Feline Insular Amyloid: Incidence in Adult Cats with No Clinicopathologic Evidence of Overt Diabetes Mellitus

Abstract

Abstract. Pancreatic tissues from 93 adult domestic cats with no clinicopathologic evidence of overt diabetes mellitus were examined for islet amyloid. Amyloid deposits were found in the pancreatic islets of 44 cats. Approximately one-third of these deposits were not seen with HE, but subsequently were identified with Congo red stain. The proportion of islets with amyloid, the intra-islet location of amyloid, and the amount of amyloid in individual islets also were characterized. In this select population of adult cats, the presence or absence of islet amyloid was not linked significantly (p = > 0.05) to age, breed, sex or primary anatomic diagnosis. Results of this study indicate that: the incidence of islet amyloid in cats is higher than previously recognized; as in man, islet amyloid can occur in cats without concurrent overt diabetes mellitus; and islet amyloid should not be considered pathognomonic for diabetes mellitus.Pancreatic islet amyloid deposits (i.e., insular amyloid) occur in man [2,3,4, 131, non-human primates [7,8, 171, raccoons [ 11, 151, and domestic and wild cats [5, 10, 11, 121. Insular amyloid in man and animals often is associated with maturityonset diabetes mellitus and is rare in juvenile-onset diabetes. A majority of human diabetics over 50 years old have amyloid deposits in their pancreatic islets [I, 4, 13, 201, but insular amyloid also has been identified in a significant number of aged, non-diabetic people [3,4,25]. The amount and frequency of insular amyloid increases with age in both diabetic and non-diabetic people [2,3].A significant relationship exists between the presence of insular amyloid and maturity-onset diabetes, but it is not known whether the amyloid causes diabetes, or arises secondarily to it. Studies of insular amyloid in man indicate that: amyloid deposits are limited to the pancreatic islets [23]; deposition apparently is independent of amyloid in other organs [21]; and systemic (primary or secondary) amyloidosis seems to have no facilitating effect on the formation of insular amyloid [21]. Histochemical, biochemical, and clinicopathologic differences between insular and systemic amyloid imply different and independent mechanisms of formation. Major precursor substances for systemic amyloid are immunoglobulin light chains in primary and myeloma-associated amyloidosis [6], and serum protein AA in secondary 310

Pathology in Captive Wild Felids at German Zoological Gardens

“…In domestic cats, amyloid deposition in pancreatic islets of Langerhans is common and can be detected in 65% of animals with diabetes mellitus [104]. However, islet amyloidosis is also described in approximately 50% of cats that lacked evidence for endocrine disease [105]. In the present study, there was no evidence for amyloidosis in islets of Langerhans within the pancreas in any of the investigated animals.…”

Generalised amyloidosis and acute liver haemorrhage in four cats

“…Insular amyloid is most common, being characterised by localised deposition of endocrineassociated amyloid in the pancreatic islets (Yano andothers 1981, Johnson andothers 1985). There is a significant association of severe insular amyloidosis with the development of maturity-onset diabetes mellitus in middle-aged and old cats (peak eight to 10 years) and the disease is considered to arise as a result of a functional islet cell abnormality, although a lesser degree of insular amyloidosis is a common incidental senile change in aged cats.…”

Metabolic Effects of Obesity and Its Interaction with Endocrine Diseases

“…44 However, they are also present in approximately 45% of older nondiabetic cats, although they are not as extensive as in diabetic cats. 45 Therefore, increased amylin secretion and amyloid deposition are not the sole determinants of beta cell failure in feline DM, although they may contribute by decreasing beta cell functional reserve. 44,46 In support of the concept that both insulin resistance and beta cell function contribute to the onset of type 2 DM, the natural history of type 2 DM in a genetically predisposed human population involves (1) a period of peripheral insulin resistance with hyperinsulinemia and euglycemia, (2) a decline in beta cell function with impaired insulin secretory response to glucose and decreased glucose tolerance, and (3) further reduction in insulin secretion with loss of hepatic insulin sensitivity and loss of control of EGP.…”