scholarly journals Insulin Administration May Trigger Type 1 Diabetes in Japanese Type 2 Diabetes Patients With Type 1 Diabetes High-Risk HLA Class II and the Insulin Gene VNTR Genotype

2014 ◽  
Vol 99 (9) ◽  
pp. E1793-E1797 ◽  
Author(s):  
Wataru Nishida ◽  
Masao Nagata ◽  
Akihisa Imagawa ◽  
Toshiaki Hanafusa ◽  
Jun Ohashi ◽  
...  
2005 ◽  
Vol 12 (1) ◽  
pp. 213-217 ◽  
Author(s):  
Ayesha A. Motala ◽  
Marc Busson ◽  
Einas M. Al-Harbi ◽  
Manal A. A. Khuzam ◽  
Emtiaz M. D. Al-Omari ◽  
...  

ABSTRACT Whereas the genetic risk for type 1 diabetes is linked to human leukocyte antigen (HLA) class II genes, the HLA association in type 2 (non-insulin-dependent) diabetes is less clear. The association between HLA class II genotypes and type 2 diabetes was examined in adult Bahrainis, an Arab population with a high prevalence of type 2 diabetes. HLA-DRB1* and -DQB1* genotyping of 86 unrelated type 2 diabetes patients (age, 51.6 ± 8.2 years; mean duration of diabetes, 7.7 ± 7.1 years) who had a strong family history of diabetes (52 of 72 versus 0 of 89 for controls, P < 0.001) and 89 healthy subjects was done by PCR-sequence-specific priming. DRB1*040101 (0.1221 versus 0.0562, P = 0.019) and DRB1*070101 (0.2151 versus 0.0843, P < 0.001) were positively associated, while DRB1*110101 (0.0698 versus 0.1461, P = 0.014) and DRB1*160101 (0.0640 versus 0.1236, P = 0.038) were negatively associated with type 2 diabetes. DRB1*040101-DQB1*0302 (0.069 versus 0.0007; P = 0.004), DRB1*070101-DQB1*0201 (0.178 versus 0.0761, P = 0.007), DRB1*070101-DQB1*050101 (0.125 versus 0.0310, P = 0.002), and DRB1*150101-DQB1*060101 (0.0756 versus 0.0281, P = 0.008) were more prevalent among patients, while DRB1*160101-DQB1*050101 (0.0702 versus 0.0349, P = 0.05) was more prevalent among controls, conferring disease susceptibility or protection, respectively. In Bahrainis with type 2 diabetes, there is a significant association with select HLA class II genotypes, which were distinct from those in type 1 diabetes.


2020 ◽  
Vol 105 (3) ◽  
pp. e245-e254 ◽  
Author(s):  
Thomas Jacobi ◽  
Lucas Massier ◽  
Nora Klöting ◽  
Katrin Horn ◽  
Alexander Schuch ◽  
...  

Abstract Context Common genetic susceptibility may underlie the frequently observed co-occurrence of type 1 and type 2 diabetes in families. Given the role of HLA class II genes in the pathophysiology of type 1 diabetes, the aim of the present study was to test the association of high density imputed human leukocyte antigen (HLA) genotypes with type 2 diabetes. Objectives and Design Three cohorts (Ntotal = 10 413) from Leipzig, Germany were included in this study: LIFE-Adult (N = 4649), LIFE-Heart (N = 4815) and the Sorbs (N = 949) cohort. Detailed metabolic phenotyping and genome-wide single nucleotide polymorphism (SNP) data were available for all subjects. Using 1000 Genome imputation data, HLA genotypes were imputed on 4-digit level and association tests for type 2 diabetes, and related metabolic traits were conducted. Results In a meta-analysis including all 3 cohorts, the absence of HLA-DRB5 was associated with increased risk of type 2 diabetes (P = 0.001). In contrast, HLA-DQB*06:02 and HLA-DQA*01:02 had a protective effect on type 2 diabetes (P = 0.005 and 0.003, respectively). Both alleles are part of the well-established type 1 diabetes protective haplotype DRB1*15:01~DQA1*01:02~DQB1*06:02, which was also associated with reduced risk of type 2 diabetes (OR 0.84; P = 0.005). On the contrary, the DRB1*07:01~DQA1*02:01~DQB1*03:03 was identified as a risk haplotype in non–insulin-treated diabetes (OR 1.37; P = 0.002). Conclusions Genetic variation in the HLA class II locus exerts risk and protective effects on non–insulin-treated type 2 diabetes. Our data suggest that the genetic architecture of type 1 diabetes and type 2 diabetes might share common components on the HLA class II locus.


1996 ◽  
Vol 47 (1-2) ◽  
pp. 153
Author(s):  
E Harfouch ◽  
P van Endert ◽  
J Timsit ◽  
C Boitard ◽  
JF Bach ◽  
...  

2016 ◽  
Vol 101 (3) ◽  
pp. 928-936 ◽  
Author(s):  
Jakob Starup-Linde ◽  
Simon Lykkeboe ◽  
Søren Gregersen ◽  
Ellen-Magrethe Hauge ◽  
Bente Lomholt Langdahl ◽  
...  

Abstract Context: Type 1 and type 2 diabetes mellitus are associated with an increased risk of fracture. Objective: The objective of the study was to compare the bone structure and density between type 1 and type 2 diabetes patients and to investigate fracture associations. Design: This was a cross-sectional study. Setting and Patients: Physician-diagnosed type 1 and type 2 diabetes patients were included from the outpatient clinics at two university hospitals participated in the study. Main Outcome Measures: Bone density and structure were assessed by dual-energy x-ray absorptiometry and high-resolution peripheral quantitative computed tomography. Blood samples were collected for bone turnover markers. Prevalent vertebral fractures were assessed by vertebral fracture assessment and x-ray, and incident fractures were collected from The Danish National Hospital Discharge Register. Results: Bone mineral density (BMD) was higher in type 2 than type 1 diabetes patients at the hip, femur, and spine; however, only the hip differed in multivariate-adjusted models. Bone tissue stiffness at the tibia was increased in type 2 diabetes patients also in adjusted models. Sclerostin levels were inversely associated with fracture in type 1 diabetes patients. The patients with the highest tertile of sclerostin had an 81% decreased risk of a fracture compared with the lowest tertile. Conclusions: Type 1 and type 2 diabetes patients differ in BMD of the hip and tissue stiffness at the tibia. Sclerostin may be a marker independent of BMD to predict fractures in type 1 diabetes patients and thus potentially of clinical importance. Studies with longer follow-up are needed.


2021 ◽  
Vol 11 (3) ◽  
pp. 230
Author(s):  
Mar Sempere-Bigorra ◽  
Iván Julián-Rochina ◽  
Omar Cauli

Background: Diabetic neuropathy is defined as the dysfunction of the peripheral nervous system in diabetic patients. It is considered a microvascular complication of diabetes mellitus. Its presence is associated with increased morbidity and mortality. Although several studies have found alterations at somatic motor, sensory levels and at the level of autonomic nervous system in diabetic patients, there is not a systematic approach regarding the differences in neuropathy between the major variants of diabetes, e.g., type 1 and 2 diabetes at both neurological and molecular level. Data sources: we systematically (Medline, Scopus, and Cochrane databases) evaluated the literature related to the difference of neuropathy in type 1 and 2 diabetes, differences in molecular biomarkers. Study characteristics: seventeen articles were selected based on pre-defined eligibility criteria. Conclusions: both superficial sensitivity (primarily thermal sensitivity to cold) and deep sensitivity (such as vibratory sensitivity), have been reported mainly in type 2 diabetes. Cardiac autonomic neuropathy is one of the diabetic complications with the greatest impact at a clinical level but is nevertheless one of the most underdiagnosed. While for type 1 diabetes patients most neuropathy alterations have been reported for the Valsalva maneuver and for the lying-to-standing test, for type 2 diabetes patients, alterations have been reported for deep-breathing test and the Valsalva test. In addition, there is a greater sympathetic than parasympathetic impairment, as indicated by the screening tests for autonomic cardiac neuropathy. Regarding subclinical inflammation markers, patients with type 2 diabetes showed higher blood levels of inflammatory markers such as high-sensitivity C-reactive protein, proinflammatory cytokines IL-6, IL-18, soluble cell adhesion molecules and E-selectin and ICAM-1, than in type 1 diabetes patients. By contrast, the blood levels of adiponectin, an adipocyte-derived protein with multiple paracrine and endocrine activities (anti-inflammatory, insulin-sensitizing and proangiogenic effects) are higher in type 1 than in type 2 diabetic patients. This review provides new insights into the clinical differences in type 1 and 2 diabetes and provide future directions in this research field.


2016 ◽  
Vol 11 (11) ◽  
pp. 1839 ◽  
Author(s):  
Ghasem Solgi ◽  
Ahmad Marzban ◽  
Javad Kiani ◽  
Mehrdad Hajilooi ◽  
Hamzeh Rezaei ◽  
...  

2011 ◽  
Vol 77 (4) ◽  
pp. 317-324 ◽  
Author(s):  
C. Weinstock ◽  
N. Matheis ◽  
S. Barkia ◽  
M.-C. Haager ◽  
A. Janson ◽  
...  

Genes ◽  
2021 ◽  
Vol 12 (3) ◽  
pp. 400
Author(s):  
Hitoe Mori ◽  
Hirokazu Takahashi ◽  
Keiichiro Mine ◽  
Ken Higashimoto ◽  
Kanako Inoue ◽  
...  

Accumulating evidence has suggested that viral infection causes type 1 diabetes due to direct β-cell damage and the triggering of autoimmune reactivity to β cells. Here, we elucidated that the tyrosine kinase 2 (Tyk2) gene, encoding an interferon receptor signaling molecule, is responsible for virus-induced diabetes in mice, and its promoter variant confers a risk of type 1 diabetes in humans. This study investigated the relationship between a TYK2 promoter variant (TYK2PV) and insulin secretion in type 2 diabetes patients. TYK2PV status was determined using direct DNA sequencing and its associations with fasting insulin, C-peptide, and homeostatic model assessment of insulin resistance (HOMA-IR) were evaluated in type 2 diabetes patients without sulfonylurea or insulin medication. Of the 172 patients assessed, 18 (10.5%) showed TYK2PV-positivity. Their body mass index (BMI) was significantly lower than in those without the variant (23.4 vs. 25.4 kg/m2, p = 0.025). Fasting insulin (3.9 vs. 6.2 μIU/mL, p = 0.007), C-peptide (1.37 vs. 1.76 ng/mL, p = 0.008), and HOMA-IR (1.39 vs. 2.05, p = 0.006) were lower in those with than in those without the variant. Multivariable analysis identified that TYK2PV was associated with fasting insulin ≤ 5 μIU/mL (odds ratio (OR) 3.63, p = 0.025) and C-peptide ≤ 1.0 ng/mL (OR 3.61, p = 0.028), and also lower insulin resistance (HOMA-IR ≤ 2.5; OR 8.60, p = 0.042). TYK2PV is associated with impaired insulin secretion and low insulin resistance in type 2 diabetes. Type 2 diabetes patients with TYK2PV should be carefully followed in order to receive the appropriate treatment including insulin injections.


2017 ◽  
Vol 75 (8) ◽  
pp. 533-538 ◽  
Author(s):  
Liliana Chevtchouk ◽  
Marcio Heitor Stelmo da Silva ◽  
Osvaldo José Moreira do Nascimento

ABSTRACT Objective To evaluate neuropathic pain and peripheral vascular disease in diabetics and compare this with the length of time since diagnosis in type 1, and type 2 diabetes. Methods A cross-sectional study with 225 diabetics chosen from their responses on the DN4 questionnaire, who were then evaluated with the ankle-brachial index (ABI), separating type 1 diabetes from type 2 diabetes. Results A higher incidence of neuropathic pain in those over 60 years of age showed an ABI > 1.3. Neuropathic pain was related to an abnormal ABI in 144 patients (64.2%). A statistically significant value was obtained in type 2 diabetes patients with more than 10 years from disease onset, 69 with altered ABI and 25 with normal ABI. There was an altered ABI (< 0.9) observed in 33% of type 1 diabetes patients and in 67% of type 2 diabetes patients. Conclusion The ABI test in type 1 diabetes and type 2 diabetes patients is important even in those who are asymptomatic. A diagnosis of more than 10 years prior, regardless of the presence of neuropathic pain or ischemic signs, altered the ABI.


Sign in / Sign up

Export Citation Format

Share Document