Background: Unstable angina pectoris
(UAP) is a type of Coronary artery disease (CAD) characterized by a series of
angina symptoms. Insulin-like growth factor 1 (IGF-1) system may be related to
CAD. However, the correlation between the IGF-1 system, metabolism, and gut
microbiota has not been studied. In the present study, we investigated
the alterations of serum IGF-1 system, metabolomics, and gut microbiota in
patients with UAP. Methods: Serum and stool samples from healthy
volunteers and UAP patients were collected. Serum metabolomics, PAPP-A, IGF-1,
IGFBP-4, STC2, hs-CRP, TNF-, and IL-6 were detected in serum samples by
LC-MS, and commercial ELISA kits, respectively. Fecal short-chain fatty acids
(SCFAs) were measured by gas chromatography. 16S rDNA was used to measure the
changes of the gut microbiota. The correlation of the above indicators was
analyzed. Results: There were 24 upregulated and 31 downregulated
metabolites in the serum of UAP patients compared to those in the controls.
Pathway analysis showed that these metabolites were enriched in pathways
including linoleic acid metabolism, amino acid metabolism, starch metabolism,
sucrose metabolism, and citrate cycle (TCA cycle), etc. Additionally,
the UAP patients had lower fecal levels of 2-hydroxyisobutyric acid and succinic
acid. 16S rDNA sequencing results showed that the relative abundances of
Bacteroidetes, Synergistetes, Lactobacillaceae,
Burkholderiaceae, Synergistaceae, and Subdoligranulum were
significantly higher in the UAP patients than the healthy subjects. Moreover, the
UAP patients had lower serum IGF-1, IGFBP-4,
and STC2 and higher serum inflammatory cytokines (hs-CRP, TNF-, and
IL-6) levels than the healthy controls. Furthermore, there was a strong
correlation between serum amino acids and IL-6, which played an important role in
the development of UAP. Conclusions: These results indicated that the
UAP patients had decreased serum IGF-1 level and imbalanced amino acids
metabolism, which may be caused by the altered gut microbiota. It may provide a
new therapeutic strategy for unstable angina pectoris.