Should I blame my genetics for my obesity?

Epidemiological studies suggest that maternal undernutrition, obesity and diabetes during gestation and lactation can all produce obesity in human offspring. During the gestational period, maternal malnutrition, obesity, type 1 and type 2 diabetes, and psychological and pharmacological stressors can all promote offspring obesity. Normal postnatal nutrition can sometimes reduce the adverse effect of some of these prenatal factors, but may also exacerbate the development of obesity and diabetes in offspring of dams that are malnourished during gestation.



The genetic background of the individual is also an important determinant of outcome when the perinatal environment is perturbed. Individuals with an obesity-prone genotype are more likely to be adversely affected by factors such as maternal obesity and high-fat diets. Many perinatal manipulations are associated with reorganization of the central neural pathways which regulate food intake, energy expenditure and storage in ways that enhance the development of obesity and diabetes in offspring. Both leptin and insulin have strong neurotrophic properties so that an excess or an absence of either of them during the perinatal period may underlie some of these adverse developmental changes. As perinatal manipulations can permanently and adversely alter the systems that regulate energy homeostasis, it behooves us to gain a better understanding of the factors during this period that promote the development of offspring obesity as a means of stemming the tide of the emerging worldwide obesity epidemic.

From: Levin BE. Synergy of nature and nurture in the development of childhood obesity. Int J Obes (Lond). 2009;33 Suppl 1:S53-6.

Children can suffer from Metabolic Syndrome too

The consequences in children health are not as clear as in the adults, but childhood obesity has been associated with risk factors for cardiovascular disease and diabetes, orthopedic problems and mental disorders. A high Body Mass Index (BMI) in the adolescence can predict a high mortality in the adult age, as well as high rates of cardiovascular diseases, even if the excess weight is lost. A number of pathologies related to obesity that were thought to be only applicable to the adults, can be found now in children, such as the “metabolic syndrome”. In fact, more than 60 % of overweight children have some other factor cardiovascular risk, like hypertension, hyperlipidemia or hyperinsulinemia, and more than 20% have two or more.

The term “metabolic syndrome” is used to describe the conjunction of abdominal obesity with hypertension, dislipemia and insulin resistance, which generally meets with endotelial malfunction, one of the first events that take place in the development of aterosclerosis. The obesity is considered, in fact, a low-grade chronic inflammatory process, since it is characterized by an increase in inflammation markers produced by adipocytes, such as C-reactive protein, tumor necrosis factor alpha, interleukin-6 and even the macrophage infiltration in the adipose tissue. In obesity, an increase in reactive oxygen species is observed, which increase proinflammatory activation pathways. Hypertrigliceridemia attributable to the increase of triglyceride-rich lipoproteins (TRL) is the most invariable metabolic alteration in obesity.

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Obesity and Lipoprotein Metabolism

The presence of visceral obesity and insulin resistance cause the increase of circulating triglyceride-rich lipoproteins (TRL), which is evidenced by an increase in plasmatic concentrations of triglycerides, apolipoprotein (apo) C-III, B-100 and B-48 and a reduction in HDL-cholesterol.

In obese subjects, this increase in plasmatic triglycerides is basically due to an impairment of TRL clearance and to an increase in VLDL secretion. Visceral obesity is related to an increase in VLDL release and unactivation of lipoprotein lipase (LPL), the enzyme in charge of TRL hydrolysis. These effects are related to insulin resistance, since this hormone controls the VLDL and chylomicron (CM) metabolism. In insulin resistance, it is not possible to suppress the hepatic apo B production, which occurs in the normal state. Also, insulin resistance suppresses the expression of the LDL receptor, which is involved in CM uptake to the liver and increases the concentration of apo CIII, the lipoprotein lipse inhibitor. For this reason, obese subjects have a higher postpranciual triglyceride response, measured either as plasmatic triglycerides or as apo B48 and apo B100 and they show a slower CM clearance rate.

Plasmatic accumulation of CM remnants (CMr) involves a major risk of atherosclerosis development, because there is a greater likelyhood of interacting with macrophages and forming foam cells. The formation of these cells is part of the inflammatory process that takes place during the formation of the atheromatous plaque and increases the proinflammatory state. In this situation, macrophages release a number of proinflammatory substances, like adhesion molecules, cytokines and eicosanoids, some of them also released by adipocytes.

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