Islet Amyloidosis and β-Cell Neogenesis in Chronic Calcifying Pancreatitis With Non-Insulin-Dependent Diabetes Mellitus

Pancreas ◽  
2009 ◽  
Vol 38 (3) ◽  
pp. 342-344 ◽  
Author(s):  
Hai-Lu Zhao ◽  
Jing Guan ◽  
Yi Sui ◽  
Lan He ◽  
Fernand F.M. Lai
Keyword(s):  
Diabetes Mellitus ◽  
Insulin Dependent Diabetes Mellitus ◽  
Insulin Dependent Diabetes ◽  
Dependent Diabetes Mellitus ◽  
Β Cell ◽  
Chronic Calcifying Pancreatitis ◽  
Insulin Dependent ◽  
Calcifying Pancreatitis

Differential β-cell response to glucose, glucagon, and arginine during progression to type I (insulin-dependent) diabetes mellitus

Metabolism ◽  
1996 ◽  
Vol 45 (3) ◽  
pp. 306-314 ◽  
Author(s):  
Lucy Chaillous ◽  
Vincent Rohmer ◽  
Didier Maugendre ◽  
Pierre Lecomte ◽  
Richard Maréchaud ◽  
...  
Keyword(s):  
Diabetes Mellitus ◽  
Cell Response ◽  
Insulin Dependent Diabetes Mellitus ◽  
Insulin Dependent Diabetes ◽  
Dependent Diabetes Mellitus ◽  
Type I ◽  
Β Cell ◽  
Insulin Dependent

scholarly journals Human Leukocyte Antigen-A24 and -DQA1*0301 in Japanese Insulin-Dependent Diabetes Mellitus: Independent Contributions to Susceptibility to the Disease and Additive Contributions to Acceleration of β-Cell Destruction*

1999 ◽  
Vol 84 (10) ◽  
pp. 3721-3725 ◽  
Author(s):  
Koji Nakanishi ◽  
Tetsuro Kobayashi ◽  
Toshio Murase ◽  
Taeko Naruse ◽  
Yoshisuke Nose ◽  
...  
Keyword(s):  
Diabetes Mellitus ◽  
Hla Antigens ◽  
Insulin Dependent Diabetes Mellitus ◽  
Insulin Dependent Diabetes ◽  
Dependent Diabetes Mellitus ◽  
Β Cell ◽  
Cell Destruction ◽  
Insulin Dependent ◽  
Hla Dqa1 ◽  
Normal Controls

Abstract The aim of this study is to identify insulin-dependent diabetes mellitus (IDDM)-susceptible HLA antigens in IDDM patients who do not have established risk allele, HLA-DQA1*0301, and analyze relationship of these HLA antigens and the degree of β-cell destruction. In 139 Japanese IDDM patients and 158 normal controls, HLA-A, -C, -B, -DR and -DQ antigens were typed. Serum C-peptide immunoreactivity response (ΔCPR) to a 100-g oral glucose load ≤ 0.033 nmol/l was regarded as complete β-cell destruction. All 14 patients without HLA-DQA1*0301 had HLA-A24, whereas only 35 of 58 (60.3%) normal controls without HLA-DQA1*0301 and only 72 of 125 (57.6%) IDDM patients with HLA-DQA1*0301 had this antigen (Pc = 0.0256 and Pc = 0.0080, respectively). ΔCPR in IDDM patients with both HLA-DQA1*0301 and HLA-A24 (0.097 ± 0.163 nmol/L, mean ± sd, n = 65) were lower than in IDDM patients with HLA-DQA1*0301 only (0.219 ± 0.237 nmol/L, n = 45, P < 0.0001) and in IDDM patients with HLA-A24 only (0.187 ± 0.198 nmol/L, n = 14, P = 0.0395). These results indicate that both HLA-DQA1*0301 and HLA-A24 contribute susceptibility to IDDM independently and accelerate β-cell destruction in an additive manner.

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