A reduced blood glucose concentrati

A reduced blood glucose concentration was associated with protein restriction or a higher level of folic acid in the maternal diet. In the progeny of dams fed with the folic acid–supplemented diet, total cholesterol content was lowered by approximately 20%. In the 16-week-old rats, the ratio of HDL cholesterol to total cholesterol was larger in those animals whose mothers were fed the diet with a normal level of protein or a diet supplemented with folic acid. Folic acid supplementation in the maternal diet was associated with a reduction of blood TAG level in the older animals, while in the 10-week-old rats, this parameter was unaffected by maternal nutrition. On the contrary, folic acid supplementation of the maternal diet has been shown to be associated with increased TAG concentration in male rat progeny (Burdge et al. 2008).
It has been postulated that negative consequences of fetal programming can be observed when there is a mismatch between prenatal and postnatal nutritional environment (Gluckman and Hanson 2008). Jones et al. (1984) found that the detrimental effect of improper maternal diet (specifically, a 50% food restriction) can be exacerbated by a nutritional challenge (a high-fat diet) in postnatal life. Protein and folic acid content in the maternal diet has been shown to influence TAG and glucose concentrations, but the effect was modified by fat intake after weaning (Burdge et al. 2008). In our study, the altered response to the high-fat diet programmed by maternal nutrition during pregnancy was detected as changed gene expression in the 10-week-old rats and central adiposity in the 16-week-old rats. Hepatic PPARγ transcription in response to the high-fat diet was dependent on maternal nutrition. Similarly, activation of PPARα gene by high-fat feeding was dependent on prenatal nutrition. The highest PPARα mRNA level following the high-fat diet was detected in the progeny of normal folic acid dams, where it was 237% of those in the progeny of folic acid–supplemented dams. Enhanced expression of the PPARα gene has an anti-obesity effect which is achieved by the activation of target genes responsible for lipid metabolism. It is also capable of decreasing the dyslipidemia associated with metabolic syndrome (Yoon 2009). We can therefore speculate that decreased PPARα expression may have an adverse effect on health, yet no such correlation was found. However, it cannot be ruled out that this effect may be detectable only after long-term high-fat feeding. An altered response to high-fat feeding programmed by maternal protein restriction, mediated by hepatic SREBP-1c expression, was previously described by Erhuma et al. (2007a).

Results (Indonesian) 1:

Konsentrasi glukosa darah berkurang adalah dikaitkan dengan protein pembatasan atau tingkat yang lebih tinggi dari asam folat dalam diet ibu. Dalam keturunan waduk-waduk yang diberi asam folat – dilengkapi diet, kolesterol total konten diturunkan oleh sekitar 20%. Pada tikus berusia 16 minggu, rasio kolesterol HDL kolesterol total adalah lebih besar dalam binatang yang diberi diet dengan tingkat normal protein atau diet dilengkapi dengan asam folat. Suplementasi asam folat dalam diet ibu adalah dikaitkan dengan penurunan darah level TAG dalam hewan yang lebih tua, sementara di tikus berusia 10 minggu, parameter ini adalah tidak terpengaruh oleh Ibu gizi. Sebaliknya, asam folat suplementasi Diet ibu telah terbukti berhubungan dengan peningkatan konsentrasi TAG dalam keturunan laki-laki tikus (Burdge et al., 2008).It has been postulated that negative consequences of fetal programming can be observed when there is a mismatch between prenatal and postnatal nutritional environment (Gluckman and Hanson 2008). Jones et al. (1984) found that the detrimental effect of improper maternal diet (specifically, a 50% food restriction) can be exacerbated by a nutritional challenge (a high-fat diet) in postnatal life. Protein and folic acid content in the maternal diet has been shown to influence TAG and glucose concentrations, but the effect was modified by fat intake after weaning (Burdge et al. 2008). In our study, the altered response to the high-fat diet programmed by maternal nutrition during pregnancy was detected as changed gene expression in the 10-week-old rats and central adiposity in the 16-week-old rats. Hepatic PPARγ transcription in response to the high-fat diet was dependent on maternal nutrition. Similarly, activation of PPARα gene by high-fat feeding was dependent on prenatal nutrition. The highest PPARα mRNA level following the high-fat diet was detected in the progeny of normal folic acid dams, where it was 237% of those in the progeny of folic acid–supplemented dams. Enhanced expression of the PPARα gene has an anti-obesity effect which is achieved by the activation of target genes responsible for lipid metabolism. It is also capable of decreasing the dyslipidemia associated with metabolic syndrome (Yoon 2009). We can therefore speculate that decreased PPARα expression may have an adverse effect on health, yet no such correlation was found. However, it cannot be ruled out that this effect may be detectable only after long-term high-fat feeding. An altered response to high-fat feeding programmed by maternal protein restriction, mediated by hepatic SREBP-1c expression, was previously described by Erhuma et al. (2007a).