Autophagy alterations in obesity, type 2 diabetes, and metabolic dysfunction-associated steatotic liver disease: the evidence from human studies

Result code in IS VaVaI

<a href="https://www.isvavai.cz/riv?ss=detail&h=RIV%2F67985823%3A_____%2F24%3A00598397" target="_blank" >RIV/67985823:_____/24:00598397 - isvavai.cz</a>

Result on the web

<a href="https://doi.org/10.1007/s11739-024-03700-w" target="_blank" >https://doi.org/10.1007/s11739-024-03700-w</a>

DOI - Digital Object Identifier

<a href="http://dx.doi.org/10.1007/s11739-024-03700-w" target="_blank" >10.1007/s11739-024-03700-w</a>

Result language

angličtina

Original language name

Autophagy alterations in obesity, type 2 diabetes, and metabolic dysfunction-associated steatotic liver disease: the evidence from human studies

Original language description

Autophagy is an evolutionarily conserved process that plays a pivotal role in the maintenance of cellular homeostasis and its impairment has been implicated in the pathogenesis of various metabolic diseases including obesity, type 2 diabetes (T2D), and metabolic dysfunction-associated steatotic liver disease (MASLD). This review synthesizes the current evidence from human studies on autophagy alterations under these metabolic conditions. In obesity, most data point to autophagy upregulation during the initiation phase of autophagosome formation, potentially in response to proinflammatory conditions in the adipose tissue. Autophagosome formation appears to be enhanced under hyperglycemic or insulin-resistant conditions in patients with T2D, possibly acting as a compensatory mechanism to eliminate damaged organelles and proteins. Other studies have proposed that prolonged hyperglycemia and disrupted insulin signaling hinder autophagic flux, resulting in the accumulation of dysfunctional cellular components that can contribute to β-cell dysfunction. Evidence from patients with MASLD supports autophagy inhibition in disease progression. Nevertheless, given the available data, it is difficult to ascertain whether autophagy is enhanced or suppressed in these conditions because the levels of autophagy markers depend on the overall metabolism of specific organs, tissues, experimental conditions, or disease duration. Owing to these constraints, determining whether the observed shifts in autophagic activity precede or result from metabolic diseases remains challenging. Additionally, autophagy-modulating strategies are shortly discussed. To conclude, more studies investigating autophagy impairment are required to gain a more comprehensive understanding of its role in the pathogenesis of obesity, T2D, and MASLD and to unveil novel therapeutic strategies for these conditions.

Czech name

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Czech description

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Type

J_imp - Article in a specialist periodical, which is included in the Web of Science database

CEP classification

—

OECD FORD branch

30308 - Nutrition, Dietetics

Project

<a href="/en/project/GF23-04100L" target="_blank" >GF23-04100L: The role of impaired autophagy and peroxisome function in NAFLD development and their targeted recovery for improved efficacy of n-3 fatty acids</a><br>

Continuities

I - Institucionalni podpora na dlouhodoby koncepcni rozvoj vyzkumne organizace

Publication year

2024

Confidentiality

S - Úplné a pravdivé údaje o projektu nepodléhají ochraně podle zvláštních právních předpisů

Name of the periodical

Internal and Emergency Medicine

ISSN

1828-0447

e-ISSN

1970-9366

Volume of the periodical

19

Issue of the periodical within the volume

5

Country of publishing house

DE - GERMANY

Number of pages

19

Pages from-to

1473-1491

UT code for WoS article

001263481600001

EID of the result in the Scopus database

2-s2.0-85197718129