Table 4.
The potential functional relevance of identified metabolites associated with diabetes and pre-term delivery
| Metabolite | Association | Potential relevance to pathophysiological aspects of diabetes and pre-term delivery | References |
|---|---|---|---|
| Glu | Increased in DM | Activates N-methyl-D-aspartate receptors in β-cells, leading to acceleration of β-cell dysfunction and apoptosis induced by hyperglycemia | [36] |
| BCAA (valine, leucine, isoleucine) | Increased in DM | Promotes insulin resistance by modulating fatty acid oxidation, mTOR, JNK and IRS1 pathways | [39, 40] |
| Phosphatidylcholines | Decreased in DM | Serum antioxidants preventing lipoprotein oxidation | [41] |
| AA | Increased in DM | Arachidonic acid triggers insulin secretion, potentially increasing risk of insulin resistance | [42] |
| GCDCA | Increased in DM | Bile acids control gut bacteria overgrowth, species population, and protect the integrity of the intestinal barrier. Alterations in GCDCA can trigger diabetes | [43] |
| DG and TG containing C18:1 and C18:2 | Increased in pre-term delivery | Serum linoleic acid is negatively correlated with visceral fat accumulation and risk of insulin resistance | [48] |
| TG17.2/36.4 and TG18.1/34.1 | Best predictors of pre-term delivery | Remains to be investigated |
Glu, glutamate; BCAA, branched chain amino acids; mTOR, The mammalian target of rapamycin; JNK, c-Jun N-terminal kinase; IRS-1, insulin receptor substrate 1; AA, arachidonic acid; GCDCA, Glycochenodeoxycholic Acid; DG, diacylglycerols; TG, triacylglycerols