The effects of macronutrients composition on hormones and substrates during a meal tolerance test in drug-naive and sitagliptin-treated individuals with type 2 diabetes: a randomized crossover study

ABSTRACT Objectives: To evaluate the effect of sitagliptin treatment in early type 2 diabetes mellitus (T2DM) and the impact of different macronutrient compositions on hormones and substrates during meal tolerance tests (MTT). Materials and methods: Half of the drug-naive patients with T2DM were randomly assigned for treatment with 100 mg of sitagliptin, q.d., or placebo for 4 weeks and then submitted to 3 consecutive MTT intercalated every 48 h. The MTTs differed in terms of macronutrient composition, with 70% of total energy from carbohydrates, proteins, or lipids. After 4 weeks of washout, a crossover treatment design was repeated. Both patients and researchers were blinded, and a repeated-measures ANOVA was employed for statistical analysis. Results: Sitagliptin treatment reduced but did not normalize fasting and post-meal glucose values in the three MTTs, with lowered area-under-glucose-curve values varying from 7% to 15%. The sitagliptin treatment also improved the insulinogenic index (+86%) and the insulin/glucose (+25%), glucagon-like peptide-1/glucose (+46%) incremental area under the curves. Patients with early T2DM maintained the lowest glucose excursion after a protein- or lipid-rich meal without any major change in insulin, C-peptide, glucagon, or NEFA levels. Conclusion: We conclude that sitagliptin treatment is tolerable and contributes to better control of glucose homeostasis in early T2DM, irrespective of macronutrient composition. The blood glucose excursion during meal ingestion is minimal in protein- or fat-rich meals, which can be a positive ally for the management of T2DM. Clinical trial no: NCT00881543

The effects of macronutrients composition on hormones and substrates during a meal tolerance test in drugnaive and sitagliptin-treated individuals with type 2 diabetes: a randomized crossover study.

Objective: To evaluate the effect of sitagliptin treatment in early type 2 diabetes mellitus (T2DM) and the impact of different macronutrient compositions on hormones and substrates during meal tolerance tests (MTT). Methods: Half of the drug-naive patients with T2DM were randomly assigned for treatment with 100 mg of sitagliptin, q.d., or placebo for 4 weeks and then submitted to 3 consecutive MTT intercalated every 48 h. The MTTs differed in terms of macronutrient composition, with 70% of total energy from carbohydrates, proteins, or lipids. After 4 weeks of washout, a crossover treatment design was repeated. Both patients and researchers were blinded, and a repeated-measures ANOVA was employed for statistical analysis. Results: Sitagliptin treatment reduced but did not normalize fasting and post-meal glucose values in the three MTTs, with lowered area-under-glucose-curve values varying from 7% to 15%. The sitagliptin treatment also improved the insulinogenic index (+86%) and the insulin/glucose (+25%), glucagon-like peptide-1/glucose (+46%) incremental area under the curves. Patients with early T2DM maintained the lowest glucose excursion after a protein- or lipid-rich meal without any major change in insulin, C-peptide, glucagon, or NEFA levels. Conclusion: We conclude that sitagliptin treatment is tolerable and contributes to better control of glucose homeostasis in early T2DM, irrespective of macronutrient composition. The blood glucose excursion during meal ingestion is minimal in protein- or fat-rich meals, which can be a positive ally for the management of T2DM. Clinical trial no: NCT00881543.

Development and internal validation of an adrenal cortical carcinoma prognostic score for predicting the risk of metastasis and local recurrence.

OBJECTIVE: To develop and internally validate a prognostic score to predict the risk of metastases or recurrence in patients with adrenal cortical carcinomas (ACC). DESIGN: Clinical, laboratory and pathological data from 129 ACC patients, treated in a tertiary centre, were retrospectively reviewed. RESULTS: Using a multivariate binary logistic regression analysis, we developed a prognostic score with five covariates: a functional pattern other than isolated hyperandrogenism, a tumour size >7·5 cm, a primary tumour classified as T3/T4, the presence of microscopic venous invasion and a mitotic index >5/50 high-power fields. The prognostic score was calibrated according to the Hosmer-Lemeshow goodness-of-fit test (P = 0·9329) and exhibited excellent overall performance (Brier score = 0·0738). Finally, the discriminatory ability of the model, determined by the area under the ROC curve (AROC ), was near perfect (AROC , 0·9611; 95% CI, 0·92676-0·99552). The prediction model was internally validated with 200 bootstrap resamples and achieved excellent performance for estimating the risk of metastasis and recurrence in eight additional patients with apparently localized disease at diagnosis. CONCLUSION: We developed and internally validated a prognostic score based on the clinicopathological data that are readily available to any attending physician. Our model can be used to accurately estimate the risk of unfavourable outcomes in ACC patients. This score could be beneficial for both patient counselling and the identification of patients in whom adjuvant mitotane is justified.

Metformin, but not glimepiride, improves carotid artery diameter and blood flow in patients with type 2 diabetes mellitus.

OBJECTIVE: To compare the effects of glimepiride and metformin on vascular reactivity, hemostatic factors and glucose and lipid profiles in patients with type 2 diabetes. METHODS: A prospective study was performed in 16 uncontrolled patients with diabetes previously treated with dietary intervention. The participants were randomized into metformin or glimepiride therapy groups. After four months, the patients were crossed over with no washout period to the alternative treatment for an additional four-month period on similar dosage schedules. The following variables were assessed before and after four months of each treatment: 1) fasting glycemia, insulin, catecholamines, lipid profiles and HbA1 levels; 2) t-PA and PAI-1 (antigen and activity), platelet aggregation and fibrinogen and plasminogen levels; and 3) the flow indices of the carotid and brachial arteries. In addition, at the end of each period, a 12-hour metabolic profile was obtained after fasting and every 2 hours thereafter. RESULTS: Both therapies resulted in similar decreases in fasting glucose, triglyceride and norepinephrine levels, and they increased the fibrinolytic factor plasminogen but decreased t-PA activity. Metformin caused lower insulin and pro-insulin levels and higher glucagon levels and increased systolic carotid diameter and blood flow. Neither metformin nor glimepiride affected endothelial-dependent or endothelial-independent vasodilation of the brachial artery. CONCLUSIONS: Glimepiride and metformin were effective in improving glucose and lipid profiles and norepinephrine levels. Metformin afforded more protection against macrovascular diabetes complications, increased systolic carotid artery diameter and total and systolic blood flow, and decreased insulin levels. As both therapies increased plasminogen levels but reduced t-PA activity, a coagulation process was likely still ongoing.

Metformin, but not glimepiride, improves carotid artery diameter and blood flow in patients with type 2 diabetes mellitus

OBJECTIVE: To compare the effects of glimepiride and metformin on vascular reactivity, hemostatic factors and glucose and lipid profiles in patients with type 2 diabetes. METHODS: A prospective study was performed in 16 uncontrolled patients with diabetes previously treated with dietary intervention. The participants were randomized into metformin or glimepiride therapy groups. After four months, the patients were crossed over with no washout period to the alternative treatment for an additional four-month period on similar dosage schedules. The following variables were assessed before and after four months of each treatment: 1) fasting glycemia, insulin, catecholamines, lipid profiles and HbA1 levels; 2) t-PA and PAI-1 (antigen and activity), platelet aggregation and fibrinogen and plasminogen levels; and 3) the flow indices of the carotid and brachial arteries. In addition, at the end of each period, a 12-hour metabolic profile was obtained after fasting and every 2 hours thereafter. RESULTS: Both therapies resulted in similar decreases in fasting glucose, triglyceride and norepinephrine levels, and they increased the fibrinolytic factor plasminogen but decreased t-PA activity. Metformin caused lower insulin and pro-insulin levels and higher glucagon levels and increased systolic carotid diameter and blood flow. Neither metformin nor glimepiride affected endothelial-dependent or endothelial-independent vasodilation of the brachial artery. CONCLUSIONS: Glimepiride and metformin were effective in improving glucose and lipid profiles and norepinephrine levels. Metformin afforded more protection against macrovascular diabetes complications, increased systolic carotid artery diameter and total and systolic blood flow, and decreased insulin levels. As both therapies increased plasminogen levels but reduced t-PA activity, a coagulation process was likely still ongoing.

Clinical approaches to preserve beta-cell function in diabetes.

In type 2 diabetes (DM2) there is progressive deterioration in beta-cell function and mass. It was found that islet function was about 50% of normal at the time of diagnosis and reduction in beta-cell mass of about 60% at necropsy (accelerated apoptosis). Among the interventions to preserve the beta-cells, those to lead to short-term improvement of beta-cell secretion are weight loss, metformin, sulfonylureas, and insulin. The long-term improvement was demonstrated with short-term intensive insulin therapy of newly diagnosed DM2, the use of antiapoptotic drugs such as glitazones, and the use of glucagon-like peptide-1 receptor agonists (GLP-1 mimetics), not inactivated by the enzyme dipeptidyl peptidase 4 and/or to inhibit that enzyme (GLP-1 enhancers). The incretin hormones are released from the gastrointestinal tract in response to nutrient ingestion to enhance glucose-dependent insulin secretion from the pancreas and overall maintenance of glucose homeostasis. From the two major incretins, GLP-1 and GIP (glucose-dependent insulinotropic polypeptide), only the first one or its mimetics or enhancers can be used for treatment. The GLP-1 mimetics exenatide and liraglutide as well as the DPP 4 inhibitors (sitagliptin and vildagliptin) were approved for treatment of DM2.

Adipose tissue at the crossroads in the development of the metabolic syndrome, inflammation and atherosclerosis.

The authors analyze insulin resistance, the metabolic syndrome and endothelial dysfunction as consequence of a common antecedent, a low grade inflammation, indicating that in obesity there is a chronically activated inflammatory state of the adipose tissue. Furthermore, the inflammatory signaling is discussed according to the adipose tissue depot, visceral or subcutaneous.

[Lipid transfer to HDl in women with type 1 diabetes]. / Transferência de lípides para a lipoproteína de alta densidade (HDl) em mulheres com diabetes melito tipo 1.

INTRODUCTION: People with type 1 diabetes mellitus (T1DM) have an increased risk of cardiovascular disease and may still have a normal lipid profile. In order to clarify whether normal HDL cholesterol levels may conceal defects in HDL function, we have studied the transfer of lipids to HDL in T1DM. METHODS: Twenty-one young women with T1DM were compared with 21 non-diabetic women. Nanoemulsion preparations were used as lipid donor to HDL: one labeled with (3)H-triglycerides and 14C-free cholesterol and the other with (3)H-cholesteryl esters and 14C-phospholipids. These preparations were incubated with plasma samples for 1h. After chemical precipitation, the supernatant containing HDL was counted for radioactivity. RESULTS: No difference in transfer was observed to nanoemulsion HDL from cholesteryl esters, triglycerides, free cholesterol and phospholipids. CONCLUSION: Simultaneous lipid transfer to HDL was not affected in T1DM patients. This suggests that the disease does not alter lipoprotein composition and transfer protein action in such way as to disturb HDL metabolism.

Adipose tissue at the crossroads in the development of the metabolic syndrome, inflammation and atherosclerosis / Tecido adiposo na encruzilhada no desenvolvimento da síndrome metabólica, inflamação e aterosclerose

The authors analyze insulin resistance, the metabolic syndrome and endothelial dysfunction as consequence of a common antecedent, a low grade inflammation, indicating that in obesity there is a chronically activated inflammatory state of the adipose tissue. Furthermore, the inflammatory signaling is discussed according to the adipose tissue depot, visceral or subcutaneous.

Os autores analisam a resistência à insulina, a síndrome metabólica e a disfunção endotelial como consequência de um antecedente comum, a inflamação de baixo nível, o que mostra que a obesidade é um estado inflamatório cronicamente ativado do tecido adiposo. Discute-se, aqui, a sinalização inflamatória de acordo com a localização do tecido adiposo subcutâneo ou visceral.

Transferência de lípides para a lipoproteína de alta densidade (HDl) em mulheres com diabetes melito tipo 1 / Lipid transfer to HDl in women with type 1 diabetes

INTRODUÇÃO: Os portadores de diabetes melito tipo 1 (DM1) possuem aumentado risco de doença cardiovascular e, ainda assim, podem apresentar perfil lipídico normal. Para esclarecer se os níveis normais de HDL podem ocultar defeitos na função, foram estudados a transferência de lípides para a HDL em DM1. MÉTODOS: Vinte e uma mulheres jovens portadoras de DM1 foram comparadas com 21 mulheres não-diabéticas. Nanoemulsões foram usadas como doadoras de lípides para HDL: uma marcada com ³H-triglicérides e 14C-colesterol livre e outra com ³H-éster de colesterol e 14C-fosfolípides. Após 1 hora de incubação com amostras de plasma, seguida por precipitação química, o sobrenadante, contendo HDL, teve a radioatividade contada. RESULTADOS: Nenhuma diferença foi encontrada nas transferências dos ésteres de colesterol, triglicérides, colesterol livre e fosfolípides para as HDL. CONCLUSÃO: A transferência de lípides para a HDL não está afetada em portadoras de DM1. Isso sugere que a doença não altera a composição de lipoproteínas e a ação de proteínas de transferência.

INTRODUCTION: People with type 1 diabetes mellitus (T1DM) have an increased risk of cardiovascular disease and may still have a normal lipid profile. In order to clarify whether normal HDL cholesterol levels may conceal defects in HDL function, we have studied the transfer of lipids to HDL in T1DM. METHODS: Twenty-one young women with T1DM were compared with 21 non-diabetic women. Nanoemulsion preparations were used as lipid donor to HDL: one labeled with ³H-triglycerides and 14C-free cholesterol and the other with ³H-cholesteryl esters and 14C-phospholipids. These preparations were incubated with plasma samples for 1h. After chemical precipitation, the supernatant containing HDL was counted for radioactivity. RESULTS: No difference in transfer was observed to nanoemulsion HDL from cholesteryl esters, triglycerides, free cholesterol and phospholipids. CONCLUSION: Simultaneous lipid transfer to HDL was not affected in T1DM patients. This suggests that the disease does not alter lipoprotein composition and transfer protein action in such way as to disturb HDL metabolism.

Glycemia and cardiovascular disease in type 1 diabetes mellitus.

OBJECTIVE: To evaluate the role of glycemic control in the development of cardiovascular disease (CVD) in type 1 diabetes mellitus (DM). METHODS: We review the literature regarding coronary atherosclerosis, coronary artery calcification, and the epidemiologic studies related to the role of glycemia and the classic risk factors for coronary artery disease (CAD) in type 1 DM. RESULTS: Four prospective studies (Wisconsin Epidemiologic Study of Diabetic Retinopathy, EURODIAB, Steno Diabetes Center Study of Adults With Type 1 DM, and Pittsburgh Epidemiology of Diabetes Complications study) do not show that glycemic control predicts CAD occurrence. Findings from the Diabetes Control and Complications Trial/Epidemiology of Diabetes Interventions and Complications study show that compared with conventional insulin therapy, intensive insulin therapy reduces CVD among patients with type 1 DM and is associated with lower prevalence of coronary artery calcification. The discrepancies between the findings from the Diabetes Control and Complications Trial/Epidemiology of Diabetes Interventions and Complications study and the Pittsburgh Epidemiology of Diabetes Complication study are likely due to differences between the study populations and the lower prevalence of renal disease in the former study. Besides duration of DM and albuminuria/overt nephropathy, insulin resistance is a major determinant of CAD associated with type 1 DM. CONCLUSIONS: Discrepant study results regarding the relationship between glycemia and CAD/coronary artery calcification may be related to the prevalence of renal disease and the presence of the metabolic syndrome. Published data suggest that addressing traditional risk factors including albuminuria, the metabolic syndrome, and inflammatory markers is better for preventing and treating CAD than focusing exclusively on glycemic control, which is still necessary for preventing microvascular complications. Furthermore, there is a synergistic effect of glycemic control and albuminuria on the development of CVD.

[The prevalence of diabetes and stress hyperglycemia in the acute myocardial infarction patients]. / Avaliação da prevalência do diabetes e da hiperglicemia de estresse no infarto agudo do miocárdio.

OBJECTIVES: To evaluate in our population the real prevalence of diabetes (DM) and stress hyperglycemia (HE) in patients with myocardial infarction (IAM) admitted in a cardiologic emergency unit. METHODS: A retrospective analysis of 2262 patients with AMI evaluating the prevalence of DM (referred and diagnosed) and stress hyperglycemia. RESULTS: Besides 12.1% of subjects were previously referred to be diabetic (men: 10.7% and women: 15.8%), diabetes was effectively diagnosed in 24.8% (M: 22.9%, W: 29.7%) and stress hyperglycemia in 13.6% HE of the patients (M: 14.3%, W: 11,7%) indicating that glycemic alterations were effectively observed in 37.2.% of the patients with IAM (M: 37.2%, W: 41.4%). In DM subjects IAM events occurred earlier, total intra-hospital mortality was higher (DM: 20.7%, ND: 13.8%, HE: 13.4%) and less surgical procedures were performed (ND 33.8%, DM: 21.7%, HE: 18.0%). CONCLUSION: The elevated DM and stress hyperglycemia prevalence observed in our study indicates that glycemic alterations is one of the most important risk factors for IAM.

[Cardiovascular disease in type 1 diabetes mellitus]. / Doença cardiovascular no diabetes melito tipo 1.

The association between type 1 diabetes and coronary heart disease has become very clear since the late 1970. It has been demonstrated that there is an important increased risk in morbidity and mortality caused by coronary artery disease in young adults with type 1 diabetes compared with the non diabetic population. The underlying pathogeneses is still poorly understood. While the role of glycemic control in the development of microvascular disease complication is well established its role in CVD in patients with DM1 remains unclear with epidemiologic studies reporting conflicting data. Recent findings from the DCCT/EDIC showed that prior intensive diabetes treatment during the DCCT was associated with less atherosclerosis, largely because of reduced level of HbA1c during the DCCT. The improvement of glycemic control itself appeared to be particularly effective in younger patients with shorter duration of the disease. Other analyses suggested the glycemia may have a stronger effect on CAD in patients without than in those with albuminúria. Other major determinants of coronary artery disease are the components of metabolic syndrome and the surrogate measure of insulin resistence: eGDR. It is proposed that patients with DM1 should have aggressive medical therapy, risk factor modification and careful monitoring not only of his blood sugar but also of the other processes involved in the atherosclerotic process, mostly the ones with family history of type 2 diabetes.

Avaliação da prevalência do diabetes e da hiperglicemia de estresse no infarto agudo do miocárdio / The prevalence of diabetes and stress hyperglycemia in the acute myocardial infarction patients

OBJETIVOS: Determinar a prevalência do diabetes melito (DM) e da hiperglicemia de estresse (HE) em pacientes com infarto agudo do miocárdio (IAM) admitidos em unidade de emergência cardiológica. MÉTODOS: Análise retrospectiva de 2.262 pacientes com IAM, avaliando, além da prevalência de diabetes referido, o diagnosticado e a hiperglicemia de estresse. RESULTADOS: Apesar de referido em 12,1 por cento dos pacientes (H: 10,7 por cento, M: 15,8 por cento), o DM ocorria efetivamente em 24,8 por cento (H: 22,9 por cento, M: 29,7 por cento) e a HE em 13,6 por cento (H: 14,3 por cento, M: 11,7 por cento) dos indivíduos dessa população. Portanto, alterações glicêmicas ocorreram em 37,4 por cento dos indivíduos com IAM (H: 37,2 por cento, M: 41,4 por cento). Nos pacientes com DM, observou-se maior precocidade etária do IAM, maior prevalência de óbitos (DM: 20,7 por cento, ND:13,8 por cento, HE: 13,4 por cento) e de procedimentos cirúrgicos (ND: 33,8 por cento, HE: 18,0 por cento, DM: 21,7 por cento). CONCLUSÃO: A elevada prevalência de DM e hiperglicemia de estresse observada em nosso estudo indica que as alterações glicêmicas constituem um dos mais importantes fatores de risco para o IAM.

OBJECTIVES: To evaluate in our population the real prevalence of diabetes (DM) and stress hyperglycemia (HE) in patients with myocardial infarction (IAM) admitted in a cardiologic emergency unit. METHODS: A retrospective analysis of 2262 patients with AMI evaluating the prevalence of DM (referred and diagnosed) and stress hyperglycemia. RESULTS: Besides 12,1 percent of subjects were previously referred to be diabetic (men: 10.7 percent and women: 15.8 percent), diabetes was effectively diagnosed in 24,8 percent (M: 22,9 percent, W: 29,7 percent) and stress hyperglycemia in 13,6 percent HE of the patients (M: 14,3 percent, W: 11,7 percent) indicating that glycemic alterations were effectively observed in 37.2. percent of the patients with IAM (M: 37,2 percent, W: 41,4 percent). In DM subjects IAM events occurred earlier, total intra-hospital mortality was higher (DM: 20.7 percent, ND: 13,8 percent, HE: 13,4 percent) and less surgical procedures were performed (ND 33.8 percent, DM: 21.7 percent, HE: 18.0 percent). CONCLUSION: The elevated DM and stress hyperglycemia prevalence observed in our study indicates that glycemic alterations is one of the most important risk factors for IAM.

Doença cardiovascular no diabetes melito tipo 1: [revisão] / Cardiovascular disease in type 1 diabetes mellitus: [review]

O risco de doença arterial coronariana (DAC) nos pacientes com diabetes melito tipo 1 (DM1) é conhecido desde o final dos anos 1970, sendo atualmente a principal causa de mortalidade na população adulta com diabetes tipo 1 de longa duração. A patogênese do processo aterosclerótico nesta doença ainda é obscura, acreditando-se que a hiperglicemia desenvolva aí um papel importante, entretanto vários estudos epidemiológicos mostraram que a associação entre doença coronariana e glicemia, em pacientes com DM1 seja fraca. Dados recentes do estudo DCCT/EDIC mostram que o grupo que recebeu tratamento insulínico intensificado durante o DCCT desenvolveu graus menores de aterosclerose, relacionado aos valores reduzidos de HbA1c durante a fase ativa do estudo, com melhor proteção nos pacientes mais jovens e com menor duração da doença. Há também evidências de que os benefícios são maiores nos pacientes sem nefropatia quando comparados aos com doença renal. Outros fatores de risco importante para o desenvolvimento de DAC em pacientes com DM1 são os mesmos descritos para DM2, incluindo os componentes da síndrome metabólica e marcadores de resistência insulínica. Sugere-se que pacientes com DM1 devam ter o melhor controle glicêmico possível, desde o início da sua doença acrescido de vigilância e tratamento rígido dos fatores de riscos clássicos para DAC, principalmente naqueles com história familiar de DM2.

The association between type 1 diabetes and coronary heart disease has become very clear since the late 1970. It has been demonstrated that there is an important increased risk in morbidity and mortality caused by coronary artery disease in young adults with type 1 diabetes compared with the non diabetic population. The underlying pathogeneses is still poorly understood. While the role of glycemic control in the development of microvascular disease complication is well established its role in CVD in patients with DM1 remains unclear with epidemiologic studies reporting conflicting data. Recent findings from the DCCT/EDIC showed that prior intensive diabetes treatment during the DCCT was associated with less atherosclerosis, largely because of reduced level of HbA1c during the DCCT. The improvement of glycemic control itself appeared to be particularly effective in younger patients with shorter duration of the disease. Other analyses suggested the glycemia may have a stronger effect on CAD in patients without than in those with albuminúria. Other major determinants of coronary artery disease are the components of metabolic syndrome and the surrogate measure of insulin resistence: eGDR. It is proposed that patients with DM1 should have aggressive medical therapy, risk factor modification and careful monitoring not only of his blood sugar but also of the other processes involved in the atherosclerotic process, mostly the ones with family history of type 2 diabetes.

Postprandial glycemia and cardiovascular disease in diabetes mellitus

The postprandial state is a factor for the development of atherosclerosis. The association of postprandial hyperglycemia and dyslipidemia with atherosclerosis (indicated by an early intima-media thickness of the carotid) supports the concept that macrovascular complications are a highly suggestive of the association of postprandial hyperglycemia and atherosclerosis. The postprandial glycemia can be considered a marker of cardiovascular risk.

Postprandial glycemia and cardiovascular disease in diabetes mellitus.

This article reviews the role of fasting and postprandial glycemia to the overall glycemic control of patients with type 2 diabetes and glucose intolerance, as well as their causal relationship upon micro and macrovascular complications. Recent studies have suggested that a third component of the glucose triad, the postprandial glucose excursions, might have a role in the overall glycemic load and might also reflect glycemic control. Epidemiological and intervention studies are presented in the article, supporting the conclusion that postprandial hyperglycemia in impaired glucose tolerance and diabetic subjects is a more powerful marker of cardiovascular disease risk than fasting hyperglycemia, then the treatment directed at specifically lowering postprandial glucose is crucial, as underlined by the American Diabetes Association.

Postprandial glycemia and cardiovascular disease in diabetes mellitus

This article reviews the role of fasting and postprandial glycemia to the overall glycemic control of patients with type 2 diabetes and glucose intolerance, as well as their causal relationship upon micro and macrovascular complications. Recent studies have suggested that a third component of the glucose triad, the postprandial glucose excursions, might have a role in the overall glycemic load and might also reflect glycemic control. Epidemiological and intervention studies are presented in the article, supporting the conclusion that postprandial hyperglycemia in impaired glucose tolerance and diabetic subjects is a more powerful marker of cardiovascular disease risk than fasting hyperglycemia, then the treatment directed at specifically lowering postprandial glucose is crucial, as underlined by the American Diabetes Association.

O presente artigo revisa o papel da glicemia de jejum e pós-prandial em relação ao controle glicêmico de pacientes com diabetes do tipo 2 e com intolerância à glicose, assim como sua relação causal sobre as complicações micro e macrovasculares. Estudos recentes têm sugerido que um terceiro componente na tríade glicêmica, as excursões glicêmicas pós-prandiais, podem ter influência sobre a carga glicêmica total, e podem também refletir sobre o controle glicêmico. Estudos epidemiológicos e de intervenção são apresentados neste artigo, suportando a conclusão de que a hiperglicemia pós-prandial na intolerância à glicose e em pacientes com diabetes é um marcador mais potente de risco cardiovascular do que a hiperglicemia de jejum, portanto o tratamento dirigido especificamente para reduzir a glicemia pós-prandial é crucial, conforme sugerido pela American Diabetes Association.