Some aspects of morphogenesis of diabetic encephalopathy
DOI:
https://doi.org/10.14739/2310-1210.2013.4.16835Keywords:
diabetes mellitus, angiopathy, diabetic encephalopathyAbstract
On the basis of the literary data and conducted large-scale research it was ascertained that diabetes mellitus raises the risk of cerebral stroke in 2-6 times, the risk of transitional ischemic attacks in 3 times in comparison with the same risk in the general population [3]. Diabetic encephalopathy in its pure form can be found in 80.7% of patients with diabetes mellitus of the 1st type, its development is caused mainly by ineffective metabolic control of autoregulation of cerebral blood flow [4]. Mixed encephalopathy is prevailed among patients with diabetes mellitus of the 2nd type; lacunar heart attack is more often developed among this category of patients [5], multiple focus of ischemic affection of white substance – leukoaraiosis regarded as the areas of increased level of water, gliosis, and demyelination of white substance is often registered [6].
Pathogeny of diabetic encephalopathy hasn’t been studied properly. It is known that it is a multifactor effect in the development of which the main role is led by the vascular dysfunction with the reduction of blood supply and ischemia of brain tissue, as well as direct toxic influence of hyperglycemia and disorder of trophism of nerve tissue [7]. Microangiopathy and macroangiopathy acquire the special meaning in encephalopathy development among patients with diabetes mellitus. The evidence of microangiopathy and macroangiopathy is identified by the disease course and prognosis.
On the ultrastructural level the changes of vessel microcircular movement are registered on the 1st month of the experimental alloxan diabetes. During electronic microscopy the thickening of basal membrane of capillaries as well as their dissection is observed. In micro vessels such phenomena as precipitation of lipoproteids, raising of the synthesis of collagen (the second type), dystrophic changes of endotheliocytes, and lowering of micropinocytosis can be found [11,12,13,14]. As the severity of diabetes mellitus is growing, damages of organelles and microclamatosis of endothelial cells are registered. The endothelial lining is getting thin. In cytoplasm of endotheliocytes there can be found multiple pores and fenesters; interendothelial junction of capillaries are getting wider and “locus of leakage”, through which form elements of blood and plasma migrate, are created [15]. Under the streptozotocin-induced diabetes considerable increase of blood-brain barrier for small molecules are registered [16].
The progress of micro-and macroangiopathy leads to the lowering of cerebral blood flow and dishemic hypoxemia that switches energetic metabolism of nerve tissue to ineffective anaerobic glycolysis. As a result, energetic deficit and lactic acidosis are developing that in its turn leads to their structural and functional abnormalities [9]. It is determined that the important role in the development of chronicle abnormalities of cerebral blood flow under diabetes mellitus is performed by endothelial dysfunction, violation of autoregulation of cerebral blood flow, raising of viscosity and aggregative properties of blood [9].
The risk of neurodegeneration and cognitive deficit is rising among insulin-resistance patients. The high level of insulin can inhibit neuron transmission and lowering the activity of cholineacetyltransferase [37]. Hypoglycemic episodes and comas accompanying the development of incisive dysmetabolic encephalopathy are particularly dangerous.
Despite great number of works on complications of diabetes mellitus of types I and II, abnormalities of cognitive functions of central nervous system are less studied. Further fundamental molecular and subcellar research of cerebrum will help to discover new links of pathogenesis of diabetic encephalopathy and maybe will open new perspectives in modern diagnostics and prevention of diabetes mellitus complications.
References
Балаболкин М.И. Диабетическая невропатия / М.И Балаболкин, В.М. Креминская // Журнал неврологии и психологии. – 2000. – №10. – C. 57–64.
Бабах В.Н. Стратегия лечения и особенности клиники психических расстройств и психосоциальных проблем у больных сахарным диабетом / В.Н. Бабах // Міжнародний ендокрінологічний журнал. – 2005. – №1. – C. 92–98.
Latha Velayudhan. Risk of developing dementia in people with diabetes and mild cognitive impairment / Latha Velayudhan, Michaela Poppe, Nicola Archer // BJP. – 2010. – Vol. 196. – Р. 36–40.
Маркин С.П. Неврологические проявления сахарного диабета / С.П. Маркин // CONSILIUM MEDICUM. Приложение Неврология/ ревматология – М., 2011. – №1. – C. 60–63.
Чугунова Л.А. Цереброваскулярные заболевания и сахарный диабет 2 типа / Л.А. Чугунова, П.Р. Камчатное, А.В. Чугунов, М.В Шестакова // Сахарный диабет. – 2006. – №1. – C. 34–40.
Stewart C. Ferguson. Cognitive Ability and Brain Structure in Type 1 Diabetes / Ferguson Stewart C., Blane Annette, Perros Petros. // Diabetes. – 2003. – Vol. 52. – Р. 149–156.
Шишкова В.Н. Взаимосвязь развития метаболических и когнитивных нарушений у пациентов с сахарным диабетом, предиабетом и метаболическим синдромом / В.Н. Шишкова // CONSILIUM MEDICUM. Приложение Неврология/ ревматология. – М., 2010. – №1. – С. 36–42.
Чугунова Л.А. Ранняя диагностика хронической ишемии мозга с применением современных иммуновоспалительных
маркеров и инструментальных методов у больных сахарным диабетом: пособие для врачей / Л.А. Чугунова, И.В. Семенова, М.В. Шестакова. – М., 2007. – C. 6–7.
Товажнянская Е.Л. Нарушение ауторегуляции мозгового кровотока как фактор развития мозговых дисциркуляций при сахарном диабете ІІ типа / Е.Л. Товажнянская, О.И Дубинская, И.О. Безуглая, М.Б. Наврузов // Міжнародний неврологічний журнал. – 2012. – №4. – C. 43–47.
Messier C. The relationships between atherosclerosis, heart disease, type 2 diabetes and dementia / C. Messier, N. Awad, M. Gagnon // Neurol. Res. – 2004. – Vol. 26 (5). – P. 567–572.
Mizutini M. Accelarated death of retinal microvascular cells in human and experimental diabetic retinopathy / M. Mizutini, T. S. Kern, M. Lorenzi // Am. J. Ophthalmol. – 1994. – Vol. 122, №3. – P. 393–403.
Chengxuan Qiu. Retinal and Cerebral Microvascular Signs and Diabetes / Qiu Chengxuan, Cotch Mary Frances, Sigurdsson Sigurdur, Garcia Melissa, [et al.] // Diabetes. – 2008. – Vol. 57. – P. 1645–1650.
Christine Maric-Bilkan. Microvascular disease precedes the
decline in renal function in the streptozotocin-induced diabetic rat/ Maric-Bilkan Christine, Flynn Elizabeth R., Chade Alejandro R. // Am J Physiol Renal Physiol. – 2012. – Vol.
– Р. 308–315.
Williams E. Electron microscopical studies of vessels in diabetic peripheral neuropathy / E Williams, W R Timperley, J D Ward, [et al.] // J Clin Pathol. – 2000. – Vol. 33. – Р. 462–470.
Варакута Е.Ю. Структурные изменения сетчатки глаза на ранней стадии аллоксанового диабета при действии света высокой интенсивности : диссертация на соискание ученой степени кандидата медицинских наук : 03.00.25 / Е.Ю. Варакута. –Томск: СГМУ, 2002. – 174 с.
Jason D. Huber. Streptozotocin-induced diabetes progressively increases blood-brain barrier permeability in specifi c brain regions in rats / Huber Jason D., VanGilder Reyna L., Houser Kimberly A. // AJP-Heart Circ Physiol. – 2006. – Vol. 291. – P. 2660–2668.
Wang M. A morphological study of the vessels in experimental diabetic rats / M. Wang, Y.H. Wang // Chung Hua Yen Ko Tsa Chih. – 1999. – Vol. 25, №8. – P. 31–34.
Sakaki V. Retinopathy in diabetic (KKA gamma) mice: diabetic microvascurar changes to the retina in KKA gamma mice revealed by light and electron microscopy / V. Sakaki, H. Nakamura, T. Shimada, H. Kibamura, [et al.] // Jpn. J. Ophthalmol. – 1996. – Vol. 40, №3. – P. 317–328.
Пашковська Н.В. Гистопатологические особенности эндотелиальной дисфункции сосудов микроциркуляторного русла головного мозга при диабетической энцефалопатии / Н.В. Пашковська // Морфологія. – 2008. – Т. 2, №1. – C. 86–90.
Morris M.C. Vitamin E and Cognitive Decline in Older Persons / M.C. Morris, D.A. Evans, J.L. Bienias, C.C. Tangney // Archives of Neurol. – 2002 – Vol. 59. – Р. 1125–1132.
Vijayakumar T.M. Mechanism Linking Cognitive Impairment and Diabetes mellitus / T.M. Vijayakumar, G.B.N. Sirisha, M.D. Farzana Begam, M.D. Dhanaraju // Europ J Appl Sciences. – 2012. – Vol. 4(1). – Р. 1–5.
Mastrocola R. Oxidative and nitrosative stress in brain mitochondria of diabetic rats / R. Mastrocola, F. Restivo, I. Vercellinatto, O. Danni // J of Endocrinol. – 2005. – Vol. 187. – Р. 37–44.
Sarkela T.M. The modulation of oxygen radical production by nitric oxide in mitochondria / T.M. Sarkela, J. Berthiaume, S. Elfering, A.A. Gybina // J of Biol Chem. – 2001. – Vol. 276. – Р. 6945–6949.
Moreira P.I. Effect of streptozotocin-induced diabetes on rat brain mitochondria / P.I. Moreira, M.S. Santos, A.M. Moreno, T. Proença, [et al.] // J of Neuroendocrinol. – 2004. – Vol. 16. – Р. 32–38.
Sherene M. Shenouda. Altered Mitochondrial Dynamics Contributes to Endothelial Dysfunction in Diabetes Mellitus /
Shenouda Sherene M., Widlansky Michael E., Chen Kai, [et al.] // Circulation. – 2011. – Vol. 124. – P. 444–453.
Новиков Ю.А. Физиология и патология эндотелия / Ю.А. Новиков // Сибирский медицинский журнал. – 2005. – №1. – C. 5–10.
Балаболкин М.И. Роль гликирования белков, окислительного стресса в патогенезе сосудистых осложнений при сахарном диабете / М.И. Балаболкин // Сахарный диабет. – 2002. – №4. – C. 5–16.
Beckman J.A. Diabetes and atherosclerosis: epidemiology, pathophysiology, and management / J.A. Beckman, M.A. Creager, P. Libby // JAMA. – 2002. – Vol. 287. – P. 2570-2581.
Бондарева В.М. Инсулин и инсулинрецепторная сигнальная система мозга / В.М. Бондарева, О.В. Чистякова // Нейрохимия. Академиздатцентр «Наука» РАН. – 2007. – Т. 24. – C. 8–20.
Головничий Ю.И. Современные представления о физиологии и патологии эндотелия сосудов головного мозга / Ю.И. Головничий, М.А. Трещинская // Український хіміотерапевтичний журнал. – 2008. – №1–2 (22). – C. 22–28.
Мельник Т.М. Особенности цереброваскулярной реактивности у больных с диабетической энцефалопатией / Т.М. Мельник // Питання експерим. та клінічної медицини. – 2011. – №1. – C. 260–264.
Cicero F.M. Diabetes mellitus, neurological pathology, diagnostic position / F.M. Cicero // Jam. – 2004. – Vol. 12. – P. 713–719.
Kyung Y.Lee. Arterial Pulsatility as an Index of Cerebral Microangiopathy in Diabetes / Y. Lee Kyung, Young H. Sohn, Jong S. Baik. // Stroke. – 2000. – Vol. 31. – Р. 1111–1115.
Cellek S. Nitrergic Neurodegeneration in Cerebral Arteries of Streptozotocin-Induced Diabetic Rats. A New Insight into Diabetic Stroke / Cellek S., Anderson P.N., Foxwell N.A. // Diabetes. – 2005. – Vol. 54. – Р. 212–219.
Северина А.С. Нарушение системы гемостаза у больных сахарным диабетом / А.С. Северина, М.В. Шестакова //Сахарный диабет. – 2004. – №1. – С. 62–67.
Мищенко Т.С. Сахарный диабет и цереброваскулярные заболевания / Т.С. Мищенко, В.Н. Перцева, В.Н. Мищенко // Новости медицины и фармации. – 2010. – № 6. – C. 16–20.
Cai X.J. C-peptide and diabetic encephalopathy / X.J. Cai, Xu H.Q., Lu Y. // Clin Med Sci J. – 2011. – Vol. 26 (2). – Р. 119–125.
Морозова О.Г. Метаболические аспекты патогенетической терапии церебральных осложнений сахарного диабета / О.Г. Морозова // Ліки України. – 2011. – №2. – C. 50–57.
Родинський О.Г. Механізми формування ураження центральної і периферичної нервової системи за умови експериментального цукрового діабету / О.Г. Родинський, В.А. Гузь // Медичні перспективи. – 2009. – Т. 14, №3. – C. 4–13
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