We therefore analyzed fasting proinsulin levels in 99 siblings of insulin-dependent diabetes mellitus (IDDM) patients, most of them discordant for diabetes for greater than 6 yr.
ERAD deficiency may contribute to the development of diabetes by affecting proinsulin processing in the ER, intracellular Ca<sup>2+</sup> concentration, and mitochondrial function.
A total of 40 individuals with diabetes (1.8% of early onset sub-group and 0.6% of adult onset sub-group) were carriers of known pathogenic missense variants in the GCK, HNF1A, HNF4A, ABCC8, and INS genes.
One hundred rats were divided into 5 groups: induced DM + RESV administration (DM + RESV; n = 20); induced DM plus placebo solution administration (DM + PLAC; n = 20); induced DM plus insulin therapy (DM + INS; n = 20); induced DM plus administration of RES and INS (DM + RESV + INS; n = 20); and nondiabetic controls (NDM; n = 20).
Analysis of HLA-DQB1 alleles in DR4+ Addison's patients with diabetes mellitus (N = 6) and without IDDM (14 of 18 individuals tested) revealed that the HLA-DQw8 allele (DQB1*0302) was significantly increased in AD patients with IDDM (chi 2 = 13.5; p = 0.001); conversely, a clustering of the HLA-DQw7 allele was detected in DR4+ Addison's patients without IDDM.
We hope to emphasize instead the homogeneity of nephropathy risk in both IDDM and NIDDM and also the idea that a common genetic susceptibility exists for all types of diabetes and is conditional on cumulative exposure to hyperglycemia.
Since after 5 years only one of the children has developed IDDM, it can be concluded autoimmune reactions towards endocrine pancreas and insulin may occur in many children without the development of manifest diabetes.
Tolerizing vaccination of NOD mice with a cDNA plasmid expressing full-length proinsulin prevented diabetes, whereas plasmids encoding ZnT8 and DβH did not.
A total of 218 sets of matched case-control questionnaire data established that paternal IDDM (odds ratio (OR) = 16.11, 95% confidence interval (CI) 1.94-133.7, p < = 0.001) is independently associated with increased risk, and higher birth order (OR = 0.64, CI 0.44-0.94, p = 0.021) and paternal age greater than 25 years (age 25-39 OR = 0.52, CI 0.30-0.89; age 40 + OR = 0.23, CI 0.08-0.67, p = 0.009) with decreased risk of diabetes.
The possible association of human growth hormone (hGH) and insulin (INS) gene regions with metabolic control in diabetes was investigated in 98 subjects with non-insulin-dependent diabetes mellitus (NIDDM); 54 control subjects from the same population were also studied.
Mutations in the preproinsulin protein that affect processing of preproinsulin to proinsulin or lead to misfolding of proinsulin are associated with diabetes.
We identified differentially expressed miRNAs in limbus vs. central cornea in normal and diabetic (DM) corneas including both type 1 (T1DM/IDDM) and type 2 (T2DM/NIDDM) diabetes.
NeuroD/BETA2 gene variability and diabetes: no associations to late-onset type 2 diabetes but an A45 allele may represent a susceptibility marker for type 1 diabetes among Danes. Danish Study Group of Diabetes in Childhood, and the Danish IDDM Epidemiology and Genetics Group.
Non-alcoholic fatty liver disease and impaired proinsulin conversion as newly identified predictors of the long-term non-response to a lifestyle intervention for diabetes prevention: results from the TULIP study.