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Updated: Jun 19, 2026

Differentiated Mouse Adipocytes in Primary Culture: A Model of Insulin Resistance
Published on: February 17, 2023
Inactivity-mediated insulin resistance is associated with upregulated pro-inflammatory fatty acids in human cell
Sara Mazzucco1, Francesco Agostini, Gianni Biolo
1Department of Medical, Technological and Translational Sciences, University of Trieste, Clinica Medica, Strada di Fiume 447, Ospedale di Cattinara, Trieste, Italy.
Background & Aims:
Low-grade systemic inflammation and pro-inflammatory pattern of cell membrane fatty acid composition characterize patients affected by type 2 diabetes and metabolic syndrome. We hypothesize that inactivity-induced insulin resistance could affect levels of pro-inflammatory fatty acids in cell membranes.
Methods:
Thirty healthy, male, young volunteers were investigated before and after 35-day experimental bed rest. Diet composition was adapted to previous dietary habits. Fatty acid composition of erythrocyte membranes was analyzed by gas-chromatography using flame ionization detector.
Results:
Following bed rest, the HOMA index of insulin resistance significantly increased by +51+/-11% (P<0.01). Bed rest was associated with increased n-6 polyunsaturated (+4.7+/-2.2%; P<0.01) and decreased monounsaturated (-4.8+/-1.5%; P<0.01) fatty acid content in erythrocyte membranes. Fractional content of arachidonic acid increased by +14+/-12% (P=0.01) following inactivity. Delta5 and Delta9 desaturase indexes, as estimated from product-to-precursor ratios, significantly diminished following bed rest from 9.6+/-0.4 to 8.4+/-0.3 (P<0.001) and from 0.72+/-0.02 to 0.69+/-0.01 (P<0.05), respectively. The n-3 fatty acids, alpha-linolenic and eicosapentaenoic, were decreased (P=0.05) following inactivity by 4.7+/-13.2% and 3.8+/-5.2%, respectively.
Conclusions:
Inactivity-mediated insulin resistance was associated with altered Delta5 and Delta9 desaturase indexes and with pro-inflammatory fatty acid pattern in erythrocyte membranes. These abnormalities could contribute to the low-grade inflammation associated to inactivity.
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