In a recent study, researchers examined the effects of aspartame (APM) on insulin resistance and atherosclerosis using animal models. The study, conducted over 12 weeks, observed significant insulin resistance in mice subjected to APM, as determined by glucose tolerance tests (GTT) and insulin tolerance tests (ITT). Additionally, the study revealed that while sucrose delayed the promotion of atherosclerosis until week 12, genetic factors played a crucial role in inhibiting early lesion formation.
The experimental setup involved keeping mice in a controlled environment at 22°C with 50%-60% humidity, following a 12-hour light and dark cycle. Each mouse was orally fed 200μL of distilled water containing varying concentrations of APM, ranging from 0.05% to 0.15%. The study aimed to explore the metabolic impacts of these substances on the development of insulin resistance and atherosclerotic lesions.
Cynomolgus monkeys were also part of the study, maintained at 18°C with 73% humidity. These primates were fed a diet including vehicle, 15% sucrose, and 0.15% APM. Blood glucose levels were meticulously monitored prior to treatment and at intervals of 15, 30, 60, 90, and 120 minutes post-treatment. The study results indicated that the addition of sucrose did not significantly affect atherosclerosis progression by weeks 4 and 8 compared to the vehicle group.
The study also highlighted the genetic aspect of atherosclerosis. Researchers discovered that genetic deletion of Cx3cr1 in macrophages significantly inhibited early-stage atherosclerotic lesion formation. This anti-atherosclerotic effect was markedly improved in Cx3cr1MΦ−/−/ApoE−/− double-knockout mice by weeks 8 and 12, suggesting potential genetic interventions for mitigating disease progression.
Further investigation into the cellular composition revealed six identified cell populations, including B cells (43.1%), T cells (32.3%), myeloid cells (16.0%), natural killer cells (7.0%), red blood cells (1.2%), and basophils (0.4%). This detailed analysis provided insights into the cellular dynamics underpinning the observed physiological changes.
Tissue analysis involved staining sections at 4°C overnight with anti-MOMA-2, followed by an hour-long staining at 37°C using an FITC-labeled goat anti-rat secondary antibody. This process allowed researchers to visualize and understand cellular interactions within the thoracic aorta's adventitia.
