**7. Animal studies**

Embryos of pregnant rats fed with a low-protein diet during the preimplantation period (0–4.25 days) show altered development in multiple organ systems; the offspring had reduced birth weights, relatively increased postnatal growth, and adult-onset hypertension [44].

Obviously, the preconception period is particularly sensitive, so that even the required nutrient deficiencies (B12 or folate or methionine) can have an effect on metabolism and blood pressure later in sheep [45]. It has recently been reported that the imbalance in B12 folic acid status and pain during pregnancy contributes to insulin resistance in childhood in humans [46].

Glucocorticoid management to pregnant rats at specific times during pregnancy to cause high blood pressure [47], insulin resistance in offspring later in life [48], changes in gene expression in the developing brain of offspring, and increased sensitivity to stress after the birth have been reported. The administration of glucocorticoids to the pregnant rat at specific points during gestation has been reported to cause hypertension [47], insulin resistance in the offspring in later life [49], alterations in gene expression in the developing brain of the offspring, and increased sensitivity to postnatal stress [50].

In mice, it may lack nutrition during pregnancy to breed showing later the following: visceral obesity, reduced lean body mass, changes in insulin sensitivity, different hepatic metabolism, decreased numbers of nephrons, high blood pressure, and altered endothelial function, together with altered appetite regulation, level of activity, and neuroendocrine control [51–54].

There are critical periods in the differentiation and maturation of the tissues and cells involved in organogenesis throughout gestation and early postnatal life. The examples are seen in the kidney, heart, and pancreas, since their functional units are formed prenatally in the human fetus.

**45**

**9. Hormones**

*Fetal-Neonatal Lifestyle Basis of the Adult Metabolic Syndrome Patients*

abnormalities might contribute to later insulin resistance.

In the kidney, maternal dietary imbalance may lead to developmentally induced deviations from the optimal ratio of body mass to nephron number. This increased risk of inadequate renal function and hypertension in later life [54]. A predisposition to renal failure and a potentially reduced life span are predicted [55]. In the pancreas insulin secretion is also affected. Nutritional stress in pregnant rats reduces the growth of the endocrine pancreas during organogenesis and increases beta-cell apoptosis [55], leading to hyperglycemia and impaired insulin secretion when the offspring become adults. In the adult male rat offspring of mothers on a protein-restricted diet, low birth weight is associated with reduced expression of components of the insulin signal transduction pathway in the skeletal muscle [56]. Similar abnormalities have been reported in infants of low birth weight, and together with the developmentally induced reduction in skeletal muscle mass, these

Developmentally induced epigenetic modifications of DNA are generally stable during the mitotic cell divisions that continue throughout a lifetime. So, developmental plasticity of fetus through cell-cell interaction can be understood as a set of programs. "Programming" is the term used to describe lifelong changes in function that follow a particular event in an earlier period of the life span. Evolutionary plasticity requires a constant modification of genetic expression that appears to be mediated, at least in part, by genetic processes such as epigenetic mechanisms as cells use to control gene expression by virtue of DNA methylation. The role of DNA methylation in gene expression can be found in Phillips [57], and by a histone modification which is a histone protein includes methylation that can impact gene expression [58].

Several studies show that skeletal muscle can be programmed, where early exposure to environmental stimuli leads to a constant change in the skeletal muscle phenotype in later life. This has been demonstrated in mammalian models where reduced nutrient availability during pregnancy weakens muscle fibers, muscle and skeletal formation (white/red fiber ratios), and birth size [59]. Epidemiological studies in human aging groups also suggest that low birth weight and gestational malnutrition are closely related to reduced muscle size, skeletal strength, and aging [59, 60].

This refers to changes in gene expression due to nongenetic structural alterations of DNA and/or histones [58]. So, remember that cell-cell interaction can be transferable in the fetus so memory of active person eventually will be available later in life for the offspring babies [58]. Thus, developmental plasticity requires both the genome and the genetic variability of the environment interactively by the mature phenotype and determines the sensitivity and subsequent environmental factors and the subsequent risk of the disease affects [61]. The effects of maternal nutrition and behavior clearly target the promoter regions of specific genes rather than being associated with global changes in DNA methylation. DNA modulates the rate of transcription to messenger RNA. The phenotypic effects of epigenetic modifica-

It plays an important role in childhood growth and continues to have anabolic effects in adults. As the stress hormone, norepinephrine affects the brain's amygdala, where attention and responses are controlled. It is also based on norepinephrine response to fight or flight, in addition to epinephrine, which raises the heart rate

tions during development may not manifest until later in life [62].

*DOI: http://dx.doi.org/10.5772/intechopen.84218*

**8. Programming**

*Fetal-Neonatal Lifestyle Basis of the Adult Metabolic Syndrome Patients DOI: http://dx.doi.org/10.5772/intechopen.84218*

In the kidney, maternal dietary imbalance may lead to developmentally induced deviations from the optimal ratio of body mass to nephron number. This increased risk of inadequate renal function and hypertension in later life [54]. A predisposition to renal failure and a potentially reduced life span are predicted [55]. In the pancreas insulin secretion is also affected. Nutritional stress in pregnant rats reduces the growth of the endocrine pancreas during organogenesis and increases beta-cell apoptosis [55], leading to hyperglycemia and impaired insulin secretion when the offspring become adults. In the adult male rat offspring of mothers on a protein-restricted diet, low birth weight is associated with reduced expression of components of the insulin signal transduction pathway in the skeletal muscle [56]. Similar abnormalities have been reported in infants of low birth weight, and together with the developmentally induced reduction in skeletal muscle mass, these abnormalities might contribute to later insulin resistance.
