**1. Introduction**

In the development period, the fetus may be exposed to an altered risk of developing diseases in adulthood. In this regard, the hypothesis called Developmental Origins of Health and Disease (DOHaD) highlights the relationship between stimuli in the early stages of life and the subsequent development of the disease [1–3]. This model studies the adaptations that occur in the fetus in response to the intrauterine environment, leading to a permanent set of homeostatic systems to assist in immediate survival and improve success in an adverse postnatal environment. However, inappropriate interpretations or environmental changes can lead to an incompatibility between prenatal predictions and postnatal reality [4, 5].

Thus, these adaptations known as predictive adaptive responses can be disadvantageous in adulthood, resulting in an increased risk of diseases that can be transmitted to future generations. In this perspective, it was established that some nutritional changes early in life can lead to an increased risk for several diseases in adulthood [6, 7].

Various studies have shown an association between maternal malnutrition and exposure to hormones during critical periods of development, with metabolic changes, with an emphasis on chronic non-communicable diseases, thyroid disorders, among others [8, 9]. The mother's malnutrition characteristic is capable of interfering with the nutritional status of adult offspring. Maternal protein restriction during lactation led to low weight of the offspring at weaning. Caloric restriction resulted in greater weight gain and resistance to leptin in adult offspring [10].

Programming at a critical stage of development can lead to changes in tissues and organs, which extend throughout life; it may also present a latency period and manifest only in adult life. More studies are emerging to explain the possible mechanisms related to metabolic programming [11, 12].

The mechanisms involved are not entirely clear, but it is believed that there is a relationship between changes in the structural development of the organs and with persistent changes at the cellular level [13]:


Molecular mechanisms suggested include acute or chronic changes in gene expression, through various avenues, where there is an epigenetic interrelation between certain genes, exposure to environmental factors, and biological events [5].

#### **Figure 1.**

*A complex network that affects adult health and disease, including hormonal and nutrition alterations, epigenetic modifications, microbiota, and the exposure to endocrine disruptors.*

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*Metabolic Programming and Nutrition DOI: http://dx.doi.org/10.5772/intechopen.92201*

nisms linked to developmental programming.

**2. The early-life origins of obesity**

diseases [15, 16].

As the epigenetic regulation during development changes, the dynamic epigenome has an unstable nature, providing a response and adaptation to environmental pressures, including nutritional changes [2]. **Figure 1** presents the principal mecha-

There is still a lot to be understood, although epigenetics helps to reveal how exposure to environmental factors, in critical periods of development, leads to changes in adult life, it is necessary to understand the post-epigenetic changes involved in the various processes that lead to the emergence of diseases [13].

Obesity is defined by an excess of adipose tissue and occurs when an imbalance in the balance of energy exists [14]. The origin of obesity is a complex process that involves genetic and environmental factors and is often associated with the development of chronic complications, such as hyperglycemia, hypertriglyceridemia, low HDL levels, and hypertension. Individuals who have at least three of these criteria are clinically diagnosed as having metabolic syndrome, which increases the risk of developing metabolic diseases, such as type 2 diabetes and cardiovascular

In 2016, more than 1.9 billion adults, 18 years and older, were overweight. Of these, over 650 million were obese; 41 million children under the age of 5 were overweight or obese, as well as over 340 million children and adolescents aged 5–19 [14]. Recognizing its etiology is essential to face the global epidemic. This creates a challenge since the pathway to obesity in many individuals begins before birth; a predisposition to obesity can occur through epigenetic and other forms of early programming, and obesity and its metabolic consequences result from physiological

It is known that a number of factors, including epigenetic signals, mitochondrial inheritance, milk composition, gut microbiota, and features of the maternal metabolic environment, such as insulin resistance, fatty acids, and inflammation, may cause developmental programming. In many cases, the effects of the prenatal perturbations are exacerbated by postnatal exposure to a high-calorie diet, acceler-

The early-life origins of obesity are supported by a number of studies, which have shown that being exposed to inappropriately nutrition levels during critical periods of development (fetal and postnatal) is associated with increased risk of obesity, insulin resistance, and type 2 diabetes in child and adult life [23, 24]. The excessive or deficient nutritional status before birth alters the development of the fat cell, the adipocyte, and results in a permanent increase in the capacity to form new cells in adipose depots (adipogenesis) or to store lipid in existing adipocytes (lipogenesis) since the adipogenesis occurs primarily during late fetal and early postnatal life, and is highly sensitive to the nutritional environment at this time, in particular to the prevailing concentrations of insulin-like growth factors, glucose,

In addition, there are animal and human data that show that obese mothers are more likely to generate to an overweight baby and that these infants are at greater risk of obesity in later life. This "intergenerational cycle of obesity" already is a well-defined phenomenon, showing that maternal obesity, maternal diabetes, and an increase in nutrient supply to the developing fetus constitute major risk factors

There is a greater propensity to develop altered energy metabolism in adult life, in particular, overweight and/or hyperphagia, after malnutrition during fetal

changes set during fetal and early postnatal development [17–19].

ated postnatal growth, stress, or other factors [20–22].

insulin, and glucocorticoids [17, 25].

for obesity in postnatal life [26–28].

### *Metabolic Programming and Nutrition DOI: http://dx.doi.org/10.5772/intechopen.92201*

*New Insights into Metabolic Syndrome*

mechanisms related to metabolic programming [11, 12].

persistent changes at the cellular level [13]:

• hyperplasia or hypertrophy;

• Metabolic differentiation process.

Various studies have shown an association between maternal malnutrition and exposure to hormones during critical periods of development, with metabolic changes, with an emphasis on chronic non-communicable diseases, thyroid disorders, among others [8, 9]. The mother's malnutrition characteristic is capable of interfering with the nutritional status of adult offspring. Maternal protein restriction during lactation led to low weight of the offspring at weaning. Caloric restriction resulted in greater weight gain and resistance to leptin in adult offspring [10]. Programming at a critical stage of development can lead to changes in tissues and organs, which extend throughout life; it may also present a latency period and manifest only in adult life. More studies are emerging to explain the possible

The mechanisms involved are not entirely clear, but it is believed that there is a relationship between changes in the structural development of the organs and with

• performance in epigenetic memory, with changes in the transcription process;

• alteration of the organ structure in vascularization, innervation, and juxtaposition, such as the position of hepatocytes, endothelial cells, and Kupffer cells,

which during organogenesis can permanently modify metabolism;

Molecular mechanisms suggested include acute or chronic changes in gene expression, through various avenues, where there is an epigenetic interrelation between certain genes, exposure to environmental factors, and biological events [5].

*A complex network that affects adult health and disease, including hormonal and nutrition alterations,* 

*epigenetic modifications, microbiota, and the exposure to endocrine disruptors.*

• abnormal cell growth under specific metabolic conditions; and

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**Figure 1.**

As the epigenetic regulation during development changes, the dynamic epigenome has an unstable nature, providing a response and adaptation to environmental pressures, including nutritional changes [2]. **Figure 1** presents the principal mechanisms linked to developmental programming.

There is still a lot to be understood, although epigenetics helps to reveal how exposure to environmental factors, in critical periods of development, leads to changes in adult life, it is necessary to understand the post-epigenetic changes involved in the various processes that lead to the emergence of diseases [13].
