(PO01-13-22) Incomplete Protein Predisposes to Cardiometabolic Defect: The Case of Lysine

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Presenting Author(s)

Carla El-Mallah, MSc
– PhD Candidate, American University of Beirut, Beirut, Beyrouth, Lebanon

Co-Author(s)

MR

Marie-Elizabeth Ragi, MSc
– American University of Beirut
OO

Omar Obeid, PhD
– American University of Beirut

Disclosure(s):

Carla El-Mallah, MSc: No relevant financial relationship(s) with ineligible companies to disclose.

Objectives: Non-communicable diseases (NCDs) are common among people with low socioeconomic status who rely on low-quality proteins, such as gluten, that are liming in lysine. This work aims at studying the effect of Lysine Deficiency (LD) on different cardiometabolic parameters to highlight its potential involvement in the development of NCDs.

Methods: The research protocol was approved by the Institutional Animal Care and Use Committee (IACUC) of the American University of Beirut. Sixteen 5 week-old male Sprague-Dawley rats were divided into 2 groups (n=8). They were maintained on a gluten-protein-based diet: the Control diet (C) contained the recommended level of lysine (9.8 g/kg), and the LD diet had a 60% lower amount. The rats had free access to their corresponding diets over the experimental period of 4 weeks.

Hematoxylin and eosin-stained adipocytes from epididymal fats were quantified, and images were used to estimate adipocyte sizes. Total RNA from liver and spleen was isolated and quantitative real-time Polymerase Chain Reaction (PCR) was performed. C-reactive protein (CRP) liver protein expression was estimated using Western Blot. Independent t-tests were conducted to check for differences between groups. Significance was set at a p-value (p) of 0.05.

Results: At the end of the experiment, the percentage of body fat was similar between groups (p=0.369), but the epididymal adipose tissue of the LD group showed hyperplasia (p=0.001) and a decrease in the adipocyte size (p=0.008). Interestingly, the toll-like receptor 4 (TLR-4) gene was overexpressed in the liver of the LD group (p=0.016) along with an increase of 85% of tumor necrosis factor-alpha (TNF-α) gene expression (p=0.027). This was accompanied by an increase of 2.3 fold in CRP protein expression in the liver (p=0.048). Furthermore, the lipid profile differed between both groups, highlighting a drop of HDL by around 23% and an increase in LDL by 14 folds in the LD group (p < 0.05).

Conclusions: LD caused an upsurge in several inflammatory markers and risk factors of cardiovascular diseases. The current data present important evidence about the relationship between lysine deficiency and some metabolic disturbances that increase the risk of NCDs.

Funding Sources: This work was funded by the University Research Board of the American University of Beirut.