ArticleThe Journal of endocrinology2011
The adaptor protein APPL1 increases glycogen accumulation in rat skeletal muscle through activation of the PI3-kinase signalling pathway.
Article in The Journal of endocrinology, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.
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Who cites it
23 citing papers in PubMed, 42 citations in OpenAlex.
- Adiponectin Resistance in Obesity: Adiponectin Leptin/Insulin Interaction.Advances in experimental medicine and biology · 2024Review
- CORP: Gene delivery into murine skeletal muscle using in vivo electroporation.Journal of applied physiology (Bethesda, Md. : 1985) · 2022Review
- Regulation of mitochondrial metabolism in murine skeletal muscle by the medium-chain fatty acid receptor Gpr84.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2019Article
- Disrupted sphingolipid metabolism following acute clozapine and olanzapine administration.Journal of biomedical science · 2018Article
- Activation of hypothalamic RIP-Cre neurons promotes beiging of WAT via sympathetic nervous system.EMBO reports · 2018Article
- Integration of GPCR Signaling and Sorting from Very Early Endosomes via Opposing APPL1 Mechanisms.Cell reports · 2017Article
- Protein kinase N2 regulates AMP kinase signaling and insulin responsiveness of glucose metabolism in skeletal muscle.American journal of physiology. Endocrinology and metabolism · 2017Article
- APPL1 prevents pancreatic beta cell death and inflammation by dampening NFκB activation in a mouse model of type 1 diabetes.Diabetologia · 2017Article
- Alternative splicing of the OCC-1 gene generates three splice variants and a novel exonic microRNA, which regulate the Wnt signaling pathway.RNA (New York, N.Y.) · 2017Article
- Adipose tissue in control of metabolism.The Journal of endocrinology · 2016Review
- Disparate metabolic response to fructose feeding between different mouse strains.Scientific reports · 2015Article
- The role of adiponectin signaling in metabolic syndrome and cancer.Reviews in endocrine & metabolic disorders · 2014Review
- APPL1 potentiates insulin sensitivity by facilitating the binding of IRS1/2 to the insulin receptor.Cell reports · 2014Article
- Regulation of adiponectin multimerization, signaling and function.Best practice & research. Clinical endocrinology & metabolism · 2014Review
- Contrasting metabolic effects of medium- versus long-chain fatty acids in skeletal muscle.Journal of lipid research · 2013Article
- Deficiency of APPL1 in mice impairs glucose-stimulated insulin secretion through inhibition of pancreatic beta cell mitochondrial function.Diabetologia · 2013Article
- Mouse strain-dependent variation in obesity and glucose homeostasis in response to high-fat feeding.Diabetologia · 2013Article
- What is the role of adiponectin in obesity related non-alcoholic fatty liver disease?World journal of gastroenterology · 2013Review
- Article
- Overexpression of the adiponectin receptor AdipoR1 in rat skeletal muscle amplifies local insulin sensitivity.Endocrinology · 2012Article
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Authors and funding
9 authors at 5 institutions in 3 countries.
Funding
Abstract
APPL1 is an adaptor protein that binds to both AKT and adiponectin receptors and is hypothesised to mediate the effects of adiponectin in activating downstream effectors such as AMP-activated protein kinase (AMPK). We aimed to establish whether APPL1 plays a physiological role in mediating glycogen accumulation and insulin sensitivity in muscle and the signalling pathways involved. In vivo electrotransfer of cDNA- and shRNA-expressing constructs was used to over-express or silence APPL1 for 1 week in single tibialis cranialis muscles of rats. Resulting changes in glucose and lipid metabolism and signalling pathway activation were investigated under basal conditions and in high-fat diet (HFD)- or chow-fed rats under hyperinsulinaemic-euglycaemic clamp conditions. APPL1 over-expression (OE) caused an increase in glycogen storage and insulin-stimulated glycogen synthesis in muscle, accompanied by a modest increase in glucose uptake. Glycogen synthesis during the clamp was reduced by HFD but normalised by APPL1 OE. These effects are likely explained by APPL1 OE-induced increase in basal and insulin-stimulated phosphorylation of IRS1, AKT, GSK3β and TBC1D4. On the contrary, APPL1 OE, such as HFD, reduced AMPK and acetyl-CoA carboxylase phosphorylation and PPARγ coactivator-1α and uncoupling protein 3 expression. Furthermore, APPL1 silencing caused complementary changes in glycogen storage and phosphorylation of AMPK and PI3-kinase pathway intermediates. Thus, APPL1 may provide a means for crosstalk between adiponectin and insulin signalling pathways, mediating the insulin-sensitising effects of adiponectin on muscle glucose disposal. These effects do not appear to require AMPK. Activation of signalling mediated via APPL1 may be beneficial in overcoming muscle 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.