lunes, 26 de junio de 2017

Obesidad e inflamación

Resultado de imagen de obesidad e inflamación
Obesity shares with most chronic diseases the presence of an inflammatory component, which
accounts for the development of metabolic disease and other associated health alterations. This
inflammatory state is reflected in increased circulating levels of pro-inflammatory proteins, and
it occurs not only in adults but also in adolescents and children. The chronic inflammatory
response has its origin in the links existing between the adipose tissue and the immune system.
Obesity, like other states of malnutrition, is known to impair the immune function, altering
leucocyte counts as well as cell-mediated immune responses. In addition, evidence has arisen
that an altered immune function contributes to the pathogenesis of obesity. This review
attempts to briefly comment on the various plausible explanations that have been proposed for
the phenomenon: (1) the obesity-associated increase in the production of leptin (pro-inflammatory)
and the reduction in adiponectin (anti-inflammatory) seem to affect the activation of
immune cells; (2) NEFA can induce inflammation through various mechanisms (such as
modulation of adipokine production or activation of Toll-like receptors); (3) nutrient excess and
adipocyte expansion trigger endoplasmic reticulum stress; and (4) hypoxia occurring in
hypertrophied adipose tissue stimulates the expression of inflammatory genes and activates
immune cells. Interestingly, data suggest a greater impact of visceral adipose tissue and central
obesity, rather than total body fat, on the inflammatory process. In summary, there is a positive
feedback loop between local inflammation in adipose tissue and altered immune response in
obesity, both contributing to the development of related metabolic complications.

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