Abstract
DM type 1 (T1D) incidence is increasing around 3% every year and represents risks for maternal and fetal health. The objective of this study was to explore the effects of diabetes on fetus liver cells in non-obese diabetic (NOD) mice. Hyperglycemic NOD (HNOD), normoglycemic NOD (NNOD) and BALB/c females were used for mating, and the fetus livers were collected at 19.5 gestation day (gd). HNOD group had reduced fetal weight (989.5±68.32 vs 1290±57.39 mg BALB/c, P<0.05) at 19.5 gd and higher glycemia (516.66±28.86 mg dl−1, P<0.001) at both 0.5 gd and 19.5 gd compared to other groups. The protein expression of albumin (ALB) was significantly reduced in HNOD group (0.9±0.2 vs 3.36±0.36 NNOD P<0.01, vs 14.1±0.49 BALB/c P<0.001). Reduced gene expression of ALB (1.34±0.12 vs 5.53±0.89 NNOD and 5.23±0.71 BALB/c, P<0.05), Hepatic Nuclear Factor-4 alpha (HNF-4α) (0.69±0.1 vs 3.66±0.36 NNOD, P<0.05) and miR-122 (0.27±0,10 vs 0.88±0.15 NNOD, P<0.05) was present in HNOD group. No difference for alpha-Fetoprotein (AFP) and gene expression was observed. In conclusion, our findings show the impacts of T1D on the expression of ALB, AFP, HNF-4α and miR-122 in fetus liver cells by using NNOD and HNOD mice.
Highlights
Diabetes mellitus (DM) is considered a worldwide public health problem and considering all types of diabetes; there was an estimated 184 million diabetic women in 2013, a number expected to rise to 288 million by 2030.1 DM type 1 (T1D) is less frequent, the data from International Diabetes Federation pointed an increase around 3% every year
Each NNOD and HNOD sample was normalized to a BALB/c sample and, the expression level of ALB, AFP, hepatocyte nuclear factor (HNF)-4α was calculated by application of ΔΔCt method and the miR-122 fold expression by 2 − ΔΔCt method
This study is the first to describe the influence of diabetes on the expression of hepatic markers (ALB, AFP), HNF-4α and miR-122 in non-obese diabetic (NOD) fetus liver
Summary
Diabetes mellitus (DM) is considered a worldwide public health problem and considering all types of diabetes; there was an estimated 184 million diabetic women in 2013, a number expected to rise to 288 million by 2030.1 DM type 1 (T1D) is less frequent, the data from International Diabetes Federation pointed an increase around 3% every year. In 2015, Brazil was found to have the third highest number of children with this form of diabetes in the world.[1] there will be an increase in. Rodent diabetic experimental models have been used to study the impacts of maternal diabetes in fetal development; few studies focused on fetal liver gene and protein expression. The non-obese diabetic (NOD) mouse is a well-characterized model of autoimmune T1D that develops spontaneous pregestational diabetes and has advantages as stable hyperglycemia throughout gestation and lack of chemical destruction of β-cells.[2,3]. MiR-122 is crucial for liver development, differentiation, homeostasis and functions.[5]
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