2022
DOI: 10.3390/cells11162581
|View full text |Cite
|
Sign up to set email alerts
|

The Stress-Responsive microRNA-34a Alters Insulin Signaling and Actions in Adipocytes through Induction of the Tyrosine Phosphatase PTP1B

Abstract: Metabolic stresses alter the signaling and actions of insulin in adipocytes during obesity, but the molecular links remain incompletely understood. Members of the microRNA-34 (miR-34 family play a pivotal role in stress response, and previous studies showed an upregulation of miR-34a in adipose tissue during obesity. Here, we identified miR-34a as a new mediator of adipocyte insulin resistance. We confirmed the upregulation of miR-34a in adipose tissues of obese mice, which was observed in the adipocyte fracti… Show more

Help me understand this report

Search citation statements

Order By: Relevance

Paper Sections

Select...
1
1
1
1

Citation Types

0
4
0

Year Published

2022
2022
2024
2024

Publication Types

Select...
6

Relationship

0
6

Authors

Journals

citations
Cited by 6 publications
(4 citation statements)
references
References 63 publications
0
4
0
Order By: Relevance
“…For instance, SIRT1 overexpression could improve insulin sensitivity and reduce insulin resistance, 829,830 while the downregulation of SIRT1 inhibits insulin-stimulated glucose transport in adipocytes in particular by inhibiting insulin signaling. 831 Conversely, hepatic SIRT1 knockdown prevented fasting hyperglycemia by decreasing hepatic glucose production and increasing hepatic insulin responsiveness. 832 SIRT2 could also promote glucose-dependent hepatic glucose uptake by deacetylating K126 of glucokinase regulatory protein.…”
Section: ) Epilepsymentioning
confidence: 99%
“…For instance, SIRT1 overexpression could improve insulin sensitivity and reduce insulin resistance, 829,830 while the downregulation of SIRT1 inhibits insulin-stimulated glucose transport in adipocytes in particular by inhibiting insulin signaling. 831 Conversely, hepatic SIRT1 knockdown prevented fasting hyperglycemia by decreasing hepatic glucose production and increasing hepatic insulin responsiveness. 832 SIRT2 could also promote glucose-dependent hepatic glucose uptake by deacetylating K126 of glucokinase regulatory protein.…”
Section: ) Epilepsymentioning
confidence: 99%
“…In diet-induced obese mice, miR-34a targets fatty acid metabolism and cholesterol biosynthesis in the liver by targeting the histone deacetylase SIRT1, which has inhibitory roles in these processes [49]. miR-34 is up-regulated in adipose tissue of obese mice and in 3T3-L1 adipocyte cells in vitro, and is involved in insulin resistance [50]. Additionally, miR-34 is overexpressed during differentiation processes involved in cytokine-mediated β-cell dysfunction in non-obese diabetic mice [51].…”
Section: Discussionmentioning
confidence: 99%
“…Noncoding RNAs (Y. Chen et al, 2021; Han et al, 2022) possess a high safety and stability in naked or encapsulated form, while miRNAs increase their applicability through imperfect base pairing, and siRNA silencing requires an exact match to the target to be effective. Recently, there is growing interest in miRNAs as regulators of gene expression for next‐generation drugs (Garbo et al, 2022), and miRNAs therapeutics for a variety of diseases are rapidly developing, such as miRNAs‐based therapeutics in cancer immunotherapy (Beck et al, 2021; Kara et al, 2022), cardiovascular disease (Amin et al, 2021; Kumari et al, 2022), Type 2 Diabetes (T2D) (Chakraborty et al, 2014; Prattichizzo et al, 2021), metabolic dysfunction and obesity (Cornejo et al, 2022; Kiran et al, 2021), neuroinflammation (L. Su et al, 2022; Xia et al, 2022) and liver diseases (Gjorgjieva et al, 2019; X. Wang et al, 2021; Zhao et al, 2019), while the relative mechanism should be further clarified.…”
Section: Conclusion and Future Perspectivesmentioning
confidence: 99%