RESUMO
Type 2 diabetes (T2DM) and its complications such as cardiomyopathy, contribute significantly to morbidity and mortality worldwide. Increased adoption of westernized diets and decreased physical activity are contributing to the obesity epidemic which, in turn, increases the risk for T2DM. Other risk factors for T2DM include insulin resistance, dyslipidemia, hypertension, metabolic syndrome, and a genetic predisposition. Risk measures for assessing these factors include family history, blood pressure, body weight, waist circumference, fasting glucose, insulin, and lipid levels, and calculated indices such as BMI, HOMA, and QUIKI. Most of these risk measures routinely done in annual check-ups, should help a primary care physician in making an early diagnosis of impending diabetic condition. The underlying mechanisms of these clinical, anthropometric and biochemical risk measures may also be involved in the etiology of diabetes and its complications. Their levels and changes over time therefore, may indeed reflect the disease process. Early and continued assessment of diabetes risk, as part of patient care, will help identify individuals most likely to develop diabetes and allow for early interventions to reduce risk factors as well as delay or may even prevent disease onset. In T2DM patients, ongoing measurement of risk markers and implementation of intervention where appropriate will improve the diabetic condition, decrease risk of cardiovascular and other complications, and decrease morbidity.
Assuntos
Cardiomiopatias/etiologia , Complicações do Diabetes/etiologia , Diabetes Mellitus Tipo 2/etiologia , Animais , Cardiomiopatias/prevenção & controle , Complicações do Diabetes/prevenção & controle , Diabetes Mellitus Tipo 2/diagnóstico , Diabetes Mellitus Tipo 2/prevenção & controle , Progressão da Doença , Dislipidemias/complicações , Diagnóstico Precoce , Feminino , Humanos , Hipertensão/complicações , Resistência à Insulina , Masculino , Obesidade/complicações , Valor Preditivo dos Testes , Prognóstico , Medição de Risco , Fatores de Risco , Fatores de Tempo , Resultado do TratamentoRESUMO
The human leukocyte receptor complex (LRC) of Chromosome 19q13.4 encodes polymorphic and highly homologous genes that are expressed by cells of the immune system and regulate their function. There is an enormous diversity at the LRC, most particularly the variable number of killer cell immunoglobulin-like receptor (KIR) genes. KIR have been associated with several disease processes due to their interaction with polymorphic human leukocyte antigen class I molecules. We have assessed haplotype compositions, linkage disequilibrium patterns and allele frequencies in two Caucasoid population samples (n=54, n=100), using a composite of single-nucleotide polymorphism (SNP) markers and high-resolution, allele-specific molecular genotyping. Particular KIR loci segregated with SNP and other markers, forming two blocks that were separated by a region with a greater history of recombination. The KIR haplotype composition and allele frequency distributions were consistent with KIR having been subject to balancing selection (Watterson's F: P=0.001). In contrast, there was a high inter - population heterogeneity measure for the LRC-encoded leukocyte immunoglobulin-like receptor A3 (LILRA3), indicating pathogen-driven disruptive selection (Wright's FST=0.32). An assessment of seven populations representative of African, Asian and Caucasoid ethnic groups (total n=593) provided little evidence for long-range LRC haplotypes. The different natural selection pressures acting on each locus may have contributed to a lack of linkage disequilibrium between them.
Assuntos
Humanos , Células Matadoras Naturais , Seleção Genética , Trinidad e TobagoRESUMO
The enzyme glycoxalase I (glyox I) is involved in metabolic detoxification, and requires glutathione (GSH) as a cofactor. Given the low concentration of whole blood GSH in children with oedematous malnutrition, it is possible that the function of this pathway may be compromised in these children. Glyox I activity was therfore assayed in erythocytes taken from 133 severely malnourished children and 21 age-matched controls. The mean values (ñSEM) for the marasmic group (marasmus: 105 ñ 4/u/gm Hb) and the group with kwashiorkor (Kwash: 103 ñ 4/u/gm Hb) were not significantly different from controls (cont: 104 ñ 2u/gm HB)>. In the group with marasmic-kwashiorkor (M-K: 88 ñ 4u/g Hb) Glyox I activity was significantly lower in controls (p < 0.005), as well as in children with marasmus (p < 0.005), and kwashiorkor (p < 0.05). Enzyme activity was lower than normal in 45 per cent of the MK group. Seven children died subsequent to admission; in five cases Glyox I activities were exceedingly low. There was a weak positive correlation between Glyox I activity and whole blood levels of GSH (r=0.215). We conclude that Glyox I activity is relatively unaffected in malnutrition, except in those with M-K and especially those who do not survive the acutely malnourished state