References

problendo

Проблемы Эндокринологии

Problems of Endocrinology

0375-96602308-1430

Endocrinology Research Centre

10.14341/probl201157664-70

problendo-4635

Research Article

Статьи

Articles

Воспаление жировой ткани (часть 5). Взаимосвязь с физиологической инсулинорезистентностью

Inflammation of adipose tissue (Part 5). The relationship with physiological insulin resistance

Shvarts

V Ia

akupunktschwarz@t-online.de

Kolberg

2011

15122011

576

ТОМ 57, №6 (2011)

6470

2011

Shvarts V.I., Kolberg B.

Данная работа распространяется под лицензией Creative Commons Attribution 4.0.

This work is licensed under a Creative Commons Attribution 4.0 License.

https://www.probl-endojournals.ru/jour/article/view/4635

В обзоре описаны результаты исследований, показывающие инсулинорезистентность как фактор физиологический, обеспечивающий энергетическими субстратами работающие органы и ткани. При физической деятельности развивается инсулинорезистентность жировых и печеночных клеток с последующим повышением выделения в кровь глюкозы и липидов. Одновременно усиливается действие инсулина в мышечных клетках, что способствует усвоению этих веществ. Противоположное изменение чувствительности к инсулину различных клеток обеспечивается повышением секреции интерлейкина-6 при мышечной активности. При иммунных процессах развивается инсулинорезистентность адипоцитов, гепатоцитов, мышечных клеток, что повышает уровень в крови глюкозы и липидов и обеспечивает возросшую потребность иммунных клеток. Механизмом развития инсулинорезистентности при иммунных процессах является активация Тoll-подобных рецепторов. При беременности повышение секреции плацентарных гормонов приводит к нарушению действия инсулина в периферических тканях, обеспечивая энергетическими и пластическими субстратами растущий плод. Состояние воспаления жировой ткани сопровождается как физиологической, так и патологической инсулинорезистентностью. Воспаление жировой ткани обсуждается как фактор, способствующий трансформации физиологической инсулинорезистентности в патологическую.

This review contains the results of investigations representing insulin resistance as a physiological factor that ensures supply of macroergic substrates for the functioning organs and tissues. Physical activity promotes the development of insulin resistance in adipose and renal cells with the resulting enhancement of the secretion of glucose and lipids into blood. Simultaneously, the insulin action in muscular cells increases which facilitates utilization of these compounds. The opposite change in insulin sensitivity of different cells is mediated through a rise in interleukin-6 secretion during muscular activity. The immune processes are associated with the development of insulin resistance in adipocytes, hepatocytes, and myocytes leading to the elevation of blood glucose and lipid levels that accounts for the enhanced requirement of immune cells in these compounds. The mechanism underlying the development of insulin resistance during immune processes consists of activation of Toll-like receptors. Increased secretion of placental hormones in the course of gestation causes disturbances in the insulin action in the peripheral tissues and thereby ensures supply of energy-rich and plastic substrates for the growing fetus. Inflammation of adipose tissue is associated with physiological and pathological insulin resistance. This condition is discussed as a factor contributing to the transformation of physiological insulin resistance to pathological one.

жировая тканьвоспалениеожирениеинсулинорезистентностьфизическая деятельностьиммунные процессыбеременность

adipose tissueinflammationadiposityinsulin resistancephysical activityimmune processes gestation

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The authors declare that there are no conflicts of interest present.