Protective effect of DRB1 locus against type 2 diabetes mellitus in Mexican Mestizos.

The aim of the study was to investigate the participation of human leukocyte antigen (HLA) class II alleles in the expression of type 2 diabetic and in nondiabetic subjects with and without family history of diabetes. The purpose was to evaluate any HLA association and to look for different patterns of insulin resistance and insulin secretion, comparing subjects with a low probability of developing diabetes, as a result of their family history. We recruited 87 healthy subjects without family history of diabetes, 48 healthy subjects with family history, and 47 type 2 diabetic patients. All of them were Mexican Mestizos of central Mexico. Using a standard 75-g oral glucose tolerance test, insulin resistance was determined and insulin secretion was assessed with the HOMA model. DRB1, DQA1 and DQB1 alleles were typed using polymerase chain reaction-sequence-specific oligonucleotide probe (PCR-SSOP) and sequence specific primers (PCR-SSP). Nondiabetic subjects had similar HOMA-IR and DeltaI 30/DeltaG 30 index (HOMA). A significant decreased frequency of DRB1*0403 (p = 0.01; odds ratio [OR] = 0.20) was demonstrated in type 2 diabetic patients, and DRB1*0701 (p = 0.02; OR = 0.17) in nondiabetics with family history of diabetes. These alleles associated with protection against type 2 diabetes, share glutamic acid at position-74 and were previously demonstrated to contribute to protection against type I diabetes.

Serum and urinary insulin-like growth factor-1 and tumor necrosis factor in neonates with and without acute renal failure.

Acute renal failure (ARF) in neonates may occur after renal ischemia. Growth factors participate in the tubular regeneration process. Insulin-like growth factor-1 (IGF-1) is produced in the kidney during the recovery phase of ARF. Tumor necrosis factor-alpha (TNFalpha) may play a role in renal apoptosis. We examined serum and urinary IGF-1 and TNFalpha in neonates with or without ARF after asphyxia, in order to assess their possible use as markers of renal damage and recovery. We studied 20 full-term asphyxiated neonates, 10 with ARF and 10 without ARF, and compared them with 13 normal newborns for 7 days after birth. Blood urea, creatinine, pH, base deficit, and serum and urine IGF-1 and TNFalpha were assessed. Neonates with ARF had more-severe acidosis than patients without ARF. All patients had lower serum IGF-1 values immediately after birth than control children. Serum IGF-1 remained low in the ARF patients. The initial urinary IGF-1 was higher in all patients compared with control newborns, and remained elevated for the rest of the study only in the ARF neonates. Serum and urinary TNFalpha concentrations were similar for all healthy and diseased neonates. Measurement of serum and urinary IGF-1 levels in ARF neonates might be of additional value for clinical assessment of ARF.