منابع مشابه
Central insulin and leptin-mediated autonomic control of glucose homeostasis.
Largely as a result of rising obesity rates, the incidence of type 2 diabetes is escalating rapidly. Type 2 diabetes results from multi-organ dysfunctional glucose metabolism. Recent publications have highlighted hypothalamic insulin- and adipokine-sensing as a major determinant of peripheral glucose and insulin responsiveness. The preponderance of evidence indicates that the brain is the maste...
متن کاملCentral nervous system and glucose homeostasis
Type 2 diabetes (T2D) is closely associated with obesity. Obesity features an abnormality in energy balance with excess energy stored in fat tissues. In T2D, the ability to regulate glucose homeostasis is compromised resulting in hyperglycemia (high levels of blood glucose). Central nervous system (CNS) plays an important role in energy and glucose homeostasis [1]. In normal situations, the neu...
متن کاملRictor/mTORC2 facilitates central regulation of energy and glucose homeostasis
Insulin signaling in the central nervous system (CNS) regulates energy balance and peripheral glucose homeostasis. Rictor is a key regulatory/structural subunit of the mTORC2 complex and is required for hydrophobic motif site phosphorylation of Akt at serine 473. To examine the contribution of neuronal Rictor/mTORC2 signaling to CNS regulation of energy and glucose homeostasis, we utilized Cre-...
متن کاملCentral insulin action in energy and glucose homeostasis.
Insulin has pleiotropic biological effects in virtually all tissues. However, the relevance of insulin signaling in peripheral tissues has been studied far more extensively than its role in the brain. An evolving body of evidence indicates that in the brain, insulin is involved in multiple regulatory mechanisms including neuronal survival, learning, and memory, as well as in regulation of energ...
متن کاملIL-1 resets glucose homeostasis at central levels.
Administration of IL-1beta results in a profound and long-lasting hypoglycemia. Here, we show that this effect can be elicited by endogenous IL-1 and is related to not only the capacity of the cytokine to increase glucose uptake in peripheral tissues but also to mechanisms integrated in the brain. We show that (i) blockade of IL-1 receptors in the brain partially counteracted IL-1-induced hypog...
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ژورنال
عنوان ژورنال: The Review of Diabetic Studies
سال: 2006
ISSN: 1613-6071,1613-0575
DOI: 10.1900/rds.2006.3.54