RESUMO
BACKGROUND: Even though excessive adipose tissue is related to chronic metabolic disturbances, not all subjects with excess weight (EW) display metabolic alterations, and not all normal-weight (NW) subjects have a metabolically healthy (MH) phenotype, probably due to gene-environment interactions. The aim of this study was to investigate the interaction effects of ADIPOQ and PPARG genetic variants in NW and EW individuals with different metabolic phenotypes. METHODS: Data on 345 adults from western Mexico were analyzed. The individuals were classified into NW and EW groups according to body mass index, and were categorized as MH or metabolically unhealthy (MUH), considering homeostatic model assessment insulin resistance (HOMA-IR) and National Cholesterol Education Program Adult Treatment Panel III (NCEP-ATP III) cut-off points for glucose, triglycerides, high-density lipoprotein cholesterol, and blood pressure. Subjects with ≤1 altered parameter were classified as MH. The single nucleotide polymorphisms (SNPs) -11377C>G, -11391G>A, +45T>G, and +276G>T for ADIPOQ and Pro12Ala for PPARG were analyzed by allelic discrimination. High-molecular-weight adiponectin isoform levels were measured by ELISA. RESULTS: Lower serum adiponectin levels were associated with the MUH phenotype in EW subjects. NW subjects with the GG or TG genotype for the +45T>G SNP had reduced odds of the MUH phenotype. Individuals who carried two copies of the GG haplotype at the -11391G>A and -11377C>G SNPs for ADIPOQ had lower serum adiponectin levels than those with zero copies. CONCLUSION: In this population, lower serum adiponectin levels were found in the EW-MUH phenotype, and no differences were observed between the NW-MH and the EW-MH phenotype. In addition, the +45T>G SNP was associated with reduced odds of the MUH phenotype.
Assuntos
Adiponectina/sangue , Transtornos do Metabolismo de Glucose/genética , Transtornos do Metabolismo dos Lipídeos/genética , Fenótipo , Adiponectina/genética , Adulto , Alelos , Antropometria , Glicemia/análise , Estudos Transversais , Ensaio de Imunoadsorção Enzimática , Feminino , Haplótipos , Humanos , Lipídeos/sangue , Masculino , Pessoa de Meia-Idade , PPAR gama/genética , Polimorfismo de Nucleotídeo ÚnicoRESUMO
AIM: To study the evolution of impaired fasting glucose (IFG), considering glucose and HbA1c levels and risk factors associated, in a period of 6 years. METHODS: We studied 94 subjects with impaired fasting glucose (IFG) that were diagnosed in 2005 and followed up to 2012. Glucose and HbA1c levels were determined. A descriptive analysis of contingence charts was performed in order to study the evolution in the development of type-2 diabetes mellitus (T2DM). RESULTS: Twenty-eight of ninety-four subjects became T2DM; 51/94 remained with IFG; and 20/94 presented normal fasting glucose. From the 28 diabetic subjects, 9 had already developed diabetes and were under treatment with oral hypoglycemic agents; 5 were diagnosed with plasma glucose < 126 mg/dL, but with HbA1c over 6.5%. In those who developed diabetes, 15/28 had a family history of T2DM in first relative degree. Also, diabetic subjects had a BMI significantly higher than nodiabetics (t test: P < 0.01). The individuals that in 2005 had the highest BMI are those who currently have diabetes. CONCLUSION: The IFG constitutes a condition of high risk of developing T2DM in a few years, especially over 110 mg/dL and in obesity patients.
Assuntos
Glicemia/metabolismo , Diabetes Mellitus Tipo 2/sangue , Jejum/sangue , Transtornos do Metabolismo de Glucose/sangue , Administração Oral , Adulto , Idoso , Idoso de 80 Anos ou mais , Biomarcadores/sangue , Índice de Massa Corporal , Chile/epidemiologia , Diabetes Mellitus Tipo 2/diagnóstico , Diabetes Mellitus Tipo 2/tratamento farmacológico , Diabetes Mellitus Tipo 2/epidemiologia , Diabetes Mellitus Tipo 2/genética , Progressão da Doença , Feminino , Seguimentos , Predisposição Genética para Doença , Transtornos do Metabolismo de Glucose/diagnóstico , Transtornos do Metabolismo de Glucose/tratamento farmacológico , Transtornos do Metabolismo de Glucose/epidemiologia , Transtornos do Metabolismo de Glucose/genética , Hemoglobinas Glicadas/metabolismo , Humanos , Hipoglicemiantes/administração & dosagem , Masculino , Pessoa de Meia-Idade , Obesidade/diagnóstico , Obesidade/epidemiologia , Linhagem , Fatores de Risco , Fatores de TempoRESUMO
Tens of dietary trials have been conducted to investigate the metabolic effects of sugar (sucrose) and its impact on human health. All of those studies took into account only the quantity of ingested sugar. By contrast, not a single study attempted to assess whether the form in which sugar is consumed plays a role in producing its metabolic effects. The failure of cohorts of researchers to specify how they administered sugar in their dietary trials may well explain why the results of those studies are extremely contradictory. These discrepant findings, understandably, resulted in conflicting opinions about sugar and in divergent guidelines about its recommended consumption. The evolutionary line of reasoning expounded in this article leads to conclude that the form in which sugar is ingested, not its quantity, constitutes the most important factor in producing the metabolic effects of sugar and its impact on human health. As a consequence, for example, the consumption of 100 g of sugar per day can be either detrimental or innocuous, depending on the form in which sugar is ingested. Specifically, the evolutionary hypothesis advanced in this paper implies that sugar can predispose to type 2 diabetes and can cause unhealthy changes in blood lipids if it is consumed in solid forms or in dense solutions containing more than 250 g/L, whereas sugar is harmless if it is consumed in more dilute concentrations. This evolutionary hypothesis, in view of its intuitively far-reaching clinical implications, should be tested by at least one dietary trial.