Abstract

Our phylogenetic theory of pathology (algorrhythm of a disease development) is based on 1) a theory of biological functions and biological reactions in vivo; 2) regulation of biological functions, reactions, and metabolic processes at three phylogenetically different levels: а) autocrine (cell level); b) paracrine (in paracrine-regulated cell communities) and c) total organism level; 3) conceptions on formation of physiological and aphysiological processes («civilization» diseases) at various stages of phylogenesis. Universal pathogenesis of essential arterial hypertension and insulin resistance syndrome is based on functional discrepancy between phylogenetically early regulatory mechanisms at the level of paracrine cell communities and phylogenetically late regulation at the organism level. Pathogenic factors of this discrepancy are impaired biological functions of homeostasis, trophology, endoecology and adaptation. An increase in the content of unesterified fatty acids in the intercellular medium results from activation of lipolysis in paracrine community cells which cannot inhibit phylogenetically late insulin, but not in insulin-dependent adipocytes. The formation of pathogenesis of each metabolic pandemia occurs dynamically at different stages of phylogenesis.

Highlights

  • Universal pathogenesis of essential arterial hypertension and insulin resistance syndrome is based on functional discrepancy between phylogenetically early regulatory mechanisms

  • Понять общность механизмов становления в филогенезе патогенеза эссенциальная артериальная гипертония (ЭАГ) и синдрома ИР как несоответствие регуляции процессов гидродинамического АД и метаболизма жирных кислот (ЖК), ГЛЮ на уровне организма и в паракринных сообществах;

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Summary

Introduction

При ЭАГ развитие деструктивно-воспалительных процессов в иных паракринных сообществах, нарушение БФ эндоэкологии и адаптации, а также гомеостаза и трофологии, системное повышение АД в проксимальном отделе артериального русла и несоответствие механизмов регуляции АД на уровне организма и в паракринных сообществах клеток являются причиной поражения органов-мишеней. Что основой патогенеза ЭАГ является нарушение энергообразования (синтез аденозинтрифосфорной кислоты – АТФ) в клетках [37], которое вызвано нарушением метаболизма субстратов (ЖК+ГЛЮ) при переносе их в межклеточной среде, метаболизма в цитозоле, а возможно, и нарушением превращения ацетил-кофермента А в митохондриях [38].

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