Thermally processed food contains advanced glycation end
products (AGEs) including Nε
-(carboxymethyl)lysine (CML).
Higher AGEs or circulating CML were shown to be associated with
pregnancy complications such as preeclampsia and gestational
diabetes. It is unclear whether this association is causal. The aim
of our study was to analyze the effects of dietary CML and
CML-containing thermally processed food on metabolism in
pregnant rats. Animals were fed with standard or with AGE-rich
diet from gestation day 1. Third group received standard diet and
CML via gavage. On gestation day 18, blood pressure was
measured, urine and blood were collected and the oral glucose
tolerance test was performed. Plasma AGEs were slightly higher
in pregnant rats fed with the AGE-rich diet (p=0.09).
A non-significant trend towards higher CML in plasma was found
in the CML group (p=0.06). No significant differences between
groups were revealed in glucose metabolism or markers of renal
functions like proteinuria and creatinine clearance. In conclusion,
this study does not support the hypothesis that dietary AGEs
such as CML might induce harmful metabolic changes or
contribute to the pathogenesis of pregnancy complications. The
short duration of the rodent gestation warrants further studies
analyzing long-term effects of AGEs/CML in preconception
nutrition.
Circulating miRNAs have been proposed as the effective diagnostic biomarkers for muscular fibrosis-associated diseases. However, circulating biomarkers for early diagnosis of contracture muscles are limited in gluteal muscle contracture (GMC) patients. Here we sought to explore the abnormally expressed miRNAs in plasma and contraction bands of GMC patients. The results showed miR-29a-3p expression in plasma and contraction bands tissue was significantly reduced in GMC patients compared with normal control. Cell viability and levels of proliferation-associated protein cyclin D1 and cyclindependent-kinase 2 (CDK2) were powerfully inhibited by miR-29a mimics and enhanced by miR-29a inhibitor compared with negative control. Furthermore, miR-29a mimics effectively impeded, while miR-29a inhibitor enhanced the expression of collagen I and collagen III, followed by the secretion of transforming growth factor β1 (TGF-β1), TGF-β3 and connective tissue growth factor (CTGF) in primary human contraction bands (CB) fibroblasts. The miR-29a-3p negatively regulated the expression of TGF-β1 through binding to the 3′ UTR region of SERPINH1 (encoding heat shock protein HSP47), but had no effect on Smad2 activity. The miR-29a-3p was inversely correlated with HSP47 in contraction bands tissue from GMC patients. Collectively, miR-29a was notably depressed and regulated cell viability and fibrosis by directly targeting HSP47 in GMC, which suggest that circulating miR-29a might be a potential biomarker for early diagnosis and provides a novel therapeutic target for GMC.