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Familial partial lipodystrophy type 2 and obesity, two adipose tissue pathologies with different inflammatory profiles

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 systemi...

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Published in:Diabetology and metabolic syndrome 2023-04, Vol.15 (1), p.77-77, Article 77
Main Authors: Treiber, Guillaume, Gonthier, Marie-Paule, Guilleux, Alice, Medjane, Samir, Bonfanti, Oriane, Cogne, Muriel, Meilhac, Olivier, Nobecourt, Estelle
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Language:English
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Summary: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. Consequently, comparison of inflammation markers between FPLD2 and obesity is of great interest to better understand the pathophysiological defects of FPLD2. To compare the levels of inflammatory biomarkers between a population of patients with FPLD2 due to the same 'Reunionese' LMNA variant and a population of patients with obesity (OB group). Adiponectin, leptin, IL-6, TNF-α and MCP-1 plasma levels were measured by enzyme-linked immuno assays for 60 subjects with FPLD2 and for 60 subjects with obesity. The populations were closely matched for age, sex, and diabetic status. Metabolic outcomes were similar between the two populations. Adiponectinemia and leptinemia were lower in the FPLD2 group than in the OB group (p 
ISSN:1758-5996
1758-5996
DOI:10.1186/s13098-023-01055-4