Insulin resistance: the conflict between biological settings of energy metabolism and human lifestyle (a glance at the problem from evolutionary viewpoint)

A biological function of the phylogenetically late humoral mediator insulin is to provide energy substrates for locomotion, i.e. movement resulting from contraction of striated muscles. Insulin is able to meet this evolutionary demand of an organism by means of the effective ATP production in the mi...

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Autores principales: Vladimir Nicolaevich Titov, Vladimir Pavlovich Shirinsky
Formato: article
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RU
Publicado: Endocrinology Research Centre 2016
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Acceso en línea:https://doaj.org/article/4f6f441151db41288db05900b8e6cdae
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spelling oai:doaj.org-article:4f6f441151db41288db05900b8e6cdae2021-11-14T09:00:20ZInsulin resistance: the conflict between biological settings of energy metabolism and human lifestyle (a glance at the problem from evolutionary viewpoint)2072-03512072-037810.14341/DM7959https://doaj.org/article/4f6f441151db41288db05900b8e6cdae2016-11-01T00:00:00Zhttps://www.dia-endojournals.ru/jour/article/view/7959https://doaj.org/toc/2072-0351https://doaj.org/toc/2072-0378A biological function of the phylogenetically late humoral mediator insulin is to provide energy substrates for locomotion, i.e. movement resulting from contraction of striated muscles. Insulin is able to meet this evolutionary demand of an organism by means of the effective ATP production in the mitochondria. Exogenous fatty acids, optimised endogenous fatty acids produced from glucose and glucose itself are the major substrates for ATP synthesis. Cells stimulated by insulin produce ω-9 С18:1 oleic acid from glucose. This fatty acid is oxidised by the mitochondria at a higher rate than exogenous and endogenous C16:0 palmitic fatty acid. In the normal state of insulin system and mitochondria, the frequent cause of insulin resistance is the non-optimal properties of dietary fatty acids supplied for oxidation by the mitochondria. Dietary excess of saturated palmitic fatty acid over monogenic oleic fatty acid causes insulin resistance to develop. Insulin resistance syndrome is the condition of in vivo energy deficiency and insufficient production of ATP for the realisation of the biological adaptation and compensation. Insulin effectively inhibits lipolysis only in phylogenetically late subcutaneous adipocytes but not in phylogenetically early visceral fat cells of the omentum. Discrepancy in the regulation of energy substrate metabolism against the background of a ‘relative biological perfection’ of higher mammals is the aetiological basis of insulin resistance.Vladimir Nicolaevich TitovVladimir Pavlovich ShirinskyEndocrinology Research Centrearticleinsulininsulin resistanceatppalmitic acidoleic acidbiological adaptationglucoseNutritional diseases. Deficiency diseasesRC620-627ENRUСахарный диабет, Vol 19, Iss 4, Pp 286-294 (2016)
institution DOAJ
collection DOAJ
language EN
RU
topic insulin
insulin resistance
atp
palmitic acid
oleic acid
biological adaptation
glucose
Nutritional diseases. Deficiency diseases
RC620-627
spellingShingle insulin
insulin resistance
atp
palmitic acid
oleic acid
biological adaptation
glucose
Nutritional diseases. Deficiency diseases
RC620-627
Vladimir Nicolaevich Titov
Vladimir Pavlovich Shirinsky
Insulin resistance: the conflict between biological settings of energy metabolism and human lifestyle (a glance at the problem from evolutionary viewpoint)
description A biological function of the phylogenetically late humoral mediator insulin is to provide energy substrates for locomotion, i.e. movement resulting from contraction of striated muscles. Insulin is able to meet this evolutionary demand of an organism by means of the effective ATP production in the mitochondria. Exogenous fatty acids, optimised endogenous fatty acids produced from glucose and glucose itself are the major substrates for ATP synthesis. Cells stimulated by insulin produce ω-9 С18:1 oleic acid from glucose. This fatty acid is oxidised by the mitochondria at a higher rate than exogenous and endogenous C16:0 palmitic fatty acid. In the normal state of insulin system and mitochondria, the frequent cause of insulin resistance is the non-optimal properties of dietary fatty acids supplied for oxidation by the mitochondria. Dietary excess of saturated palmitic fatty acid over monogenic oleic fatty acid causes insulin resistance to develop. Insulin resistance syndrome is the condition of in vivo energy deficiency and insufficient production of ATP for the realisation of the biological adaptation and compensation. Insulin effectively inhibits lipolysis only in phylogenetically late subcutaneous adipocytes but not in phylogenetically early visceral fat cells of the omentum. Discrepancy in the regulation of energy substrate metabolism against the background of a ‘relative biological perfection’ of higher mammals is the aetiological basis of insulin resistance.
format article
author Vladimir Nicolaevich Titov
Vladimir Pavlovich Shirinsky
author_facet Vladimir Nicolaevich Titov
Vladimir Pavlovich Shirinsky
author_sort Vladimir Nicolaevich Titov
title Insulin resistance: the conflict between biological settings of energy metabolism and human lifestyle (a glance at the problem from evolutionary viewpoint)
title_short Insulin resistance: the conflict between biological settings of energy metabolism and human lifestyle (a glance at the problem from evolutionary viewpoint)
title_full Insulin resistance: the conflict between biological settings of energy metabolism and human lifestyle (a glance at the problem from evolutionary viewpoint)
title_fullStr Insulin resistance: the conflict between biological settings of energy metabolism and human lifestyle (a glance at the problem from evolutionary viewpoint)
title_full_unstemmed Insulin resistance: the conflict between biological settings of energy metabolism and human lifestyle (a glance at the problem from evolutionary viewpoint)
title_sort insulin resistance: the conflict between biological settings of energy metabolism and human lifestyle (a glance at the problem from evolutionary viewpoint)
publisher Endocrinology Research Centre
publishDate 2016
url https://doaj.org/article/4f6f441151db41288db05900b8e6cdae
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