Publications by authors named "G Treiber"

Background: Coronary artery calcium score (CACS) refines the cardiovascular disease (CVD) risk prediction in patients with Type-2 diabetes (T2D). We aimed to identify the determinants for high CACS in CVD-free patients with T2D.

Methods: We studied 796 patients with T2D with CACS measured in three centers: two in continental France and a third in the Reunion Island.

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Introduction: The transition to metabolically unhealthy obesity (MUO) is driven by the limited expandability of adipose tissue (AT). Familial Partial Lipodystrophy type 2 (FPLD2) is an alternative model for AT dysfunction that is suitable for comparison with obesity. While MUO is associated with low-grade systemic inflammation, studies of inflammation in FPLD2 have yielded inconsistent results.

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Aim: Subjects with Familial Partial Lipodystrophy type 2 (FPLD2) are at high risk to develop diabetes. To better understand the natural history and variability of this disease, we studied glucose tolerance, insulin response to an oral glucose load, and metabolic markers in the largest cohort to date of subjects with FPLD2 due to the same LMNA variant.

Methods: A total of 102 patients aged > 18 years, with FPLD2 due to the LMNA 'Reunionese' variant p.

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The annual Virtual Hospital Diabetes Meeting was hosted by Diabetes Technology Society on April 1 and April 2, 2022. This meeting brought together experts in diabetes technology to discuss various new developments in the field of managing diabetes in hospitalized patients. Meeting topics included (1) digital health and the hospital, (2) blood glucose targets, (3) software for inpatient diabetes, (4) surgery, (5) transitions, (6) coronavirus disease and diabetes in the hospital, (7) drugs for diabetes, (8) continuous glucose monitoring, (9) quality improvement, (10) diabetes care and educatinon, and (11) uniting people, process, and technology to achieve optimal glycemic management.

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Aims: LMNA-linked familial partial lipodystrophy type 2 (FPLD2) leads to insulin resistance-associated metabolic complications and cardiovascular diseases. We aimed to characterise the disease phenotype in a cohort of patients carrying an LMNA founder variant.

Methods: We collected clinical and biological data from patients carrying the monoallelic or biallelic LMNA p.

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