Liraglutide Increases Serum Levels of MicroRNA-27b, -130a and -210 in Patients with Type 2 Diabetes Mellitus: A Novel Epigenetic Effect

Liraglutide has shown favourable effects on several cardiometabolic risk factors, beyond glucose control. MicroRNAs (miRNAs) regulate gene expression, resulting in post-transcriptional modifications of cell response and function. Specific miRNAs, including miRNA-27b, miRNA-130a, and miRNA-210, play...

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Published inMetabolites Vol. 10; no. 10; p. 391
Main Authors Giglio, Rosaria Vincenza, Nikolic, Dragana, Volti, Giovanni Li, Stoian, Anca Pantea, Banerjee, Yajnavalka, Magan-Fernandez, Antonio, Castellino, Giuseppa, Patti, Angelo Maria, Chianetta, Roberta, Castracani, Carlo Castruccio, Montalto, Giuseppe, Rizvi, Ali A., Sesti, Giorgio, Rizzo, Manfredi
Format Journal Article
LanguageEnglish
Published Basel MDPI AG 30.09.2020
MDPI
Subjects
Angiogenesis
Apoptosis
Atherosclerosis
Biomarkers
Blood pressure
cardiometabolic risk
Cardiovascular disease
Cell growth
Cholesterol
Diabetes
Diabetes mellitus (non-insulin dependent)
Endothelial cells
epigenetic
Epigenetics
Gene expression
Glucose
Heart attacks
Hemoglobin
Homeostasis
Ischemia
liraglutide
Metabolic disorders
Metformin
MicroRNAs
miRNA
Mortality
Oxidative stress
Polymerase chain reaction
Post-transcription
Risk factors
Serum levels
Triglycerides
type-2 diabetes
Online AccessGet full text

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Abstract Liraglutide has shown favourable effects on several cardiometabolic risk factors, beyond glucose control. MicroRNAs (miRNAs) regulate gene expression, resulting in post-transcriptional modifications of cell response and function. Specific miRNAs, including miRNA-27b, miRNA-130a, and miRNA-210, play a role in cardiometabolic disease. We aimed to determine the effect of liraglutide on the serum levels of miRNA-27b, miRNA-130a and miRNA-210. Twenty-five subjects with type-2 diabetes mellitus (T2DM), naïve to incretin-based therapy, were treated with liraglutide (1.2 mg/day as an add-on to metformin) for 4 months. miRNAs were quantified using real-time polymerase chain reaction. After liraglutide treatment, we found significant reductions in fasting glucose (from 9.8 ± 5.3 to 6.7 ± 1.6 mmol/L, p = 0.0042), glycosylated haemoglobin (HbA1c) (from 8.1 ± 0.8 to 6.6 ± 1.0%, p = 0.0008), total cholesterol (from 5.0 ± 1.0 to 4.0 ± 0.7 mmol/L, p = 0.0011), triglycerides (from 1.9 ± 1.0 to 1.5 ± 0.8 mmol/L, p = 0.0104) and low-density lipoprotein cholesterol (from 2.9 ± 1.2 to 2.2 ± 0.6 mmol/L, p = 0.0125), while the serum levels of miRNA-27b, miRNA-130a and miRNA-210a were significantly increased (median (interquartile range, IQR) changes: 1.73 (7.12) (p = 0.0401), 1.91 (3.64) (p = 0.0401) and 2.09 (11.0) (p = 0.0486), respectively). Since the changes in miRNAs were independent of changes in all the metabolic parameters investigated, liraglutide seems to exert a direct epigenetic effect in T2DM patients, regulating microRNAs involved in the maintenance of endothelial cell homeostasis. These changes might be implicated in liraglutide’s benefits and may represent useful targets for cardiometabolic management.
AbstractList Liraglutide has shown favourable effects on several cardiometabolic risk factors, beyond glucose control. MicroRNAs (miRNAs) regulate gene expression, resulting in post-transcriptional modifications of cell response and function. Specific miRNAs, including miRNA-27b, miRNA-130a, and miRNA-210, play a role in cardiometabolic disease. We aimed to determine the effect of liraglutide on the serum levels of miRNA-27b, miRNA-130a and miRNA-210. Twenty-five subjects with type-2 diabetes mellitus (T2DM), naïve to incretin-based therapy, were treated with liraglutide (1.2 mg/day as an add-on to metformin) for 4 months. miRNAs were quantified using real-time polymerase chain reaction. After liraglutide treatment, we found significant reductions in fasting glucose (from 9.8 ± 5.3 to 6.7 ± 1.6 mmol/L, p = 0.0042), glycosylated haemoglobin (HbA1c) (from 8.1 ± 0.8 to 6.6 ± 1.0%, p = 0.0008), total cholesterol (from 5.0 ± 1.0 to 4.0 ± 0.7 mmol/L, p = 0.0011), triglycerides (from 1.9 ± 1.0 to 1.5 ± 0.8 mmol/L, p = 0.0104) and low-density lipoprotein cholesterol (from 2.9 ± 1.2 to 2.2 ± 0.6 mmol/L, p = 0.0125), while the serum levels of miRNA-27b, miRNA-130a and miRNA-210a were significantly increased (median (interquartile range, IQR) changes: 1.73 (7.12) (p = 0.0401), 1.91 (3.64) (p = 0.0401) and 2.09 (11.0) (p = 0.0486), respectively). Since the changes in miRNAs were independent of changes in all the metabolic parameters investigated, liraglutide seems to exert a direct epigenetic effect in T2DM patients, regulating microRNAs involved in the maintenance of endothelial cell homeostasis. These changes might be implicated in liraglutide's benefits and may represent useful targets for cardiometabolic management.Liraglutide has shown favourable effects on several cardiometabolic risk factors, beyond glucose control. MicroRNAs (miRNAs) regulate gene expression, resulting in post-transcriptional modifications of cell response and function. Specific miRNAs, including miRNA-27b, miRNA-130a, and miRNA-210, play a role in cardiometabolic disease. We aimed to determine the effect of liraglutide on the serum levels of miRNA-27b, miRNA-130a and miRNA-210. Twenty-five subjects with type-2 diabetes mellitus (T2DM), naïve to incretin-based therapy, were treated with liraglutide (1.2 mg/day as an add-on to metformin) for 4 months. miRNAs were quantified using real-time polymerase chain reaction. After liraglutide treatment, we found significant reductions in fasting glucose (from 9.8 ± 5.3 to 6.7 ± 1.6 mmol/L, p = 0.0042), glycosylated haemoglobin (HbA1c) (from 8.1 ± 0.8 to 6.6 ± 1.0%, p = 0.0008), total cholesterol (from 5.0 ± 1.0 to 4.0 ± 0.7 mmol/L, p = 0.0011), triglycerides (from 1.9 ± 1.0 to 1.5 ± 0.8 mmol/L, p = 0.0104) and low-density lipoprotein cholesterol (from 2.9 ± 1.2 to 2.2 ± 0.6 mmol/L, p = 0.0125), while the serum levels of miRNA-27b, miRNA-130a and miRNA-210a were significantly increased (median (interquartile range, IQR) changes: 1.73 (7.12) (p = 0.0401), 1.91 (3.64) (p = 0.0401) and 2.09 (11.0) (p = 0.0486), respectively). Since the changes in miRNAs were independent of changes in all the metabolic parameters investigated, liraglutide seems to exert a direct epigenetic effect in T2DM patients, regulating microRNAs involved in the maintenance of endothelial cell homeostasis. These changes might be implicated in liraglutide's benefits and may represent useful targets for cardiometabolic management.
Liraglutide has shown favourable effects on several cardiometabolic risk factors, beyond glucose control. MicroRNAs (miRNAs) regulate gene expression, resulting in post-transcriptional modifications of cell response and function. Specific miRNAs, including miRNA-27b, miRNA-130a, and miRNA-210, play a role in cardiometabolic disease. We aimed to determine the effect of liraglutide on the serum levels of miRNA-27b, miRNA-130a and miRNA-210. Twenty-five subjects with type-2 diabetes mellitus (T2DM), naïve to incretin-based therapy, were treated with liraglutide (1.2 mg/day as an add-on to metformin) for 4 months. miRNAs were quantified using real-time polymerase chain reaction. After liraglutide treatment, we found significant reductions in fasting glucose (from 9.8 ± 5.3 to 6.7 ± 1.6 mmol/L, p = 0.0042), glycosylated haemoglobin (HbA1c) (from 8.1 ± 0.8 to 6.6 ± 1.0%, p = 0.0008), total cholesterol (from 5.0 ± 1.0 to 4.0 ± 0.7 mmol/L, p = 0.0011), triglycerides (from 1.9 ± 1.0 to 1.5 ± 0.8 mmol/L, p = 0.0104) and low-density lipoprotein cholesterol (from 2.9 ± 1.2 to 2.2 ± 0.6 mmol/L, p = 0.0125), while the serum levels of miRNA-27b, miRNA-130a and miRNA-210a were significantly increased (median (interquartile range, IQR) changes: 1.73 (7.12) (p = 0.0401), 1.91 (3.64) (p = 0.0401) and 2.09 (11.0) (p = 0.0486), respectively). Since the changes in miRNAs were independent of changes in all the metabolic parameters investigated, liraglutide seems to exert a direct epigenetic effect in T2DM patients, regulating microRNAs involved in the maintenance of endothelial cell homeostasis. These changes might be implicated in liraglutide’s benefits and may represent useful targets for cardiometabolic management.
Liraglutide has shown favourable effects on several cardiometabolic risk factors, beyond glucose control. MicroRNAs (miRNAs) regulate gene expression, resulting in post-transcriptional modifications of cell response and function. Specific miRNAs, including miRNA-27b, miRNA-130a, and miRNA-210, play a role in cardiometabolic disease. We aimed to determine the effect of liraglutide on the serum levels of miRNA-27b, miRNA-130a and miRNA-210. Twenty-five subjects with type-2 diabetes mellitus (T2DM), naïve to incretin-based therapy, were treated with liraglutide (1.2 mg/day as an add-on to metformin) for 4 months. miRNAs were quantified using real-time polymerase chain reaction. After liraglutide treatment, we found significant reductions in fasting glucose (from 9.8 ± 5.3 to 6.7 ± 1.6 mmol/L, p = 0.0042), glycosylated haemoglobin (HbA1c) (from 8.1 ± 0.8 to 6.6 ± 1.0%, p = 0.0008), total cholesterol (from 5.0 ± 1.0 to 4.0 ± 0.7 mmol/L, p = 0.0011), triglycerides (from 1.9 ± 1.0 to 1.5 ± 0.8 mmol/L, p = 0.0104) and low-density lipoprotein cholesterol (from 2.9 ± 1.2 to 2.2 ± 0.6 mmol/L, p = 0.0125), while the serum levels of miRNA-27b, miRNA-130a and miRNA-210a were significantly increased (median (interquartile range, IQR) changes: 1.73 (7.12) ( p = 0.0401), 1.91 (3.64) ( p = 0.0401) and 2.09 (11.0) ( p = 0.0486), respectively). Since the changes in miRNAs were independent of changes in all the metabolic parameters investigated, liraglutide seems to exert a direct epigenetic effect in T2DM patients, regulating microRNAs involved in the maintenance of endothelial cell homeostasis. These changes might be implicated in liraglutide’s benefits and may represent useful targets for cardiometabolic management.
Author Chianetta, Roberta
Castellino, Giuseppa
Patti, Angelo Maria
Banerjee, Yajnavalka
Magan-Fernandez, Antonio
Volti, Giovanni Li
Montalto, Giuseppe
Stoian, Anca Pantea
Sesti, Giorgio
Nikolic, Dragana
Giglio, Rosaria Vincenza
Castracani, Carlo Castruccio
Rizvi, Ali A.
Rizzo, Manfredi
AuthorAffiliation 5 Division of Endocrinology, Diabetes and Metabolism, University of South Carolina School of Medicine, Columbia, SC 29203, USA
6 Division of Endocrinology, Metabolism, and Lipids Emory University School of Medicine, Atlanta, GA 30322, USA
3 Department of Diabetes, Nutrition and Metabolic Diseases, Carol Davila University of Medicine and Pharmacy, 050474 Bucharest, Romania; ancastoian@yahoo.com
4 College of Medicine, Mohammed Bin Rashid University of Medicine and Health Sciences, Dubai, UAE; Yajnavalka.Banerjee@mbru.ac.ae
1 Department of Health Promotion Sciences Maternal and Infantile Care, Internal Medicine and Medical Specialties (PROMISE), University of Palermo, 90127 Palermo, Italy; rosaria.vincenza.giglio@alice.it (R.V.G.); dragana.nikolic@unipa.it (D.N.); amaganf@ugr.es (A.M.-F.); castellinogiusy@gmail.com (G.C.); pattiangelomaria@gmail.com (A.M.P.); chianetta.roberta8@gmail.com (R.C.); giuseppe.montalto@unipa.it (G.M.); manfredi.rizzo@unipa.it (M.R.)
2 Department of Biomedical and Bi
AuthorAffiliation_xml – name: 7 Department of Clinical and Molecular Medicine, University of Rome La Sapienza, 00182 Rome, Italy; giorgio.sesti@uniroma1.it
– name: 1 Department of Health Promotion Sciences Maternal and Infantile Care, Internal Medicine and Medical Specialties (PROMISE), University of Palermo, 90127 Palermo, Italy; rosaria.vincenza.giglio@alice.it (R.V.G.); dragana.nikolic@unipa.it (D.N.); amaganf@ugr.es (A.M.-F.); castellinogiusy@gmail.com (G.C.); pattiangelomaria@gmail.com (A.M.P.); chianetta.roberta8@gmail.com (R.C.); giuseppe.montalto@unipa.it (G.M.); manfredi.rizzo@unipa.it (M.R.)
– name: 2 Department of Biomedical and Biotechnological Sciences, University of Catania, 95125 Catania, Italy; livolti@unict.it (G.L.V.); carlo.castruccio@unict.it (C.C.C.)
– name: 5 Division of Endocrinology, Diabetes and Metabolism, University of South Carolina School of Medicine, Columbia, SC 29203, USA
– name: 3 Department of Diabetes, Nutrition and Metabolic Diseases, Carol Davila University of Medicine and Pharmacy, 050474 Bucharest, Romania; ancastoian@yahoo.com
– name: 6 Division of Endocrinology, Metabolism, and Lipids Emory University School of Medicine, Atlanta, GA 30322, USA
– name: 4 College of Medicine, Mohammed Bin Rashid University of Medicine and Health Sciences, Dubai, UAE; Yajnavalka.Banerjee@mbru.ac.ae
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These authors contributed equally to the work.
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Snippet Liraglutide has shown favourable effects on several cardiometabolic risk factors, beyond glucose control. MicroRNAs (miRNAs) regulate gene expression,...
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StartPage 391
SubjectTerms Angiogenesis
Apoptosis
Atherosclerosis
Biomarkers
Blood pressure
cardiometabolic risk
Cardiovascular disease
Cell growth
Cholesterol
Diabetes
Diabetes mellitus (non-insulin dependent)
Endothelial cells
epigenetic
Epigenetics
Gene expression
Glucose
Heart attacks
Hemoglobin
Homeostasis
Ischemia
liraglutide
Metabolic disorders
Metformin
MicroRNAs
miRNA
Mortality
Oxidative stress
Polymerase chain reaction
Post-transcription
Risk factors
Serum levels
Triglycerides
type-2 diabetes
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Title Liraglutide Increases Serum Levels of MicroRNA-27b, -130a and -210 in Patients with Type 2 Diabetes Mellitus: A Novel Epigenetic Effect
URI https://www.proquest.com/docview/2548904361
https://www.proquest.com/docview/2448406663
https://pubmed.ncbi.nlm.nih.gov/PMC7599907
https://doaj.org/article/2794467510104e2abc37bb9488f3c68c
Volume 10
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