ArticleThe Biochemical journal2013
AS160 deficiency causes whole-body insulin resistance via composite effects in multiple tissues.
Article in The Biochemical journal, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 43 papers, 1 of them a synthesis that pooled it.
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Who cites it
43 citing papers in PubMed, 1 synthesis or guideline pooled it, 91 citations in OpenAlex.
- Genetic variants modulate gene expression statin response in human lymphoblastoid cell lines.BMC genomics · 2020Pooled it
- Trial
- AS160 Overexpression Protects Against β-Cell Failure in Hyperglycemic Mice by Interacting With HSPA8 to Regulate Mitophagy.Acta physiologica (Oxford, England) · 2026Article
- Nuclear entry of AS160 as a transcriptional regulator of satellite cells for muscle regeneration.Nature communications · 2025Article
- Skeletal muscle from TBC1D4 p.Arg684Ter variant carriers is severely insulin resistant but exhibits normal metabolic responses during exercise.Nature metabolism · 2024Article
- Effect of acute exercise in carriers of TBC1D4 mutation.Nature metabolism · 2024Article
- Phosphorylation of AS160-serine 704 is not essential for exercise-increase in insulin-stimulated glucose uptake by skeletal muscles from female or male rats.American journal of physiology. Endocrinology and metabolism · 2024Article
- Complex rearrangement in TBC1D4 in an individual with diabetes due to severe insulin resistance syndrome.European journal of human genetics : EJHG · 2024Article
- Deletion of Tbc1d4/As160 abrogates cardiac glucose uptake and increases myocardial damage after ischemia/reperfusion.Cardiovascular diabetology · 2023Article
- A Cardiac Amino-Terminal GRK2 Peptide Inhibits Maladaptive Adipocyte Hypertrophy and Insulin Resistance During Diet-Induced Obesity.JACC. Basic to translational science · 2022Article
- AKT ISOFORMS-AS160-GLUT4: The defining axis of insulin resistance.Reviews in endocrine & metabolic disorders · 2021Review
- Physical activity attenuates postprandial hyperglycaemia in homozygous TBC1D4 loss-of-function mutation carriers.Diabetologia · 2021Article
- A peptide of the amino-terminus of GRK2 induces hypertrophy and yet elicits cardioprotection after pressure overload.Journal of molecular and cellular cardiology · 2021Article
- Insulin-stimulated glucose uptake partly relies on p21-activated kinase (PAK)2, but not PAK1, in mouse skeletal muscle.The Journal of physiology · 2020Article
- Olive Leaf Polyphenols (OLPs) Stimulate GLUT4 Expression and Translocation in the Skeletal Muscle of Diabetic Rats.International journal of molecular sciences · 2020Article
- Glucose transporters in adipose tissue, liver, and skeletal muscle in metabolic health and disease.Pflugers Archiv : European journal of physiology · 2020Review
- Glucose transporters in cardiovascular system in health and disease.Pflugers Archiv : European journal of physiology · 2020Review
- Excess Accumulation of Lipid Impairs Insulin Sensitivity in Skeletal Muscle.International journal of molecular sciences · 2020Review
- In vivo glucoregulation and tissue-specific glucose uptake in female Akt substrate 160 kDa knockout rats.PloS one · 2020Article
- Article
Corrections and comments
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Authors and funding
9 authors at 3 institutions in 2 countries.
Funding
Abstract
AS160 (Akt substrate of 160 kDa) is a Rab GTPase-activating protein implicated in insulin control of GLUT4 (glucose transporter 4) trafficking. In humans, a truncation mutation (R363X) in one allele of AS160 decreased the expression of the protein and caused severe postprandial hyperinsulinaemia during puberty. To complement the limited studies possible in humans, we generated an AS160-knockout mouse. In wild-type mice, AS160 expression is relatively high in adipose tissue and soleus muscle, low in EDL (extensor digitorum longus) muscle and detectable in liver only after enrichment. Despite having lower blood glucose levels under both fasted and random-fed conditions, the AS160-knockout mice exhibited insulin resistance in both muscle and liver in a euglycaemic clamp study. Consistent with this paradoxical phenotype, basal glucose uptake was higher in AS160-knockout primary adipocytes and normal in isolated soleus muscle, but their insulin-stimulated glucose uptake and overall GLUT4 levels were markedly decreased. In contrast, insulin-stimulated glucose uptake and GLUT4 levels were normal in EDL muscle. The liver also contributes to the AS160-knockout phenotype via hepatic insulin resistance, elevated hepatic expression of phosphoenolpyruvate carboxykinase isoforms and pyruvate intolerance, which are indicative of increased gluconeogenesis. Overall, as well as its catalytic function, AS160 influences expression of other proteins, and its loss deregulates basal and insulin-regulated glucose homoeostasis, not only in tissues that normally express AS160, but also by influencing liver function.
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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.