RESUMO
BACKGROUND: Visfatin is an adipokine, associated with obesity and possibly glucose regulation. OBJECTIVE: The aim of this study was to examine the association of visfatin and its genetic variants with adiposity, cardiometabolic risk factors and obesity-related morbidities in obese children. METHODS: Anthropometric measurements, dual energy X-ray absorptiometry scan, fasting blood samples and oral glucose tolerance tests were performed for 243 obese children. We screened the visfatin gene of 24 obese subjects and then performed genotyping of identified genetic variants in other 219 obese children through direct DNA sequencing. RESULTS: Fasting serum visfatin correlated with measures of obesity and liver enzymes and was elevated in obese children with abnormal glucose tolerance and non-alcoholic fatty liver disease. The two upstream single nucleotide polymorphisms, -3187G>A (rs11977021) and -1537C>T (rs61330082), were at complete linkage disequilibrium. The AA genotype of -3187G>A was associated with higher serum visfatin (6.17 ± 0.76 ng mL(-1) vs. 3.92 ± 0.44 ng mL(-1)) and higher triglyceride (1.39 ± 0.08 mmol L(-1) vs. 1.19 ± 0.07 mmol L(-1)) as compared with the GG genotype. There was also a significant linear increase in serum visfatin across GG to GA to AA genotype of -3187G>A, indicating possible additive effect of A allele. The dominant GA + AA genotype model of +21426G>A (rs2302559) was associated with lower serum visfatin (3.83 ± 0.56 ng mL(-1) vs. 5.13 ± 0.34 ng mL(-1)) and lower plasma glucose (4.37 ± 0.08 mmol L(-1) vs. 4.77 ± 0.12 mmol L(-1)) as compared with the GG genotype. CONCLUSION: Visfatin and its genetic variants were associated with adiposity, obesity-related morbidities and adverse cardiometabolic parameters. This supported our hypothesis that visfatin plays a significant role in the development of obesity-related morbidities and cardiometabolic risk.
Assuntos
Citocinas/genética , Angiopatias Diabéticas/etiologia , Nicotinamida Fosforribosiltransferase/genética , Hepatopatia Gordurosa não Alcoólica/etiologia , Obesidade Mórbida/complicações , Obesidade Mórbida/genética , Polimorfismo de Nucleotídeo Único , Absorciometria de Fóton , Glicemia/metabolismo , Índice de Massa Corporal , Doenças Cardiovasculares/etiologia , Criança , Citocinas/sangue , Angiopatias Diabéticas/genética , Angiopatias Diabéticas/fisiopatologia , Feminino , Variação Genética , Genótipo , Teste de Tolerância a Glucose , Humanos , Desequilíbrio de Ligação , Masculino , Nicotinamida Fosforribosiltransferase/sangue , Hepatopatia Gordurosa não Alcoólica/genética , Hepatopatia Gordurosa não Alcoólica/fisiopatologia , Obesidade Mórbida/fisiopatologia , Medição de Risco , Fatores de Risco , Análise de Sequência de DNARESUMO
BACKGROUND: Hamsters are popular household pets and anaphylaxis after their bites have described. However, the putative allergen has not been identified. OBJECTIVE: This study was conducted to identify the allergen causing dwarf hamster (Phodopus sungoris) bite-induced anaphylaxis. METHODS: Two children with hamster bite-induced anaphylaxis were enrolled. They both had negative results to skin testing and specific IgE to hamster epithelium. However, they were both allergic to Dermatophagoides pteronyssinus (Der p). Identification of the putative IgE-binding allergens from the hamster saliva was performed using immunoblot analysis. RESULTS: A specific IgE-binding component at 21 kD in the hamster saliva was identified. ELISA inhibition tests showed partial inhibition with Der p. CONCLUSIONS: The putative allergen from the hamster saliva causing dwarf hamster-induced anaphylaxis was identified. Possible cross-reactivity with Der p was demonstrated. Further studies will be needed to identify the exact nature and function of this allergen.