PATHOGENESIS OF FELINE DIABETES-MELLITUS

Authors
Citation
Ta. Lutz et Js. Rand, PATHOGENESIS OF FELINE DIABETES-MELLITUS, The Veterinary clinics of North America. Small animal practice, 25(3), 1995, pp. 527-552
Citations number
147
Categorie Soggetti
Veterinary Sciences
ISSN journal
01955616
Volume
25
Issue
3
Year of publication
1995
Pages
527 - 552
Database
ISI
SICI code
0195-5616(1995)25:3<527:POFD>2.0.ZU;2-W
Abstract
Diabetes mellitus may occur as a primary disease process or secondary to destruction of beta cells or insulin resistance caused by another d isease. Primary diabetes in humans was subdivided initially based on t he clinical characteristics of the disease, such as age of onset, insu lin dependence, and susceptibility to ketosis. In most human diabetics , the clinical features correspond well to the underlying pathology. H ence, insulin-dependent diabetes is generally used to describe type 1 diabetes, which is caused by immune-mediated destruction of beta cells .' Noninsulin-dependent diabetes is used to describe type 2 diabetes, associated with islet amyloid deposition.(53) Direct translation of th is terminology to feline diabetes has lead to confusion and inaccurate classification. Although there is strong evidence that type 1 and typ e 2 diabetes both occur in cats, type 2 seems to be more frequent, and in contrast to humans, most cats are insulin dependent. In this artic le, the terms Spe I and type 2 diabetes are used to imply a specific u nderlying pathology, and insulin-dependence or non-dependence is used only as a description of the clinical characteristics of the disease. Therefore, insulin-dependent diabetes may occur as a result of either type 1 or type 2 diabetes or secondary diabetes. Impaired glucose tole rance replaces the terms latent and subclinical diabetes,(90) and refe rs to cats with increased glucose concentration or glucose half-life a fter a glucose tolerance test, and fasting normoglycemia or mild hyper glycemia.(61, 95) In cats and humans, impaired glucose tolerance is as sociated with type 2 diabetes, obesity, and stress reactions to diseas e (Link KRJ, Rand JS, unpublished data, 1994).(22, 91, 95)