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Семь этиологических факторов становления синдрома резистентности к инсулину
Семь этиологических факторов становления синдрома резистентности к инсулину
Титов В.Н. Семь этиологических факторов становления синдрома резистентности к инсулину. Consilium Medicum. 2018 (4): 68–74. DOI: 10.26442/2075-1753_2018.4.68-74
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Аннотация
Биологическая роль инсулина – регуляция метаболизма в первую очередь жирных кислот (ЖК) и во вторую – глюкозы; инсулин регулирует превращение в филогенезе плотоядных (рыбоядных) животных океана в травоядные на суше. Семь этиологических факторов синдрома резистентности к инсулину: 1) соматические клетки не поглощают глюкозу, пока есть возможность поглощать ЖК; поглощение клетками ЖК всегда более активно. Чтобы клетки поглощали глюкозу, инсулин лишает их возможности поглощать ЖК в форме неэтерифицированных ЖК (НЭЖК); 2) инсулин обеспечивает наиболее высокую производительность митохондрий в наработке аденозинтрифосфата (АТФ) и высокие параметры кинетики особей. Инсулин опосредованно регулирует метаболизм клетками глюкозы; глюкоза – субстрат для синтеза олеиновой мононенасыщенной ЖК. Среди длинноцепочечных ЖК митохондрии окисляют ее наиболее активно, нарабатывая АТФ; 3) инсулин не может блокировать освобождение в среду НЭЖК, если в висцеральных жировых клетках сальника липолиз активировал филогенетически более ранний гормон. Инсулин блокирует липолиз только в подкожных адипоцитах; 4) биохимическая активность пальмитиновой насыщенной ЖК (НЖК) низкая; высока она у олеиновой мононенасыщенной ЖК (МЖК). В становлении биологической функции локомоции инсулин экспрессирует синтез de novo двух ферментов: пальмитоил-КоА-элонгазы и стеарил-КоА-десатуразы. Они превращают всю синтезированную гепатоцитами пальмитиновую НЖК в высокоактивную олеиновую МЖК; 5) инсулин превращает в олеиновую МЖК только пальмитиновую НЖК, которую гепатоциты синтезировали из глюкозы de novo, но не НЖК плотоядной (мясной) пищи; 6) клетки поглощают ЖК в форме олеиновых триглицеридов путем апоЕ/В-100-эндоцитоза много активнее, чем пальмитиновые триглицериды путем апоВ-100-эндоцитоза; 7) недостаток наработки митохондриями АТФ в биологической функции трофологии при окислении митохондриями пальмитиновой НЖК приходится компенсировать путем активации биологической функции адаптации, биологической реакции эндотрофии, липолиза в висцеральных жировых клетках сальника и освобождения НЭЖК. Высокий уровень в крови НЭЖК – наиболее частая причина синдрома резистентности к инсулину.
Ключевые слова: инсулин, жирные кислоты, глюкоза, резистентность к инсулину, филогенез.
Ключевые слова: инсулин, жирные кислоты, глюкоза, резистентность к инсулину, филогенез.
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Biological role of insulin is metabolic processes regulation of, firstly, fatty acids (FA) and, secondly, of glucose. Insulin is known to regulate phylogenetic transformation of sarcophagous (ichthyophagous) animals of the ocean to herbivorous animals on land. Seven etiologic factors of insulin resistance syndrome: 1) somatic cells do not absorb glucose while they are able to absorb FA; FA absorption is always more active. To force cells to absorb glucose insulin deprives them of FA in non-esterified FA form (NEFA) absorption opportunity; 2) insulin warrants the highest mitochondria productivity in adenosine triphosphate (ATP) production and high animal unit kinetics parameters. Insulin indirectly regulates glucose metabolism; glucose is a substrate for olein monounsaturated FA synthesis. Among long chain FA mitochondria oxidize it most actively, producing ATP; 3) insulin cannot block NEFA release if lipolysis in visceral fatty omentum cells was activated by phylogenetically earlier hormone. Isulin blocks lipolysis only in subcutaneous adipocytes; 4) biochemical activity of palmitic saturated FA (SFA) is low; it is high in olein monounsaturated FA (MFA). In such biological function as locomotion development insulin expresses de novo synthesis of two enzymes: palmytoil-CoA-elongase and stearoyl-CoA-desaturase. These enzymes turn all hepatocyte synthesized palmitate SFA to highly active olein MFA; 5) insulin turns to olein MFA only palmitate SFA which was synthesized from glucose de novo but not from meat food SFA; 6) cells absorb FA in olein triglycerides form by apoE/В-100-endocytosis more actively than palmitate triglycerides by apoВ-100-endocytosis; 7) lack of ATP mitochondria production in trophology biologic function in mitochondria oxidation of palmitate SFA is to be compensated by biologic adaptation function activation, biologic endotrophy reaction, lypolysis in visceral fatty omentum cells and NEFA release. High NEFA serum level is the most common reason for insulin resistance syndrome.
Key words: insulin, fatty acids, glucose, insulin resistance, phylogenesis.
Key words: insulin, fatty acids, glucose, insulin resistance, phylogenesis.
Полный текст
Список литературы
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1. Tejlor D. Zdorov'e po Darvinu. Pochemu my boleem i kak eto svyazano s evolyuciej. M.: Al'pina Pablisher, 2016. [in Russian]
2. Irawati D, Mamo J, Dhaliwal SS et al. Plasma triglyceride and high density lipoprotein cholesterol are poor surrogate markers of pro-atherogenic chylomicron remnant homeostasis in subjects with the metabolic syndrome. Lipids Health Dis 2016; 15 (1): 169. https://search.crossref.org/funding?q=501100001797...4
3. Titov V.N. Klinicheskaya biohimiya. Kurs lekcij. M.: INFRA-M, 2017. [in Russian]
4. Botham KM, Wheeler-Jones CP. Postprandial lipoproteins and the molecular regulation of vascular homeostasis. Prog Lipid Res 2013; 52 (4): 446–64.
5. Zakiev ER, Nikiforov NG, Orekhov AN. Cell-Based models for development of antiatherosclerotic therapies. Biomed Res Int 2017; 2017: 5198723. https://www.ncbi.nlm.nih.gov/pubmed/28286766
6. Ugolev A.M. Estestvennye tekhnologii biologicheskih sistem. L.: Nauka, 1987. [in Russian]
7. Scheithauer TP, Dallinga-Thie GM, de Vos WM et al. Causality of small and large intestinal microbiota in weight regulation and insulin resistance. Mol Metab 2016; 5 (9): 759–70.
8. Bullon P, Marin-Aguilar F, Roman-Malo L. AMPK/Mitochondria in metabolic diseases. EXS 2016; 107: 129–52.
9. Goodpaster BH, Sparks LM. Metabolic flexibility in health and disease. Cell Metab 2017; 25 (5): 1027–36.
10. Garg SG, Martin WF. Mitochondria, the cell cycle, and the origin of sex via a syncytial eukaryote common ancestor. Genome Biol Evol 2016; 8 (6): 1950–70.
11. Jin ES, Beddow SA, Malloy CR, Samuel VT. Hepatic glucose production pathways after three days of a high-fat diet. Metabolism 2013; 62 (1): 152–62.
12. Buldak L, Dulava-Buldak A, Labuzek K, Okopien B. Effects of 90-day hypolipidemic treatment on insulin resistance, adipokines and proinflammatory cytokines in patients with mixed hyperlipidemia and impaired fasting glucose. Int J Clin Pharmacol Ther 2012; 50 (11): 805–13.
13. Okuyama H, Langsjoen PH, Ohara N et al. Medicines and vegetable oils as hidden causes of cardiovascular disease and diabetes. Pharmacology 2016; 98 (3–4): 134–70.
14. Titov V.N. Izofermenty stearil-koenzim A-desaturazy i dejstvie insulina v svete filogeneticheskoj teorii patologii. Oleinovaya zhirnaya kislota v realizacii biologicheskoj funkcii trofologii i lokomocii. Klin. laboratornaya diagnostika. 2013; 11: 16–26. [in Russian]
15. Lisicyn D.M., Razumovskij S.D., Tishenin M.A., Titov V.N. Kineticheskie parametry okisleniya ozonom individual'nyh zhirnyh kislot. Byulleten' eksperimental'noj biologii i mediciny. 2004; 138 (11): 517–9. [in Russian]
16. Capurso C, Capurso A. From excess adiposity to insulin resistance: the role of free fatty acids. Vascul Pharmacol 2012; 57 (2–4): 91–7.
17. Jeschke MG, Boehning D. Endoplasmic reticulum stress and insulin resistance post-trauma: similarities to type 2 diabetes. J Cell Mol Med 2012; 16 (3): 437–44.
18. Saltykova M.M. Adaptaciya k holodu kak sredstvo usileniya antioksidantnoj zashchity. Ros. fiziologich. zhurn. 2017; 103 (7): 712–26. [in Russian]
19. Kraegen EW, Cooney GJ, Ye J, Thompson AL. Triglycerides, fatty acids and insulin resistance – hyperinsulinemia. Exp Clin Endocrinol Diabetes 2001; 109 (4): S516–S526.
20. Valera LM, Ortega A, Bermudez B et al. A high-fat meal promotes lipid-load and apolipoprotein B-48 receptor transcriptional activity in circulating monocytes. Am J Clin Nutr 2011; 93 (5): 918–25.
21. Filipou A, Teng KT, Berry SE, Sanders TA. Palmitic acid in the sn-2 position of dietary triacylglycerols does not affect insulin secretion or glucose homeostasis in healthy men and women. Eur J Clin Nutr 2014; 68 (9): 1036–41.
22. Connor WE, Lin DS, Colvis C. Differential mobilization of fatty acids from adipose tissue. J Lipid Res 1996; 37: 290–8.
23. Longo G, Soto AM. Why do we need theories? Prog Biophys Mol Biol 2016; 122 (1): 4–10.
24. Li LO, Grevengoed TJ, Paul DS et al. Compartmentalized acyl-CoA metabolism in skeletal muscle regulates systemic glucose homeostasis. Diabetes 2015; 64 (1): 23–35.
25. Agren JJ, Ravandi A, Kuksis A, Steiner G. Structural and compositional changes in very low density lipoprotein triacylglycerols during basal lipolysis. Eur J Biochem 2002; 269 (24): 6223–32.
26. Bei F, JiaJ, Jia YQ et al. Long-term effect of early postnatal overnutrition on insulin resistance and serum fatty acid profiles in male rats. Lipids Health Dis 2015; 14: 96–109.
27. Titov V.N., Malyshev P.P., Amelyushkina V.A. i dr. Dejstvie statinov: aktivaciya lipoliza i pogloshcheniya insulinozavisimymi kletkami lipoproteinov ochen' nizkoj plotnosti, povyshenie biodostupnosti polienovyh zhirnyh kislot i ponizhenie holesterina lipoproteinov nizkoj plotnosti. Klin. laboratornaya diagnostika. 2015; 10: 4–12. [in Russian]
28. Van Capalleveen JC, Bernelot Moens SJ, Yang X et al. Apolipoprotein C-III levels and Incident coronary artery disease risk: the EPIC-Norfolk prospective population study. Arterioscler Thromb Vasc Biol 2017; 37 (6): 1206–12.
29. Drouin-Chartier JP, Tremblay AJ, Hogue JC et al. C-reactive protein levels are inversely correlated with the apolipoprotein B-48-containing triglyceride-rich lipoprotein production rate in insulin resistant men. Metabolism 2017; 68: 163–72.
30. Titov V.N., Saltykova M.M. Stanovlenie filogeneza funkcii metabolizma podkozhnyh insulinzavisimyh adipocitov. Etiologicheskij faktor i patogenez ozhireniya kak metabolicheskoj pandemii. Klin. laboratornaya diagnostika. 2017; 62 (1): 4–12. [in Russian]
31. Jesckhe MG, Finnerty CC, Herndon DN et al. Severe injury is associated with insulin resistance, endoplasmic reticulum stress response, and unfolded protein response. Ann Surg 2012; 255 (2): 370–8.
2. Irawati D, Mamo J, Dhaliwal SS et al. Plasma triglyceride and high density lipoprotein cholesterol are poor surrogate markers of pro-atherogenic chylomicron remnant homeostasis in subjects with the metabolic syndrome. Lipids Health Dis 2016; 15 (1): 169. https://search.crossref.org/funding?q=501100001797...4
3. Titov V.N. Klinicheskaya biohimiya. Kurs lekcij. M.: INFRA-M, 2017. [in Russian]
4. Botham KM, Wheeler-Jones CP. Postprandial lipoproteins and the molecular regulation of vascular homeostasis. Prog Lipid Res 2013; 52 (4): 446–64.
5. Zakiev ER, Nikiforov NG, Orekhov AN. Cell-Based models for development of antiatherosclerotic therapies. Biomed Res Int 2017; 2017: 5198723. https://www.ncbi.nlm.nih.gov/pubmed/28286766
6. Ugolev A.M. Estestvennye tekhnologii biologicheskih sistem. L.: Nauka, 1987. [in Russian]
7. Scheithauer TP, Dallinga-Thie GM, de Vos WM et al. Causality of small and large intestinal microbiota in weight regulation and insulin resistance. Mol Metab 2016; 5 (9): 759–70.
8. Bullon P, Marin-Aguilar F, Roman-Malo L. AMPK/Mitochondria in metabolic diseases. EXS 2016; 107: 129–52.
9. Goodpaster BH, Sparks LM. Metabolic flexibility in health and disease. Cell Metab 2017; 25 (5): 1027–36.
10. Garg SG, Martin WF. Mitochondria, the cell cycle, and the origin of sex via a syncytial eukaryote common ancestor. Genome Biol Evol 2016; 8 (6): 1950–70.
11. Jin ES, Beddow SA, Malloy CR, Samuel VT. Hepatic glucose production pathways after three days of a high-fat diet. Metabolism 2013; 62 (1): 152–62.
12. Buldak L, Dulava-Buldak A, Labuzek K, Okopien B. Effects of 90-day hypolipidemic treatment on insulin resistance, adipokines and proinflammatory cytokines in patients with mixed hyperlipidemia and impaired fasting glucose. Int J Clin Pharmacol Ther 2012; 50 (11): 805–13.
13. Okuyama H, Langsjoen PH, Ohara N et al. Medicines and vegetable oils as hidden causes of cardiovascular disease and diabetes. Pharmacology 2016; 98 (3–4): 134–70.
14. Titov V.N. Izofermenty stearil-koenzim A-desaturazy i dejstvie insulina v svete filogeneticheskoj teorii patologii. Oleinovaya zhirnaya kislota v realizacii biologicheskoj funkcii trofologii i lokomocii. Klin. laboratornaya diagnostika. 2013; 11: 16–26. [in Russian]
15. Lisicyn D.M., Razumovskij S.D., Tishenin M.A., Titov V.N. Kineticheskie parametry okisleniya ozonom individual'nyh zhirnyh kislot. Byulleten' eksperimental'noj biologii i mediciny. 2004; 138 (11): 517–9. [in Russian]
16. Capurso C, Capurso A. From excess adiposity to insulin resistance: the role of free fatty acids. Vascul Pharmacol 2012; 57 (2–4): 91–7.
17. Jeschke MG, Boehning D. Endoplasmic reticulum stress and insulin resistance post-trauma: similarities to type 2 diabetes. J Cell Mol Med 2012; 16 (3): 437–44.
18. Saltykova M.M. Adaptaciya k holodu kak sredstvo usileniya antioksidantnoj zashchity. Ros. fiziologich. zhurn. 2017; 103 (7): 712–26. [in Russian]
19. Kraegen EW, Cooney GJ, Ye J, Thompson AL. Triglycerides, fatty acids and insulin resistance – hyperinsulinemia. Exp Clin Endocrinol Diabetes 2001; 109 (4): S516–S526.
20. Valera LM, Ortega A, Bermudez B et al. A high-fat meal promotes lipid-load and apolipoprotein B-48 receptor transcriptional activity in circulating monocytes. Am J Clin Nutr 2011; 93 (5): 918–25.
21. Filipou A, Teng KT, Berry SE, Sanders TA. Palmitic acid in the sn-2 position of dietary triacylglycerols does not affect insulin secretion or glucose homeostasis in healthy men and women. Eur J Clin Nutr 2014; 68 (9): 1036–41.
22. Connor WE, Lin DS, Colvis C. Differential mobilization of fatty acids from adipose tissue. J Lipid Res 1996; 37: 290–8.
23. Longo G, Soto AM. Why do we need theories? Prog Biophys Mol Biol 2016; 122 (1): 4–10.
24. Li LO, Grevengoed TJ, Paul DS et al. Compartmentalized acyl-CoA metabolism in skeletal muscle regulates systemic glucose homeostasis. Diabetes 2015; 64 (1): 23–35.
25. Agren JJ, Ravandi A, Kuksis A, Steiner G. Structural and compositional changes in very low density lipoprotein triacylglycerols during basal lipolysis. Eur J Biochem 2002; 269 (24): 6223–32.
26. Bei F, JiaJ, Jia YQ et al. Long-term effect of early postnatal overnutrition on insulin resistance and serum fatty acid profiles in male rats. Lipids Health Dis 2015; 14: 96–109.
27. Titov V.N., Malyshev P.P., Amelyushkina V.A. i dr. Dejstvie statinov: aktivaciya lipoliza i pogloshcheniya insulinozavisimymi kletkami lipoproteinov ochen' nizkoj plotnosti, povyshenie biodostupnosti polienovyh zhirnyh kislot i ponizhenie holesterina lipoproteinov nizkoj plotnosti. Klin. laboratornaya diagnostika. 2015; 10: 4–12. [in Russian]
28. Van Capalleveen JC, Bernelot Moens SJ, Yang X et al. Apolipoprotein C-III levels and Incident coronary artery disease risk: the EPIC-Norfolk prospective population study. Arterioscler Thromb Vasc Biol 2017; 37 (6): 1206–12.
29. Drouin-Chartier JP, Tremblay AJ, Hogue JC et al. C-reactive protein levels are inversely correlated with the apolipoprotein B-48-containing triglyceride-rich lipoprotein production rate in insulin resistant men. Metabolism 2017; 68: 163–72.
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Авторы
В.Н.Титов
ФГБУ «Национальный медицинский исследовательский центр кардиологии» Минздрава России. 121552, Россия, Москва, ул. 3-я Черепковская, д. 15А
vn_titov@mail.ru
ФГБУ «Национальный медицинский исследовательский центр кардиологии» Минздрава России. 121552, Россия, Москва, ул. 3-я Черепковская, д. 15А
________________________________________________
V.N.Titov
National Medical Research Center of Cardiology of the Ministry of Health of the Russian Federation. 121552, Russian Federation, Moscow, ul. 3-ia Cherepkovskaia, d. 15a
vn_titov@mail.ru
National Medical Research Center of Cardiology of the Ministry of Health of the Russian Federation. 121552, Russian Federation, Moscow, ul. 3-ia Cherepkovskaia, d. 15a
vn_titov@mail.ru
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