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Updated: Aug 2, 2025
Isolation, Characterization, and Purification of Macrophages from Tissues Affected by Obesity-related Inflammation
Published on: April 3, 2017
Familial partial lipodystrophy type 2 and obesity, two adipose tissue pathologies with different inflammatory
Guillaume Treiber1,2, Marie-Paule Gonthier2, Alice Guilleux3
1Department of Endocrinology, Diabetes and Nutrition, GHSR, Centre Hospitalo-Universitaire de la Réunion, Saint-Pierre, La Réunion, France.
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. Consequently, comparison of inflammation markers between FPLD2 and obesity is of great interest to better understand the pathophysiological defects of FPLD2.
Objective:
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).
Methods:
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.
Results:
Metabolic outcomes were similar between the two populations. Adiponectinemia and leptinemia were lower in the FPLD2 group than in the OB group (p < 0.01 for both), while MCP-1 levels were higher in the FPLD2 than in the OB group (p < 0.01). Levels of other inflammatory markers were not significantly different.
Conclusions:
Insulin-resistant patients with FPLD2 and obesity share common complications related to AT dysfunction. Inflammatory biomarker analyses demonstrated that MCP-1 levels and adiponectin levels differ between patients with FPLD2 and patients with obesity. These two AT pathologies thus appear to have different inflammatory profiles.
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