Etiology

• Most cases of DM in ferrets are iatrogenic as a result of aggressive pancreatectomy to debulk insulinomas Insulinoma. Any ferret undergoing (partial) pancreatectomy for treatment of insulinoma should be considered at risk for developing DM.
• Causes may include:
  • Lack of insulin production, ie an absolute insulin deficiency, eg secondary to immune-mediated pancreatitis, ie type-I DM.
  • Insulin resistance (peripheral), ie a relative insulin deficiency resulting from diminished response to insulin, ie type-II DM.
  • Glucagonoma, resulting in excessive production and release of glucagon in the circulation.
• In the literature, one case report described pathological findings consistent with a type-I DM:
  • Histologically, the ferret’s pancreas not only contained fewer beta cells, but cells also lacked immunoreactivity for insulin.
  • In addition, focal lymphoplasmacytic inflammation was present in the pancreatic tissue, consistent with an immune-mediated pancreatitis, as has been found in dogs with DM.
• Another report described presence of diabetes mellitus and ketoacidosis in a ferret fed solely on sweet cereals, suggesting that a diet high in glycemic index may play a role in diabetogenesis in ferrets, similar to other species. Findings in this ferret were thought to be the result of a peripheral insulin resistance brought on by the high-sugar diet, consistent with a type-II DM.
• Two other ferrets with spontaneous DM were found to have concurrent hyperadrenocorticism Hyperadrenocorticism/hyperandrogenism:
  • It may be theorized that DM in these ferrets occurred due to peripheral insulin resistance brought on by increased blood cortisol concentrations resulting from adrenal gland disease.
  • Unfortunately, cortisol levels were not reported in either of the two ferrets, thereby rendering it uncertain whether and to what degree adrenal gland disease played a role in DM diagnosed in these ferrets.
  • Alternatively, gonadotropin-releasing hormone (which had been administered in one of the ferrets to manage its hyperadrenocorticism) may also have played a role in the peripheral insulin resistance, as has been reported in humans.
• Another reported case was suggested to be secondary to steroid treatment.