involved in the defense of oxidative stress, ER stress, proinflammatory cytokines
and chemokines, cell cycle control and growth, as well as metabolic pathways for
lipid formation and storage. Moreover, several genes are differentially expressed in
the prediabetic and diabetic states, while being genetically associated with diabetes-related traits in human genome-wide association studies (Chadt et al. 2012).
Several (but not mutually exclusive) pathophysiological pathways involved in
nutrition-induced impairments of b-cells have now been established (Fig. 10.2),
and novel aspects such as epigenetic modifications of DNA and associated proteins
are currently under investigation (Chadt et al. 2012).
10.4 Obesity: Feed Your Genes Right
Obesity can be defined as a condition of abnormal or excess fat accumulation in
adipose tissue, to the extent that health may be impaired. Body Mass Index (BMI),
calculated as [(weight in kg)/(height in m)
2 ], is considered to be the most useful
population-level measure of obesity, and a simple index to classify underweight,
overweight, and obesity in adults (WHO 2000).
Obesity is a major public health concern worldwide, contributing to increased
morbidity and mortality. It has emerged as a significant cause of diabetes, cardiovascular disease (CVD), and renal insufficiency. The accelerated worldwide
increase of obesity prevalence has been named ‘‘globesity,’’ with considerable
variations observed between and within countries. Coincidentally, epidemiological
patterns, food habits, and lifestyles are changing very fast. Obesity affects both
sexes and all ages, and, in Latin America, it increases with age and is always more
prevalent in women, especially those from lower social strata (Aballay et al. 2013).
Many national and international agencies recommend an increased intake of
fruits and vegetables in order to decrease the risk of developing lifestyle related
diseases including overweight and obesity (WHO 2003). Different examples of
dynamic changes in DNA methylation patterns due to the restriction or supplementation with different nutrients related to obesity have been reported. In neonatal exposure to a DNA-hypomethylating compound such as bisphenol A has
been associated with higher body weight, although its effects were prevented by
diet supplemented with different methyl donors such as folic acid or genistein.
Genistein-induced hypermethylation of the Agouti gene decreasing its expression
and protecting offspring from obesity. In fact, transgenerational amplification of
body weight has been prevented by a promethylating dietary supplement. In this
sense, maternal supraphysiological methyl group (folate, cobalamin, choline, and
betaine) supply, and a low-protein diet in rodents throughout pregnancy modify
DNA methylation of some key metabolic genes (agouti, glucocorticoid receptor,
and PPAR-a). All these data strongly suggest that epigenetic mechanisms may be
boosted or impaired by dietary factors in the mother and could be involved in
obesity susceptibility in the offspring (Campión et al. 2009).
304
R. Campos-Vega et al.
and chemokines, cell cycle control and growth, as well as metabolic pathways for
lipid formation and storage. Moreover, several genes are differentially expressed in
the prediabetic and diabetic states, while being genetically associated with diabetes-related traits in human genome-wide association studies (Chadt et al. 2012).
Several (but not mutually exclusive) pathophysiological pathways involved in
nutrition-induced impairments of b-cells have now been established (Fig. 10.2),
and novel aspects such as epigenetic modifications of DNA and associated proteins
are currently under investigation (Chadt et al. 2012).
10.4 Obesity: Feed Your Genes Right
Obesity can be defined as a condition of abnormal or excess fat accumulation in
adipose tissue, to the extent that health may be impaired. Body Mass Index (BMI),
calculated as [(weight in kg)/(height in m)
2 ], is considered to be the most useful
population-level measure of obesity, and a simple index to classify underweight,
overweight, and obesity in adults (WHO 2000).
Obesity is a major public health concern worldwide, contributing to increased
morbidity and mortality. It has emerged as a significant cause of diabetes, cardiovascular disease (CVD), and renal insufficiency. The accelerated worldwide
increase of obesity prevalence has been named ‘‘globesity,’’ with considerable
variations observed between and within countries. Coincidentally, epidemiological
patterns, food habits, and lifestyles are changing very fast. Obesity affects both
sexes and all ages, and, in Latin America, it increases with age and is always more
prevalent in women, especially those from lower social strata (Aballay et al. 2013).
Many national and international agencies recommend an increased intake of
fruits and vegetables in order to decrease the risk of developing lifestyle related
diseases including overweight and obesity (WHO 2003). Different examples of
dynamic changes in DNA methylation patterns due to the restriction or supplementation with different nutrients related to obesity have been reported. In neonatal exposure to a DNA-hypomethylating compound such as bisphenol A has
been associated with higher body weight, although its effects were prevented by
diet supplemented with different methyl donors such as folic acid or genistein.
Genistein-induced hypermethylation of the Agouti gene decreasing its expression
and protecting offspring from obesity. In fact, transgenerational amplification of
body weight has been prevented by a promethylating dietary supplement. In this
sense, maternal supraphysiological methyl group (folate, cobalamin, choline, and
betaine) supply, and a low-protein diet in rodents throughout pregnancy modify
DNA methylation of some key metabolic genes (agouti, glucocorticoid receptor,
and PPAR-a). All these data strongly suggest that epigenetic mechanisms may be
boosted or impaired by dietary factors in the mother and could be involved in
obesity susceptibility in the offspring (Campión et al. 2009).
304
R. Campos-Vega et al.