Premium
Interleukin‐1β and Insulin Elicit Different Neuroendocrine Responses to Hypoglycemia
Author(s) -
Ota Kazuki,
Wildmann Johannes,
Ota Taeko,
Besedovsky Hugo O.,
Del Rey Adriana
Publication year - 2009
Publication title -
annals of the new york academy of sciences
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.712
H-Index - 248
eISSN - 1749-6632
pISSN - 0077-8923
DOI - 10.1111/j.1749-6632.2008.03981.x
Subject(s) - hypoglycemia , insulin , medicine , interleukin , endocrinology , immunology , cytokine
Interleukin (IL)‐1β induces a prolonged hypoglycemia in mice that is not caused by a reduction in food intake and is dissociable from insulin effects. There is a peripheral component in the hypoglycemia that the cytokine induces resulting from an increased glucose uptake, an effect that can be exerted in a paracrine fashion at the site where IL‐1 is locally produced. However, the maintenance of hypoglycemia is controlled at brain levels because the blockade of IL‐1 receptors in the central nervous system inhibits this effect to a large extent. Furthermore, there is evidence that the cytokine interferes with counter regulation to hypoglycemia. Here we report that administration of IL‐1 or long‐lasting insulin results in different changes in food intake and in neuroendocrine mechanisms 8 h following induction of the same degree of hypoglycemia (40–45% decrease in glucose blood levels). Insulin, but not IL‐1, caused an increase in food intake and an endocrine response that tends to reestablish euglycemia. Conversely, a decrease in noradrenergic and an increase in serotonergic activity in the hypothalamus occur in parallel with a reduction of glucose blood levels only in IL‐1‐treated mice, effects that can contribute to the maintenance of hypoglycemia. These results are compatible with the proposal that IL‐1 acting in the brain can reset glucose homeostasis at a lower level. The biologic significance of this effect is discussed.