One-hour post-load hyperglycemia combined with HbA1c identifies pre-diabetic individuals with a higher cardio-metabolic risk burden

Fiorentino, Teresa Vanessa; Sesti, Franz; Andreozzi, Francesco; Pedace, Elisabetta; Sciacqua, Angela; Hribal, Marta Letizia; Perticone, Francesco; Sesti, Giorgio

doi:10.1016/j.atherosclerosis.2016.08.020

Cited by 38 publications

(38 citation statements)

References 38 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Ideally, these new inquiries will incorporate the latest advances that stratify DM characterization into a range of diabetic subgroups (Tuomi et al 2014). The recent discovery that combining the 1 hour post glucose load OGTT with HbA1c identifies subsets of individuals at high risk for both DM and cardiovascular disease (Bergman et al 2016; Fiorentino et al 2016) may be another particularly suitable approach for development in the setting of Chagas disease.…”

Section: Discussionmentioning

confidence: 99%

Alterations in pancreatic β cell function and Trypanosoma cruzi infection: evidence from human and animal studies

et al. 2016

View full text Add to dashboard Cite

The parasite Trypanosoma cruzi causes a persistent infection, Chagas disease, affecting millions of persons in endemic areas of Latin America. As a result of immigration, this disease has now been diagnosed in non-endemic areas worldwide. Although, the heart and gastrointestinal tract are the most studied, the insulin secreting β cell of the endocrine pancreas is also a target of infection. In this review, we summarize available clinical and laboratory evidence to determine whether T. cruzi-infection-mediated changes of β cell function is likely to contribute to the development of hyperglycemia and diabetes. Our literature survey indicates that T. cruzi infection of humans and of experimental animals relates to altered secretory behavior of β cells. The mechanistic basis of these observations appears to be a change in stimulus-secretion pathway function rather than the loss of insulin producing β cells. Whether this attenuated insulin release ultimately contributes to the pathogenesis of diabetes in human Chagas disease however, remains to be determined. Since the etiologies of diabetes are multifactorial including genetic and life-style factors, the use of cell- and animal-based investigations, allowing direct manipulation of these factors, are important tools in testing if reduced insulin secretion has a causal influence on diabetes in the setting of Chagas disease. Long-term clinical investigations will be required to investigate this link in humans.

show abstract

Section: Discussionmentioning

confidence: 99%

Alterations in pancreatic β cell function and Trypanosoma cruzi infection: evidence from human and animal studies

et al. 2016

View full text Add to dashboard Cite

show abstract

“…The design of the CATAMERI study has been previously reported [14,[25][26][27]. The study cohorts include 2055 participants used to estimate the linear relationship between fasting plasma glucose and HbA1c in the study population to calculate the predicted HbA1c value, and 1120 individuals in whom hepatic steatosis was assessed by ultrasonography.…”

Section: Methodsmentioning

confidence: 99%

“…The study cohorts include 2055 participants used to estimate the linear relationship between fasting plasma glucose and HbA1c in the study population to calculate the predicted HbA1c value, and 1120 individuals in whom hepatic steatosis was assessed by ultrasonography. All participants were consecutively recruited at the Department of Medical and Surgical Sciences of the University ''Magna Graecia" of Catanzaro [14,[25][26][27]. Exclusion criteria included: history of type 1 or type 2 diabetes mellitus, heart failure, end stage renal disease, haemoglobinopathies or anemia, history of malignant disease, gastrointestinal diseases associated with bleeding or malabsorption, autoimmune diseases, acute or chronic infections, positivity for antibodies to hepatitis C virus (HCV) or hepatitis B surface antigen (HBsAg), accumulation diseases such as amyloidosis and hemochromatosis, history of drug abuse, self-reporting alcohol consumption of >20 g/day, and history of treatments known to induce liver injury including tamoxifen, glucocorticoids, tetracycline, estrogens, methotrexate, and amiodarone.…”

Section: Methodsmentioning

confidence: 99%

“…Nevertheless, no studies have been carried out to assess the correlation between HGI and NAFLD in subjects without type 2 diabetes. To address this issue, we sought to evaluate whether HGI is associated with hepatic steatosis and related biomarkers in a large cohort of adult White subjects participating to the CATAnzaro MEtabolic RIsk factors (CATAMERI) study [14,[25][26][27].…”

Section: Introductionmentioning

confidence: 99%

See 1 more Smart Citation

Association between hemoglobin glycation index and hepatic steatosis in non-diabetic individuals

Fiorentino

Marini

Succurro

et al. 2017

Diabetes Research and Clinical Practice

Self Cite

View full text Add to dashboard Cite

Hemoglobin glycation indexHepatic steatosis Non-enzymatic protein glycation A B S T R A C TAims: Hemoglobin glycation index (HGI), which is the difference between the observed value of HbA1 and the predicted HbA1c based on plasma glucose levels, represents a measure of the degree of non-enzymatic glycation of hemoglobin and it has been found to be positively associated with diabetic complications. Herein we investigated whether HGI is associated with hepatic steatosis and related biomarkers in subjects without diabetes.Methods: 1120 White individuals without diabetes were stratified in quartiles according to HGI levels. Hepatic steatosis was diagnosed by ultrasonography.Results: As compared with subjects in the lowest quartile of HGI those in the intermediate and high HGI groups displayed an unfavorable cardio-metabolic risk profile having significantly higher values of body mass index (BMI), waist circumference, % fat mass, total cholesterol, triglycerides, inflammatory markers such as high sensitivity C reactive protein, erythrocytes sedimentation rate, complement C3, platelets and white blood cell count, hepatic insulin resistance assessed by the liver IR index and lower concentrations of highdensity lipoprotein. HGI was positively associated with the biomarker of liver damage alanine aminotransferase, and fatty liver index, an indicator of hepatic steatosis. In a logistic regression analysis adjusted for age, gender and BMI individuals in the highest quartile of HGI exhibited a 1.6-fold increased odd of having hepatic steatosis (95% CI: 1.03-2.41; p = 0.03) as compared with subjects in the lowest quartile of HGI.Conclusions: Higher levels of HGI may identify subjects without diabetes at increased risk of having hepatic steatosis.

show abstract

“…A large body of studies have demonstrated that prediabetes conditions are not only associated with incident diabetes but also predict cardiovascular morbidity and mortality . Importantly, it has been reported that individuals with HbA1c‐defined prediabetes display a worse cardio‐metabolic phenotype associated with subclinical organ damage, and higher levels of HbA1c have been found to be associated with a greater risk of cardiovascular diseases (CVD) independently from the common cardiovascular risk factors in non‐diabetic individuals …”

Section: Introductionmentioning

confidence: 99%

One‐hour post‐load hyperglycemia combined with HbA1c identifies individuals with higher risk of cardiovascular diseases: Cross‐sectional data from the CATAMERI study

Fiorentino

Succurro

Andreozzi

et al. 2018

Diabetes Metabolism Res

Self Cite

View full text Add to dashboard Cite

Aims A value of 1‐hour post‐load plasma glucose (PG) ≥155 mg/dL combined with the recently established HbA1c diagnostic thresholds for prediabetes increases the ability to predict diabetes and to detect subclinical cardiovascular organ damage. Herein, we evaluated whether a value of 1‐hour PG ≥155 mg/dL may recognize non‐diabetic individuals with an increased risk of cardiovascular diseases (CVD) within HbA1c‐defined glycemic categories. Materials and Methods The prevalence of composite and individual CVD, including coronary artery disease (CAD) and cerebrovascular disease, was assessed in 1010 non‐diabetic individuals. Results Within the group with HbA1c <5.7%, a higher proportion of subjects with 1‐hour PG ≥ 155 mg/dL had composite CVD and individual CAD in comparison to those having 1‐hour PG˂155 mg/dL. Similarly, within the group with HbA1c‐defined prediabetes (5.7%‐6.4%), the prevalence of composite CVD and individual CAD in subjects with 1‐hour PG ≥155 mg/dL was higher than in the group with individuals having 1‐hour PG < 155 mg/dL. In a logistic regression analysis adjusted for several CVD risk factors individuals with HbA1c <5.7% and 1‐hour PG ≥ 155 mg/dL and those with HbA1c 5.7% to 6.4% and 1‐hour PG ≥ 155 mg/dL had a 4.5‐ (95%CI: 1.02‐20.44) and 6.2‐ (95%CI: 1.29‐29.74) fold increased risk of composite CVD and 6.2‐ (95%CI: 1.05–36.32) and 8.0‐ (95%CI: 1.25‐51.70) fold increased risk of having CAD, respectively, in comparison to individuals with HbA1c <5.7% and 1‐hour PG < 155 mg/dL. Conclusions 1‐hour post‐load hyperglycemia may identify a subset of individuals within HbA1c‐defined glycemic categories at higher risk of having CVD.

show abstract

One-hour post-load hyperglycemia combined with HbA1c identifies pre-diabetic individuals with a higher cardio-metabolic risk burden

Cited by 38 publications

References 38 publications

Alterations in pancreatic β cell function and Trypanosoma cruzi infection: evidence from human and animal studies

Alterations in pancreatic β cell function and Trypanosoma cruzi infection: evidence from human and animal studies

Association between hemoglobin glycation index and hepatic steatosis in non-diabetic individuals

One‐hour post‐load hyperglycemia combined with HbA1c identifies individuals with higher risk of cardiovascular diseases: Cross‐sectional data from the CATAMERI study

Contact Info

Product

Resources

About