Staphylococcus aureus and Insulin Resistance: A Research Paper Summary

This research paper summary analyzes how Staphylococcus aureus causes insulin resistance during infection. The study shows that insulin signaling defects cause insulin resistance and are inhibited by lipopolysaccharide, TNF, and diacylglycerol.

Running head: RESEARCH PAPER SUMMARY 1
Research Paper Summary.
Student’s Name
Institutional Affiliation

RESEARCH PAPER SUMMARY 2
Research Paper Summary
Summary
Insulin resistance predisposes people to Staphylococcus aureus colonization. Insulin, a
peptide hormone, is produced by B-cells found in the pancreatic islets. S. aureus colonization
occurs frequently in obese people than in healthy individuals. S. aureus infection leads to insulin
resistance (Jung and Choi, 2014). Consequently, this happens due to the production of eLtaS that
inhibits glucose uptake. This, paper analyses how Staphylococcus aureus causes insulin
resistance especially during infection. C57BL/6J mice were used for the study and Roche
diagnostics utilized to determine glucose levels in the blood. To facilitate cell differentiation,
C2C12 cells were immersed in a high glucose solution that contained 2% horse serum45.
Bacterial growth conditions and strains entailed growing S. aureus in a solution of brain heart
infusion. GTT was done by injecting glucose while ITT was performed by injecting insulin.
Subsequently, insulin levels were determined through the use of insulin ELISA kit. PVC,
polyvinyl chloride, was vital in testing if eLtaS binds to insulin. Other important activities
carried out were western blotting, GC-TOF/MS analysis, and labeling cells using ITC-insulin.
Data processing which entailed peak alignment, chromatogram acquisition, peak finding, and
signal deconvolution was done using the ChromaTOF software. ANOVA was essential for
statistical analysis. The research shows that insulin signaling defects cause insulin resistance.
The defects are inhibited by lipopolysaccharide39, TNF and diacylglycerol. Superantigen TSST-
1 of s. aureus causes chronic inflammation which hinders glucose tolerance. Additionally, this
happens by enhancing the secretion of inflammatory factors17. Infection of s. aureus is
responsible for impairing glucose tolerance through the production of eLtaS. In addition, eLtaS
is an insulin binding factor. Reduced glucose tolerance is basically a pre-diabetic condition of

RESEARCH PAPER SUMMARY 3
hyperglycemia-related insulin resistance. The condition considerably raises the threat of getting
type 2 diabetes. According to the research, exogenous eLtaS greatly decreased glucose tolerance
precisely in C57BL/6J mice (Liu et al., 2018). eLtaStrans mice revealed a pre-diabetic phenotype
comprising of increased water and food intake, postprandial hyperglycemia, and diminished
glucose tolerance. Therefore, contemporary research reveals that s. aureus is greatly involved in
causing insulin resistance.
Questions
Question 1
Does eLtaS bind directly to insulin?
Question 2
Does s. aureus cause insulin resistance?

RESEARCH PAPER SUMMARY 4
References
Jung, U. J., & Choi, M. S. (2014). Obesity and its metabolic complications: the role of
adipokines and the relationship between obesity, inflammation, insulin resistance,
dyslipidemia and nonalcoholic fatty liver disease. International journal of molecular
sciences, 15(4), 6184-6223.
Liu, Y., Liu, F. J., Guan, Z. C., Dong, F. T., Cheng, J. H., Gao, Y. P., ... & Ma, C. M. (2018).
The extracellular domain of Staphylococcus aureus LtaS binds insulin and induces
insulin resistance during infection. Nature microbiology, 3(5), 622.