ArticleThe Journal of physiology2008
In vivo inhibition of focal adhesion kinase causes insulin resistance.
Article in The Journal of physiology, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 papers.
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Who cites it
26 citing papers in PubMed, 47 citations in OpenAlex.
- The focal adhesion kinases regulate leptin action and the weight reducing effect of HDAC6 inhibition.Nature communications · 2026Article
- Mechanomedicine for Addressing Skeletal Muscle Insulin Resistance.Endocrine reviews · 2025Review
- Focal Adhesion Kinase Orchestrates GLUT4 Translocation and Glucose Uptake via Cytoskeletal Turnover in Primary Adipocytes.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2025Article
- Hidden pathway: the role of extracellular matrix in type 2 diabetes mellitus-related sarcopenia.Frontiers in endocrinology · 2025Review
- Mechanical Stretch Control of Adipocyte AKT Signaling and the Role of FAK and ROCK Mechanosensors.Bioengineering (Basel, Switzerland) · 2024Article
- Link between insulin resistance and skeletal muscle extracellular matrix remodeling.Endocrine connections · 2023Review
- Older postmenopausal women with lower lean mass have hypermethylated sites in the PI3K-Akt pathway.Frontiers in physiology · 2023Article
- Hepatocyte phosphatase DUSP22 mitigates NASH-HCC progression by targeting FAK.Nature communications · 2022Article
- Involvement of the extracellular matrix and integrin signalling proteins in skeletal muscle glucose uptake.The Journal of physiology · 2022Review
- The association of laminin levels with insulin resistance and non-alcoholic hepatosteatosis.Diabetology & metabolic syndrome · 2021Article
- Fat mass- and obesity-associated (FTO) gene promoted myoblast differentiation through the focal adhesion pathway in chicken.3 Biotech · 2020Article
- Genetic deletion of microRNA biogenesis in muscle cells reveals a hierarchical non-clustered network that controls focal adhesion signaling during muscle regeneration.Molecular metabolism · 2020Article
- ADAMTS9 Regulates Skeletal Muscle Insulin Sensitivity Through Extracellular Matrix Alterations.Diabetes · 2019Article
- Multifaceted Interweaving Between Extracellular Matrix, Insulin Resistance, and Skeletal Muscle.Cells · 2018Review
- The Vasculature in Prediabetes.Circulation research · 2018Review
- FAK tyrosine phosphorylation is regulated by AMPK and controls metabolism in human skeletal muscle.Diabetologia · 2018Article
- Integrin-Linked Kinase Is Necessary for the Development of Diet-Induced Hepatic Insulin Resistance.Diabetes · 2017Article
- The extracellular matrix and insulin resistance.Trends in endocrinology and metabolism: TEM · 2015Review
- Integrin α1-null mice exhibit improved fatty liver when fed a high fat diet despite severe hepatic insulin resistance.The Journal of biological chemistry · 2015Article
- Paxillin and focal adhesion kinase colocalise in human skeletal muscle and its associated microvasculature.Histochemistry and cell biology · 2014Article
Corrections and comments
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Authors and funding
3 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Focal adhesion kinase (FAK), a non-receptor tyrosine kinase, has recently been implicated in the regulation of insulin resistance in vitro. However, its in vivo validation has not been attempted due to lethality of FAK knockout. Hence, to ascertain the role of FAK in the development of insulin resistance in vivo, we have down-regulated FAK expression by delivering FAK-specific small interfering RNA (siRNA) in mice using hydrodynamic tail vein injection. Here, we show for the first time that FAK silencing (57 +/- 0.05% in muscle and 80 +/- 0.08% in liver) exacerbates insulin signalling and causes hyperglycaemia (251.68 +/- 8.1 mg dl(-1)) and hyperinsulinaemia (3.48 +/- 0.06 ng ml(-1)) in vivo. FAK-silenced animals are less glucose tolerant and have physiological and biochemical parameters similar to that of high fat diet (HFD)-fed insulin-resistant animals. Phosphorylation and expression of insulin receptor substrate 1 (IRS-1) was attenuated by 40.2 +/- 0.03% and 35.2 +/- 0.6% in muscle and 52.3 +/- 0.04% and 40.2 +/- 0.03% in liver in FAK-silenced mice. Akt-Ser473-phosphorylation decreased in muscle and liver (50.3 +/- 0.03% and 70.2 +/- 0.02%, respectively) in FAK-silenced mice. This, in part, explains the mechanism of development of insulin resistance in FAK-silenced mice. The present study provides direct evidence that FAK is a crucial mediator of insulin resistance in vivo. Considering the lethality of FAK gene knockout the approach of this study will provide a new strategy for in vivo inhibition of FAK. Furthermore, the study should certainly motivate chemists to synthesize new chemical entities for FAK activation. This may shed light on new drug development against insulin resistance.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.