Figure 3. POPs modulated the outcomes of farmed salmon intake.

In three separate studies, mice fed VHF/S (n = 31) and VHF/S_-POPs (n = 25) for 8 weeks were screened for insulin resistance-induced metabolic disorders. (A) Concentrations of 7PCBs and DDTs in epididymal fat of animals (5 mice per group). (B) Body weight gain (25–31 mice per group). (C) Quantification of adipose tissue. Total fat pad includes epididymal, retroperitoneal and inguinal fat pad (8–11 mice per group). (D) Representative H&E staining (upper panel) and immunohistochemical detection of the macrophage-specific antibody F4/80 (lower panel) in epididymal fat (4–5 mice per group). Note the important infiltration of macrophages in epididymal fat (arrows) of mice fed VHF/S compared with VHF/S_-POPs . (E) Real-time PCR determination of mRNA expression of Mac-2a, iNOS, TNFα and IL-6 in epididymal fat (5 mice per group). (F) Glucose tolerance test. Mice were injected with glucose and blood glucose assessed at indicated time points (8–13 mice per group). (G) Glucose-stimulated insulin release. Plasma insulin levels were measured before and 15 min after glucose injection (6–10 mice per group). (H) Insulin tolerance test. Random-fed mice were injected with insulin and blood glucose assessed at indicated time points (8–16 mice per group). (I) Muscle glucose uptake. Ex vivo soleus muscles were incubated without or with insulin, and glucose uptake assessed (6–12 mice per group). (J) TAG concentrations in gastrocnemius muscles (6–10 mice per group). (K) 3T3-L1 preadipocytes were treated with a weak differentiation cocktail containing cortisone and exposed to the organochlorine pesticide pp′-DDE. Graphic shows fold stimulation of lipid accumulation quantified by Oil red O staining. Results are expressed relative to vehicle-treated cells for three independent experiments. *p<0.05 vs. VHF/S or vehicle-treated cells.