheless, normal imaging findings do not completely exclude HST, as microadenomas or hyperplasia may remain undetected^5,6. 

Clinical Importance for Long-Term Management 

Recognising HST has important implications that extend well beyond explaining poor diabetic control. Addressing the underlying disease allows clinicians to have informed discussions with caregivers regarding prognosis and available treatment options. 

Definitive interventions, particularly hypophysectomy, have been associated with the longest survival times, excellent control of IGF-1 concentrations, and high caregiver satisfaction, although availability, cost, perioperative risks, and the need for lifelong medication must be considered. Other options, including radiotherapy, pasireotide, cabergoline, or management directed primarily at the diabetic consequences of HST, each have distinct advantages and limitations that should be individualised according to the patient and caregiver circumstances¹. 

Importantly, identification of HST shifts the clinical objective from repeatedly escalating insulin doses alone toward managing the underlying endocrine disorder whenever feasible. 

Practical Clinical Insights 

For practicing veterinarians, HST should become part of the routine differential diagnosis whenever managing feline diabetes, not only in severely insulin-resistant patients. Incorporating IGF-1 screening into discussions with caregivers of diabetic cats can facilitate earlier recognition of this frequently underdiagnosed condition. Maintaining awareness that most affected cats lack obvious physical changes helps prevent missed diagnoses, while interpreting IGF-1 results within the context of treatment timing improves diagnostic accuracy. Recognising HST early enables a more comprehensive treatment strategy and supports informed decision-making regarding long-term diabetic management while tailoring therapy to the individual patient and caregiver. 

References 

1. Taylor S, Cannon M, Church D, Fleeman L, Fracassi F, Gilor C, Mott J, Niessen S. 2025 iCatCare consensus guidelines on the diagnosis and management of diabetes mellitus in cats. Journal of feline medicine and surgery. 2025 Nov;27(11):1098612X251399103. https://journals.sagepub.com/doi/pdf/10.1177/1098612X251399103 

2. Niessen SJ, Forcada Y, Mantis P, Lamb CR, Harrington N, Fowkes R, Korbonits M, Smith K, Church DB. Studying cat (Felis catus) diabetes: beware of the acromegalic imposter. PLoS One. 2015 May 29;10(5):e0127794. https://journals.plos.org/plosone/article/file?id=10.1371/journal.pone.0127794&type=printable 

3. Berg RI, Nelson RW, Feldman EC, Kass PH, Pollard R, Refsal KR. Serum insulin‐like growth factor‐I concentration in cats with diabetes mellitus and acromegaly. Journal of veterinary internal medicine. 2007 Sep;21(5):892-8. https://onlinelibrary.wiley.com/doi/pdfdirect/10.1111/j.1939-1676.2007.tb03040.x 

4. Schaefer S, Kooistra HS, Riond B, Suchodolski JS, Steiner JM, Prins M, Zini E, Reusch CE. Evaluation of insulin-like growth factor-1, total thyroxine, feline pancreas-specific lipase and urinary corticoid-to-creatinine ratio in cats with diabetes mellitus in Switzerland and the Netherlands. Journal of feline medicine and surgery. 2017 Aug;19(8):888-96. https://journals.sagepub.com/doi/pdf/10.1177/1098612X16664390 

5. Scudder C, Church D. Feline comorbidities: hypersomatotropism-induced diabetes in cats. Journal of Feline Medicine and Surgery. 2024 Feb;26(2):1098612X241226690. https://journals.sagepub.com/doi/pdf/10.1177/1098612X241226690 

6. Miller MA, Piotrowski SL, Donovan TA, Scott-Moncrieff JC, Owen TJ, McCue JP, DuSold DM, Ramos-Vara JA, Weng HY, Chen AV, Martin LG. Feline pituitary adenomas: correlation of histologic and immunohistochemical characteristics with clinical findings and case outcome. Veterinary pathology. 2021 Mar;58(2):266-75. https://journals.sagepub.com/doi/pdf/10.1177/0300985820978309