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Your search keyword '"Grespan, Eleonora"' showing total 4 results
Start Over Author "Grespan, Eleonora" Publisher american diabetes association
4 results on '"Grespan, Eleonora"'

1. Profiles of Glucose Metabolism in Different Prediabetes Phenotypes, Classified by Fasting Glycemia, 2-Hour OGTT, Glycated Hemoglobin, and 1-hour OGTT: An IMI DIRECT Study

Author

Tura, Andrea, primary, Grespan, Eleonora, primary, Göbl, Christian S., primary, Koivula, Robert W., primary, Franks, Paul W., primary, Pearson, Ewan R., primary, Walker, Mark, primary, Forgie, Ian M., primary, Giordano, Giuseppe N., primary, Pavo, Imre, primary, Ruetten, Hartmut, primary, Dermitzakis, Emmanouil T., primary, McCarthy, Mark I., primary, Pedersen, Oluf, primary, Schwenk, Jochen M., primary, Adamski, Jerzy, primary, Masi, Federico De, primary, Tsirigos, Konstantinos D., primary, Brunak, Søren, primary, Viñuela, Ana, primary, Mahajan, Anubha, primary, McDonald, Timothy J., primary, Kokkola, Tarja, primary, Vangipurapu, Jagadish, primary, Cederberg, Henna, primary, Laakso, Markku, primary, Rutters, Femke, primary, Elders, Petra J.M., primary, Koopman, Anitra D.M., primary, Beulens, Joline W., primary, Ridderstråle, Martin, primary, Hansen, Tue H., primary, Allin, Kristine H., primary, Hansen, Torben, primary, Vestergaard, Henrik, primary, Mari, Andrea, primary, and Consortium, IMI DIRECT, primary

Published
2021
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2. Profiles of Glucose Metabolism in Different Prediabetes Phenotypes, Classified by Fasting Glycemia, 2-Hour OGTT, Glycated Hemoglobin, and 1-Hour OGTT: An IMI DIRECT Study.

Author

Tura, Andrea, Grespan, Eleonora, Göbl, Christian S., Koivula, Robert W., Franks, Paul W., Pearson, Ewan R., Walker, Mark, Forgie, Ian M., Giordano, Giuseppe N., Pavo, Imre, Ruetten, Hartmut, Dermitzakis, Emmanouil T., McCarthy, Mark I., Pedersen, Oluf, Schwenk, Jochen M., Adamski, Jerzy, De Masi, Federico, Tsirigos, Konstantinos D., Brunak, Søren, and Viñuela, Ana

Subjects
*GLYCOSYLATED hemoglobin, *GLUCOSE metabolism, *INSULIN sensitivity, *PREDIABETIC state, *TYPE 2 diabetes
Abstract

Differences in glucose metabolism among categories of prediabetes have not been systematically investigated. In this longitudinal study, participants (N = 2,111) underwent a 2-h 75-g oral glucose tolerance test (OGTT) at baseline and 48 months. HbA1c was also measured. We classified participants as having isolated prediabetes defect (impaired fasting glucose [IFG], impaired glucose tolerance [IGT], or HbA1c indicative of prediabetes [IA1c]), two defects (IFG+IGT, IFG+IA1c, or IGT+IA1c), or all defects (IFG+IGT+IA1c). β-Cell function (BCF) and insulin sensitivity were assessed from OGTT. At baseline, in pooling of participants with isolated defects, they showed impairment in both BCF and insulin sensitivity compared with healthy control subjects. Pooled groups with two or three defects showed progressive further deterioration. Among groups with isolated defect, those with IGT showed lower insulin sensitivity, insulin secretion at reference glucose (ISRr), and insulin secretion potentiation (P < 0.002). Conversely, those with IA1c showed higher insulin sensitivity and ISRr (P < 0.0001). Among groups with two defects, we similarly found differences in both BCF and insulin sensitivity. At 48 months, we found higher type 2 diabetes incidence for progressively increasing number of prediabetes defects (odds ratio >2, P < 0.008). In conclusion, the prediabetes groups showed differences in type/degree of glucometabolic impairment. Compared with the pooled group with isolated defects, those with double or triple defect showed progressive differences in diabetes incidence. [ABSTRACT FROM AUTHOR]

Published
2021
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4. Defective Amplifying Pathway of β-Cell Secretory Response to Glucose in Type 2 Diabetes: Integrated Modeling of In Vitro and In Vivo Evidence.

Author

Grespan, Eleonora, Giorgino, Toni, Arslanian, Silva, Natali, Andrea, Ferrannini, Ele, and Mari, Andrea

Subjects
*GLUCOSE metabolism, *ANIMAL experimentation, *BIOCHEMISTRY, *BIOLOGICAL models, *BIOLOGICAL transport, *BLOOD sugar, *CELL physiology, *CELLULAR signal transduction, *COMPARATIVE studies, *COMPUTER simulation, *CYTOPLASM, *IMMUNITY, *INSULIN, *INSULIN resistance, *ISLANDS of Langerhans, *PHENOMENOLOGY, *RESEARCH methodology, *MEDICAL cooperation, *METABOLISM, *MICE, *TYPE 2 diabetes, *RESEARCH, *TISSUE culture, *EVALUATION research, RESEARCH evaluation
Abstract

In vivo studies have investigated the role of β-cell dysfunction in type 2 diabetes (T2D), whereas in vitro research on islets has elucidated key mechanisms that control the insulin secretion rate. However, the relevance of the cellular mechanisms identified in vitro (i.e., the triggering and amplifying pathways) has not been established in vivo. Furthermore, the mechanisms underpinning β-cell dysfunction in T2D remain undetermined. We propose a unifying explanation of several characteristic features of insulin secretion both in vitro and in vivo by using a mathematical model. The model describes the triggering and amplifying pathways and reproduces a variety of in vitro and in vivo tests in subjects with and without T2D, identifies the mechanisms modulating first-phase insulin secretion rate in response to basal hyperglycemia or insulin resistance, and shows that β-cell dysfunction in T2D can be explained by an impaired amplifying pathway with no need to postulate defects in intracellular calcium handling. [ABSTRACT FROM AUTHOR]

Published
2018
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