Epigenetic influence of long non-coding RNAs on the development of insulin resistance in metabolically associated fatty liver disease (part 1) DOI Creative Commons
А.Е. Абатуров, В.С. Березенко, Anna Nikulina

и другие.

INTERNATIONAL JOURNAL OF ENDOCRINOLOGY (Ukraine), Год журнала: 2025, Номер 21(2), С. 226 - 236

Опубликована: Апрель 1, 2025

Insulin resistance (IR) of metabolic origin is a pathological condition, which based on decrease in the response insulin-sensitive cells to insulin stimulation. It often accompanies metabolically associated fatty liver disease (MAFLD) and pathogenetic basis type 2 diabetes mellitus (T2DM). MAFLD with high risk developing T2DM, its presence increases likelihood T2DM by approximately two times during next five years patient’s life. Long non-coding RNAs are directly involved development IR, determination level their expression can significantly increase effectiveness diagnosis prognosis disease. Today, among assumptions explaining mechanisms IR development, lipocentric glucocentric hypotheses dominate. The hypothesis idea that consequence lipotoxic effect excessive intracellular content free acids derivatives (diacylglycerol, cera­mides). postulates due recurrent manifestations hyperglycemia, accompanied generation advanced glycation end products. Insulin-resistant tissue characterized increased activity gluconeogenesis, depletion glycogen depot decreased secretion triglycerides. Hepatic steatosis leads gluconeogenesis. Selective hepatic primary event systemic disruption insulin-­associated signaling pathway, subsequently peripheral tissues. Numerous long RNAs, such as H19, MALAT1, MEG3, MIAT, SRA, others, MAFLD. case resistance, Blnc1, EPB41L4A-AS1, HCG18, HOTAIR, HOTTIP, LncARSR, MAYA, NONMMUT031874.2. At same time, decreases represented B4GALT1-AS1/LncSHGL, MEG3.

Язык: Английский

Histones post-translational modifications associated with the development of metabolic dysfunction-associated fatty liver disease. Part 3. Histon acetylation DOI Creative Commons
А.Е. Абатуров, Anna Nikulina

GASTROENTEROLOGY, Год журнала: 2025, Номер 59(1), С. 56 - 67

Опубликована: Март 25, 2025

Based on the analysis of literature sources from Pubmed, MEDLINE, The Cochrane Library, Embase databases, authors article highlight general provisions regarding histone acetylation. They emphasize that it is acetylation lysine residue key post-translational modification histones by epigenetic mechanisms gene expression regulation. To date, at least 2000 human proteins have been identified can be modified residues About 1000 in liver tissue undergo Acetylation mediated acetyltransferases (HAT/KAT) and usually associated with active transcription due to its ability decondense chromatin. In contrast, deacetylases (HDAC/KDAC) remove acetyl group and, thus, restore compact form state target sites determined balance activity between processes deacetylation N-terminal regions molecules. Histone hyperacetylation caused both increased HAT/KAT decreased HDAC expression. catalyze transfer an acetyl-CoA epsilon-amino lysine, neutralizing positive charge weakening interaction DNA molecule. always chromatin opening activation transcription. increase representation acetylated markers progression metabolic dysfunction-associated fatty disease (MAFLD). A particularly high level (hyperacetylation) MAFLD noted K9, K14 K18 3. Today, determine region certain genes are considered as potential targets for drug treatment. Studying influence morphological changes development disorders basis will allow developing effective methods treatment patients MAFLD.

Язык: Английский

Процитировано

0
Epigenetic influence of long non-coding RNAs on the development of insulin resistance in metabolically associated fatty liver disease (part 1) DOI Creative Commons
А.Е. Абатуров, В.С. Березенко, Anna Nikulina

и другие.

INTERNATIONAL JOURNAL OF ENDOCRINOLOGY (Ukraine), Год журнала: 2025, Номер 21(2), С. 226 - 236

Опубликована: Апрель 1, 2025

Insulin resistance (IR) of metabolic origin is a pathological condition, which based on decrease in the response insulin-sensitive cells to insulin stimulation. It often accompanies metabolically associated fatty liver disease (MAFLD) and pathogenetic basis type 2 diabetes mellitus (T2DM). MAFLD with high risk developing T2DM, its presence increases likelihood T2DM by approximately two times during next five years patient’s life. Long non-coding RNAs are directly involved development IR, determination level their expression can significantly increase effectiveness diagnosis prognosis disease. Today, among assumptions explaining mechanisms IR development, lipocentric glucocentric hypotheses dominate. The hypothesis idea that consequence lipotoxic effect excessive intracellular content free acids derivatives (diacylglycerol, cera­mides). postulates due recurrent manifestations hyperglycemia, accompanied generation advanced glycation end products. Insulin-resistant tissue characterized increased activity gluconeogenesis, depletion glycogen depot decreased secretion triglycerides. Hepatic steatosis leads gluconeogenesis. Selective hepatic primary event systemic disruption insulin-­associated signaling pathway, subsequently peripheral tissues. Numerous long RNAs, such as H19, MALAT1, MEG3, MIAT, SRA, others, MAFLD. case resistance, Blnc1, EPB41L4A-AS1, HCG18, HOTAIR, HOTTIP, LncARSR, MAYA, NONMMUT031874.2. At same time, decreases represented B4GALT1-AS1/LncSHGL, MEG3.

Язык: Английский

Процитировано

0