CENEXA   05419
CENTRO DE ENDOCRINOLOGIA EXPERIMENTAL Y APLICADA
Unidad Ejecutora - UE
capítulos de libros
Título:
Unhealthy Diet Intake during the Peri-Natal and Adult Periods: Detrimental Neuroendocrine and Metabolic Effects
Autor/es:
SPINEDI E; GIOVAMBATTISTA A; REBOLLEDO OR; GAILLARD RC; GAGLIARDINO JJ
Libro:
Fructose: Synthesis, Functions and Health Implications
Editorial:
Nova Science Publishers, Inc
Referencias:
Lugar: Hauppauge, New York; Año: 2012; p. 1 - 36
Resumen:
Consumption of unhealthy diets (so called ¨modern diets¨) in early/late life might play a key role in the development of obesity, metabolic syndrome (MS) and type 2 diabetes (T2DM). Due to the epidemic growth profile of these diseases with their negative socioeconomic impact, this unhealthy habit becomes a relevant preventive target factor to improve human longevity/life quality and to reduce the current economic load for the public health system worldwide. We have currently reviewed data from studies addressing the impact of the intake of an iso-caloric fructose-rich diet (FRD) by either lactating mothers or adult individuals on metabolic and endocrine adipose tissue (AT) functions. Data from several hypothalamic functions, peripheral metabolic markers, and the pattern of the AT adipokine production were also compiled from experiments performed in those two conditions. Since one of the most important derangements caused by the intake of an excess of fructose is an overall enhancement in oxidative stress (OS) rate, the studies revisited have explored both its indirect and direct consequences upon body weight, food intake, hypothalamic function, adipoinsular axis activity, and the sensitivity of various tissues to insulin and leptin stimuli. The role of the AT dysfunction generated after feeding individuals with a FRD has also been deeply examined. Data collected clearly indicate that the intake of a FRD triggers the development of several features similar to those found in the human phenotype of MS, e.g., hyperadiposity, impaired glucose tolerance, dyslipemia, insulin- and leptin-resistance, enhanced prothrombotic risk and dysfunction of the hypothalamic satiety signal. Moreover, the intake of this diet negatively affects several of the above mentioned functions regardless of whether this interventional diet is applied directly or indirectly and earlier or later to an organism over development. This evidence must help health policy makers to develop/implement appropriate strategies to promote healthy dietary habits in the general population to prevent the development of chronic diseases such as obesity and T2DM, thus improving the population life quality and decreasing the heavy load of these diseases upon health care budgets and society overall.