Insulin and IGF-1 receptor autocrine loops are not required for Exendin-4 induced changes to pancreatic β-cell bioenergetic parameters and metabolism in BRIN-BD11 cells
•Chronic GLP-1R stimulation promotes β-cell metabolic reprogramming.•IGF-1R and IR are important for β-cell development, function and proliferation.•GLP-1 enhanced metabolic phenotype is independent of IR and IGF-1R autocrine loops.•Enhanced metabolism can contribute to GLP-1 pro-survival abilities....
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| Veröffentlicht in: | Peptides (New York, N.Y. : 1980) Jg. 100; S. 140 - 149 |
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| ISSN: | 0196-9781, 1873-5169, 1873-5169 |
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| Abstract | •Chronic GLP-1R stimulation promotes β-cell metabolic reprogramming.•IGF-1R and IR are important for β-cell development, function and proliferation.•GLP-1 enhanced metabolic phenotype is independent of IR and IGF-1R autocrine loops.•Enhanced metabolism can contribute to GLP-1 pro-survival abilities.
Pharmacological long lasting Glucagon-like peptide-1 (GLP-1) analogues, such as Exendin-4, have become widely used diabetes therapies. Chronic GLP-1R stimulation has been linked to β-cell protection and these pro-survival actions of GLP-1 are dependent on the activation of the mammalian target of rapamycin (mTOR) leading to accumulation of Hypoxia inducible factor 1 alpha (HIF-1α). Recent studies from our lab indicate that prolonged GLP-1R stimulation promotes metabolic reprograming of β-cells towards a highly glycolytic phenotype and activation of the mTOR/HIF-1α pathway was required for this action. We hypothesised that GLP-1 induced metabolic changes depend on the activation of mTOR and HIF-1α, in a cascade that occurs after triggering of a potential Insulin-like growth factor 1 receptor (IGF-1R) or the Insulin receptor (IR) autocrine loops. Loss of function of these receptors, through the use of small interfering RNA, or neutralizing antibodies directed towards their products, was undertaken in conjunction with functional assays. Neither of these strategies mitigated the effect of GLP-1 on glucose uptake, protein expression or bioenergetic flux. Our data indicates that activation of IGF-1R and/or the IR autocrine loops resulting in β-cell protection and function, involve mechanisms independent to the enhanced metabolic effects resulting from sustained GLP-1R activation. |
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| AbstractList | •Chronic GLP-1R stimulation promotes β-cell metabolic reprogramming.•IGF-1R and IR are important for β-cell development, function and proliferation.•GLP-1 enhanced metabolic phenotype is independent of IR and IGF-1R autocrine loops.•Enhanced metabolism can contribute to GLP-1 pro-survival abilities.
Pharmacological long lasting Glucagon-like peptide-1 (GLP-1) analogues, such as Exendin-4, have become widely used diabetes therapies. Chronic GLP-1R stimulation has been linked to β-cell protection and these pro-survival actions of GLP-1 are dependent on the activation of the mammalian target of rapamycin (mTOR) leading to accumulation of Hypoxia inducible factor 1 alpha (HIF-1α). Recent studies from our lab indicate that prolonged GLP-1R stimulation promotes metabolic reprograming of β-cells towards a highly glycolytic phenotype and activation of the mTOR/HIF-1α pathway was required for this action. We hypothesised that GLP-1 induced metabolic changes depend on the activation of mTOR and HIF-1α, in a cascade that occurs after triggering of a potential Insulin-like growth factor 1 receptor (IGF-1R) or the Insulin receptor (IR) autocrine loops. Loss of function of these receptors, through the use of small interfering RNA, or neutralizing antibodies directed towards their products, was undertaken in conjunction with functional assays. Neither of these strategies mitigated the effect of GLP-1 on glucose uptake, protein expression or bioenergetic flux. Our data indicates that activation of IGF-1R and/or the IR autocrine loops resulting in β-cell protection and function, involve mechanisms independent to the enhanced metabolic effects resulting from sustained GLP-1R activation. Pharmacological long lasting Glucagon-like peptide-1 (GLP-1) analogues, such as Exendin-4, have become widely used diabetes therapies. Chronic GLP-1R stimulation has been linked to β-cell protection and these pro-survival actions of GLP-1 are dependent on the activation of the mammalian target of rapamycin (mTOR) leading to accumulation of Hypoxia inducible factor 1 alpha (HIF-1α). Recent studies from our lab indicate that prolonged GLP-1R stimulation promotes metabolic reprograming of β-cells towards a highly glycolytic phenotype and activation of the mTOR/HIF-1α pathway was required for this action. We hypothesised that GLP-1 induced metabolic changes depend on the activation of mTOR and HIF-1α, in a cascade that occurs after triggering of a potential Insulin-like growth factor 1 receptor (IGF-1R) or the Insulin receptor (IR) autocrine loops. Loss of function of these receptors, through the use of small interfering RNA, or neutralizing antibodies directed towards their products, was undertaken in conjunction with functional assays. Neither of these strategies mitigated the effect of GLP-1 on glucose uptake, protein expression or bioenergetic flux. Our data indicates that activation of IGF-1R and/or the IR autocrine loops resulting in β-cell protection and function, involve mechanisms independent to the enhanced metabolic effects resulting from sustained GLP-1R activation.Pharmacological long lasting Glucagon-like peptide-1 (GLP-1) analogues, such as Exendin-4, have become widely used diabetes therapies. Chronic GLP-1R stimulation has been linked to β-cell protection and these pro-survival actions of GLP-1 are dependent on the activation of the mammalian target of rapamycin (mTOR) leading to accumulation of Hypoxia inducible factor 1 alpha (HIF-1α). Recent studies from our lab indicate that prolonged GLP-1R stimulation promotes metabolic reprograming of β-cells towards a highly glycolytic phenotype and activation of the mTOR/HIF-1α pathway was required for this action. We hypothesised that GLP-1 induced metabolic changes depend on the activation of mTOR and HIF-1α, in a cascade that occurs after triggering of a potential Insulin-like growth factor 1 receptor (IGF-1R) or the Insulin receptor (IR) autocrine loops. Loss of function of these receptors, through the use of small interfering RNA, or neutralizing antibodies directed towards their products, was undertaken in conjunction with functional assays. Neither of these strategies mitigated the effect of GLP-1 on glucose uptake, protein expression or bioenergetic flux. Our data indicates that activation of IGF-1R and/or the IR autocrine loops resulting in β-cell protection and function, involve mechanisms independent to the enhanced metabolic effects resulting from sustained GLP-1R activation. Pharmacological long lasting Glucagon-like peptide-1 (GLP-1) analogues, such as Exendin-4, have become widely used diabetes therapies. Chronic GLP-1R stimulation has been linked to β-cell protection and these pro-survival actions of GLP-1 are dependent on the activation of the mammalian target of rapamycin (mTOR) leading to accumulation of Hypoxia inducible factor 1 alpha (HIF-1α). Recent studies from our lab indicate that prolonged GLP-1R stimulation promotes metabolic reprograming of β-cells towards a highly glycolytic phenotype and activation of the mTOR/HIF-1α pathway was required for this action. We hypothesised that GLP-1 induced metabolic changes depend on the activation of mTOR and HIF-1α, in a cascade that occurs after triggering of a potential Insulin-like growth factor 1 receptor (IGF-1R) or the Insulin receptor (IR) autocrine loops. Loss of function of these receptors, through the use of small interfering RNA, or neutralizing antibodies directed towards their products, was undertaken in conjunction with functional assays. Neither of these strategies mitigated the effect of GLP-1 on glucose uptake, protein expression or bioenergetic flux. Our data indicates that activation of IGF-1R and/or the IR autocrine loops resulting in β-cell protection and function, involve mechanisms independent to the enhanced metabolic effects resulting from sustained GLP-1R activation. |
| Author | Cruzat, Vinicius Newsholme, Philip Carlessi, Rodrigo Rowlands, Jordan |
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| CitedBy_id | crossref_primary_10_12688_f1000research_20602_1 crossref_primary_10_3389_fendo_2018_00672 crossref_primary_10_2147_DMSO_S415934 crossref_primary_10_31146_1682_8658_ecg_197_1_104_109 crossref_primary_10_1007_s12672_022_00536_8 crossref_primary_10_1016_j_bcp_2023_115831 crossref_primary_10_3390_antiox11010108 |
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| Keywords | GLP-1 Bioenergetics BRIN-BD11 beta cells Diabetes Metabolism Insulin Exendin-4 |
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| SubjectTerms | Animals Autocrine Communication - drug effects Bioenergetics BRIN-BD11 beta cells Diabetes Diabetes Mellitus - drug therapy Diabetes Mellitus - metabolism Diabetes Mellitus - pathology Energy Metabolism - drug effects Exenatide - administration & dosage Exendin-4 GLP-1 Glucagon-Like Peptide-1 Receptor - genetics Glucose - metabolism Humans Hypoxia-Inducible Factor 1, alpha Subunit - genetics Insulin Insulin - genetics Insulin-Secreting Cells - drug effects Metabolism Rats Receptor, IGF Type 1 - genetics Receptor, Insulin - genetics TOR Serine-Threonine Kinases - genetics |
| Title | Insulin and IGF-1 receptor autocrine loops are not required for Exendin-4 induced changes to pancreatic β-cell bioenergetic parameters and metabolism in BRIN-BD11 cells |
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