Diabetes mellitus (DM) is nowadays a major global health problem affecting more than 200 million people worldwide. It is one of the most severe metabolic disorders in humans characterized by hyperglycemia due to a relative or an absolute lack of insulin or the action of insulin on its target tissue or both. Many neurodegenerative disorders, such as diabetic encephalopathy and Alzheimer's disease (AD), are associated with the type 1, insulindependent, and the type 2, non-insulin-dependent, diabetes mellitus (DM1 and DM2). Manifestations of these disorders in diabetic patients include alterations in neurotransmission, electrophysiological abnormalities, structural changes and cognitive deficit (Biessels et al., 2001). In the recent time attention to the neurological consequences of DM in the CNS has increased considerably. Many approaches and tools have been used to study etiology and pathogenesis of DM and DM-associated neurodegenerative disorders, and their diagnostics and treatment. The most perspective approaches are based on a combined use of the methods of biochemistry, molecular biology and physiology, they include clinical investigations of diabetic patients and the experimental models of DM and their complications, such as the model of DM1 induced by streptozotocin (STZ) treatment of young or adult rodents, the neonatal model of DM2 induced by the STZ treatment of newborn rats, and also the models of spontaneous DM and nutritional background causing DM2, as well as the models produced by transgenic manipulations or gene knockout techniques are all successfully used to study the molecular, cellular and morphological changes in diabetic brain (Shafrir, 2010). A severe hyperglycemia in DM1, mild hyperglycemia typical of DM2, and recurrent hypoglycemia induced by inadequate insulin therapy are the major factors responsible for the development of CNS complications in DM. The brain is mainly a glucose-dependent organ, which can be damaged by hyperas well as by hypoglycemia (Scheen, 2010). Being a major problem in clinical practice, hypoglycemia unawareness is associated with an increased risk of coma. Note that low blood glucose level induces negative mood states, primarily self-reported “nervousness” (Boyle & Zrebiec, 2007). Moreover, patients with a history of severe hypoglycemia show a much higher level of anxiety compared to other DM patients (Wredling, 1992). The prolonged influence of mild hypoglycemia on the brain leads to deregulation of many processes in CNS, which underlines the importance of scrupulously avoiding even mild hypoglycemic episodes in patients with DM. Hypoglycemia induces
Hormonal Signaling Systems of the Brain in Diabetes Mellitus
O. Chistyakova,K. Derkach,V. Bondareva
Published 2011 in Unknown venue
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2011
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Unknown venue
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2011-12-09
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Biology, Medicine
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