The Role of Calcium, Lipid Membranes and Islet Amyloid Polypeptide in the Onset of Type 2 Diabetes: Innocent Bystanders or Partners in a Crime?
| Autor: | Carmelo La Rosa, Antonino Raudino, Danilo Milardi, Loredana Randazzo, Michele Sciacca |
|---|---|
| Jazyk: | angličtina |
| Rok vydání: | 2014 |
| Předmět: |
Genetically modified mouse
medicine.medical_specialty obesity endocrine system diseases Amyloid Endocrinology Diabetes and Metabolism Type 2 diabetes lcsh:Diseases of the endocrine glands. Clinical endocrinology Pathogenesis Endocrinology Internal medicine Extracellular medicine Genetic predisposition Genetic Predisposition to Disease type II diabetes mellitus geography geography.geographical_feature_category lcsh:RC648-665 calcium business.industry amyloid Membranes Artificial free fatty acids Opinion Article Islet medicine.disease Diabetes Mellitus Type 2 Calcitonin membranes business genetic predisposition |
| Zdroj: | Frontiers in endocrinology (Lausanne) 5 (2014). doi:10.3389/fendo.2014.00216 info:cnr-pdr/source/autori:Milardi D.; Sciacca M.F.M.; Randazzo L.; Raudino A.; Rosa C.L./titolo:The role of calcium, lipid membranes and islet amyloid polypeptide in the onset of type 2 diabetes: Innocent bystanders or partners in a crime?/doi:10.3389%2Ffendo.2014.00216/rivista:Frontiers in endocrinology (Lausanne)/anno:2014/pagina_da:/pagina_a:/intervallo_pagine:/volume:5 Frontiers in Endocrinology Frontiers in Endocrinology, Vol 5 (2014) |
| ISSN: | 1664-2392 |
| DOI: | 10.3389/fendo.2014.00216 |
| Popis: | Type II diabetes mellitus (T2DM) is one of the most disabling age-related pathologies in developed countries (1). Its incidence is constantly growing: the number of people affected by T2DM worldwide grew from 28 million cases in 1985 to around 168 million in 2001, with an estimate of 350 million cases in 2030 (2). Despite the intense research efforts focusing on T2DM in the last 20 years, the cause of the underlying pathology is still unclear. Islet Amyloid Polypeptide (IAPP) is an amyloidogenic protein, member of the calcitonin family (3), which is known to be involved in the mechanisms lying at the root of T2DM pathogenesis (4, 5). Indeed, although the correlation between islet β-cell death and amyloid fibril formation is still a matter of debate, recent studies, performed on transgenic mice, show that IAPP aggregation can mediate β-cell failure in T2DM (6). Indeed, despite human and rat variants of IAPP differing by only six amino acids, the two variants behave in a completely different way. In particular, rat IAPP (rIAPP) is unable to form amyloid aggregates under normal conditions (7) and rats do not develop T2DM in analogous conditions. Human IAPP (hIAPP) amyloid aggregates are detectable in pancreas’ extracellular space in 90% of patients (4), while only 10% of patients do not have detectable amyloid deposits. We propose that T2DM etiology might be clarified by studying the close relationships between three apparently independent issues: (i) amyloid toxicity; (ii) genetic factors; and (iii) environmental risk factors related to lifestyle and diet. |
| Databáze: | OpenAIRE |
| Externí odkaz: |
|