Mechanisms of obesogenic adipocyte signaling in mouse 3T3-L1 cells in response to plasma from C57BL/6 mice exposed to traffic-generated emissions and high-fat diet.
Year: 2026
Type: article
Abstract: Recent studies have demonstrated a strong correlation between exposure to traffic-generated air pollutants and the development of metabolic disorders, including obesity. We have reported that exposure to a mixture of vehicle emissions (MVE) promotes increased angiotensin II (Ang II) levels, associated with adipocyte hypertrophy and lipid accumulation in C57BL/6 mice; and this effect is further exacerbated by high-fat (HF) diet consumption. To elucidate the underlying mechanisms, mouse adipocyte 3T3-L1 cells were utilized to test the hypothesis that circulating Ang II mediates obesogenic outcomes via the Ang II type 1 (AT 1 ) receptor following MVE exposure. Plasma from three mo-old male C57BL/6 mice, fed either a high-fat (HF) or low-fat (LF) diet and exposed to either filtered-air (FA) or 100 µg PM/m 3 MVE for 6 hr/day for 30 days was collected and applied to the cell culture media (1:40 dilution) for 48 hrs. A subset of cells was pretreated with losartan (10 −6 mol/l), an AT 1 receptor antagonist, for 30 min. 3T3-L1 adipocytes treated with plasma from either HF diet-fed or MVE-exposed animals, regardless of diet, exhibited adipocyte hypertrophy. Plasma from the MVE+HF diet group induced increased adipocyte mRNA expression of the Ang II type 2 (AT 2 ) receptor, angiotensinogen (AGT), glucose transporter-4 (GLUT-4), peroxisome proliferator-activated receptor gamma (PPARγ) and leptin, compared to either the LF or HF+FA controls; most of these effects were normalized by losartan treatment. These findings indicate that Ang II – AT 1 signaling mediate alterations obesogenic responses in 3T3-L1 adipocytes following exposure to traffic-generated pollution, in combination with a HF diet.
Source: Toxicology Reports
Authors: U. Suwannasual, A.K. Lund
Language: English
Subfield: Health, Toxicology and Mutagenesis
Field: Environmental Science
Domain: Physical Sciences
Open Access status: gold
Estimated APC paid: $2,530
Awards: G3115184984, G7611009456
OpenAlex ID: W7166194251
