The promise(s) of mesenchymal stem cell therapy in averting preclinical diabetes: lessons from in vivo and in vitro model systems

Obesity (Ob) poses a significant risk factor for the onset of metabolic syndrome with associated complications, wherein the Mesenchymal Stem Cell (MSC) therapy shows pre-clinical success. Here, we explore the therapeutic applications of human Placental MSCs (P-MSCs) to address Ob-associated Insulin...

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Published inScientific reports Vol. 11; no. 1; pp. 16983 - 18
Main Authors Kotikalapudi, Nagasuryaprasad, Sampath, Samuel Joshua Pragasam, Sukesh Narayan, Sinha, R., Bhonde, Nemani, Harishankar, Mungamuri, Sathish Kumar, Venkatesan, Vijayalakshmi
Format Journal Article
LanguageEnglish
Published London Nature Publishing Group UK 20.08.2021
Nature Publishing Group
Nature Portfolio
Subjects
1-Phosphatidylinositol 3-kinase
631/45/127
631/45/320
631/532
631/532/2074
631/80/86/2367
Adipocytes
Adipocytes - metabolism
Adipose tissue
Adipose Tissue - metabolism
AKT protein
Animals
Blood glucose
Blood Glucose - metabolism
Cell therapy
Cells, Cultured
Cytokines
Cytokines - metabolism
Diabetes mellitus
Diabetes Mellitus, Experimental - blood
Diabetes Mellitus, Experimental - prevention & control
Diabetes Mellitus, Experimental - therapy
Diabetes Mellitus, Type 2 - blood
Diabetes Mellitus, Type 2 - etiology
Diabetes Mellitus, Type 2 - prevention & control
Diabetes Mellitus, Type 2 - therapy
Female
Glucose
Glucose Transporter Type 4 - metabolism
Homeostasis
Humanities and Social Sciences
Humans
Insulin
Insulin - metabolism
Insulin resistance
Macrophages - metabolism
Mesenchymal Stem Cell Transplantation
Mesenchymal stem cells
Mesenchymal Stem Cells - cytology
Metabolic disorders
Metabolic syndrome
Models, Biological
multidisciplinary
Obesity - complications
Palmitic acid
Peripheral blood
Phosphatidylinositol 3-Kinases - metabolism
Placenta
Placenta - cytology
Pregnancy
Protein Transport
Proto-Oncogene Proteins c-akt - metabolism
Rats
Risk factors
Science
Science (multidisciplinary)
Signal Transduction
Stem cells
Therapeutic applications
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Abstract Obesity (Ob) poses a significant risk factor for the onset of metabolic syndrome with associated complications, wherein the Mesenchymal Stem Cell (MSC) therapy shows pre-clinical success. Here, we explore the therapeutic applications of human Placental MSCs (P-MSCs) to address Ob-associated Insulin Resistance (IR) and its complications. In the present study, we show that intramuscular injection of P-MSCs homed more towards the visceral site, restored HOMA-IR and glucose homeostasis in the WNIN/GR-Ob (Ob-T2D) rats. P-MSC therapy was effective in re-establishing the dysregulated cytokines. We report that the P-MSCs activates PI3K-Akt signaling and regulates the Glut4-dependant glucose uptake and its utilization in WNIN/GR-Ob (Ob-T2D) rats compared to its control. Our data reinstates P-MSC treatment's potent application to alleviate IR and restores peripheral blood glucose clearance evidenced in stromal vascular fraction (SVF) derived from white adipose tissue (WAT) of the WNIN/GR-Ob rats. Gaining insights, we show the activation of the PI3K-Akt pathway by P-MSCs both in vivo and in vitro (palmitate primed 3T3-L1 cells) to restore the insulin sensitivity dysregulated adipocytes. Our findings suggest a potent application of P-MSCs in  pre-clinical/Ob-T2D management.
AbstractList Obesity (Ob) poses a significant risk factor for the onset of metabolic syndrome with associated complications, wherein the Mesenchymal Stem Cell (MSC) therapy shows pre-clinical success. Here, we explore the therapeutic applications of human Placental MSCs (P-MSCs) to address Ob-associated Insulin Resistance (IR) and its complications. In the present study, we show that intramuscular injection of P-MSCs homed more towards the visceral site, restored HOMA-IR and glucose homeostasis in the WNIN/GR-Ob (Ob-T2D) rats. P-MSC therapy was effective in re-establishing the dysregulated cytokines. We report that the P-MSCs activates PI3K-Akt signaling and regulates the Glut4-dependant glucose uptake and its utilization in WNIN/GR-Ob (Ob-T2D) rats compared to its control. Our data reinstates P-MSC treatment's potent application to alleviate IR and restores peripheral blood glucose clearance evidenced in stromal vascular fraction (SVF) derived from white adipose tissue (WAT) of the WNIN/GR-Ob rats. Gaining insights, we show the activation of the PI3K-Akt pathway by P-MSCs both in vivo and in vitro (palmitate primed 3T3-L1 cells) to restore the insulin sensitivity dysregulated adipocytes. Our findings suggest a potent application of P-MSCs in pre-clinical/Ob-T2D management.
Obesity (Ob) poses a significant risk factor for the onset of metabolic syndrome with associated complications, wherein the Mesenchymal Stem Cell (MSC) therapy shows pre-clinical success. Here, we explore the therapeutic applications of human Placental MSCs (P-MSCs) to address Ob-associated Insulin Resistance (IR) and its complications. In the present study, we show that intramuscular injection of P-MSCs homed more towards the visceral site, restored HOMA-IR and glucose homeostasis in the WNIN/GR-Ob (Ob-T2D) rats. P-MSC therapy was effective in re-establishing the dysregulated cytokines. We report that the P-MSCs activates PI3K-Akt signaling and regulates the Glut4-dependant glucose uptake and its utilization in WNIN/GR-Ob (Ob-T2D) rats compared to its control. Our data reinstates P-MSC treatment's potent application to alleviate IR and restores peripheral blood glucose clearance evidenced in stromal vascular fraction (SVF) derived from white adipose tissue (WAT) of the WNIN/GR-Ob rats. Gaining insights, we show the activation of the PI3K-Akt pathway by P-MSCs both in vivo and in vitro (palmitate primed 3T3-L1 cells) to restore the insulin sensitivity dysregulated adipocytes. Our findings suggest a potent application of P-MSCs in  pre-clinical/Ob-T2D management.
Obesity (Ob) poses a significant risk factor for the onset of metabolic syndrome with associated complications, wherein the Mesenchymal Stem Cell (MSC) therapy shows pre-clinical success. Here, we explore the therapeutic applications of human Placental MSCs (P-MSCs) to address Ob-associated Insulin Resistance (IR) and its complications. In the present study, we show that intramuscular injection of P-MSCs homed more towards the visceral site, restored HOMA-IR and glucose homeostasis in the WNIN/GR-Ob (Ob-T2D) rats. P-MSC therapy was effective in re-establishing the dysregulated cytokines. We report that the P-MSCs activates PI3K-Akt signaling and regulates the Glut4-dependant glucose uptake and its utilization in WNIN/GR-Ob (Ob-T2D) rats compared to its control. Our data reinstates P-MSC treatment's potent application to alleviate IR and restores peripheral blood glucose clearance evidenced in stromal vascular fraction (SVF) derived from white adipose tissue (WAT) of the WNIN/GR-Ob rats. Gaining insights, we show the activation of the PI3K-Akt pathway by P-MSCs both in vivo and in vitro (palmitate primed 3T3-L1 cells) to restore the insulin sensitivity dysregulated adipocytes. Our findings suggest a potent application of P-MSCs in pre-clinical/Ob-T2D management.Obesity (Ob) poses a significant risk factor for the onset of metabolic syndrome with associated complications, wherein the Mesenchymal Stem Cell (MSC) therapy shows pre-clinical success. Here, we explore the therapeutic applications of human Placental MSCs (P-MSCs) to address Ob-associated Insulin Resistance (IR) and its complications. In the present study, we show that intramuscular injection of P-MSCs homed more towards the visceral site, restored HOMA-IR and glucose homeostasis in the WNIN/GR-Ob (Ob-T2D) rats. P-MSC therapy was effective in re-establishing the dysregulated cytokines. We report that the P-MSCs activates PI3K-Akt signaling and regulates the Glut4-dependant glucose uptake and its utilization in WNIN/GR-Ob (Ob-T2D) rats compared to its control. Our data reinstates P-MSC treatment's potent application to alleviate IR and restores peripheral blood glucose clearance evidenced in stromal vascular fraction (SVF) derived from white adipose tissue (WAT) of the WNIN/GR-Ob rats. Gaining insights, we show the activation of the PI3K-Akt pathway by P-MSCs both in vivo and in vitro (palmitate primed 3T3-L1 cells) to restore the insulin sensitivity dysregulated adipocytes. Our findings suggest a potent application of P-MSCs in pre-clinical/Ob-T2D management.
Abstract Obesity (Ob) poses a significant risk factor for the onset of metabolic syndrome with associated complications, wherein the Mesenchymal Stem Cell (MSC) therapy shows pre-clinical success. Here, we explore the therapeutic applications of human Placental MSCs (P-MSCs) to address Ob-associated Insulin Resistance (IR) and its complications. In the present study, we show that intramuscular injection of P-MSCs homed more towards the visceral site, restored HOMA-IR and glucose homeostasis in the WNIN/GR-Ob (Ob-T2D) rats. P-MSC therapy was effective in re-establishing the dysregulated cytokines. We report that the P-MSCs activates PI3K-Akt signaling and regulates the Glut4-dependant glucose uptake and its utilization in WNIN/GR-Ob (Ob-T2D) rats compared to its control. Our data reinstates P-MSC treatment's potent application to alleviate IR and restores peripheral blood glucose clearance evidenced in stromal vascular fraction (SVF) derived from white adipose tissue (WAT) of the WNIN/GR-Ob rats. Gaining insights, we show the activation of the PI3K-Akt pathway by P-MSCs both in vivo and in vitro (palmitate primed 3T3-L1 cells) to restore the insulin sensitivity dysregulated adipocytes. Our findings suggest a potent application of P-MSCs in  pre-clinical/Ob-T2D management.
ArticleNumber 16983
Author Nemani, Harishankar
Venkatesan, Vijayalakshmi
Mungamuri, Sathish Kumar
Kotikalapudi, Nagasuryaprasad
Sukesh Narayan, Sinha
R., Bhonde
Sampath, Samuel Joshua Pragasam
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  email: v.venkateshan@gmail.com
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– reference: 34584190 - Sci Rep. 2021 Sep 28;11(1):19627
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Snippet Obesity (Ob) poses a significant risk factor for the onset of metabolic syndrome with associated complications, wherein the Mesenchymal Stem Cell (MSC) therapy...
Abstract Obesity (Ob) poses a significant risk factor for the onset of metabolic syndrome with associated complications, wherein the Mesenchymal Stem Cell...
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SubjectTerms 1-Phosphatidylinositol 3-kinase
631/45/127
631/45/320
631/532
631/532/2074
631/80/86/2367
Adipocytes
Adipocytes - metabolism
Adipose tissue
Adipose Tissue - metabolism
AKT protein
Animals
Blood glucose
Blood Glucose - metabolism
Cell therapy
Cells, Cultured
Cytokines
Cytokines - metabolism
Diabetes mellitus
Diabetes Mellitus, Experimental - blood
Diabetes Mellitus, Experimental - prevention & control
Diabetes Mellitus, Experimental - therapy
Diabetes Mellitus, Type 2 - blood
Diabetes Mellitus, Type 2 - etiology
Diabetes Mellitus, Type 2 - prevention & control
Diabetes Mellitus, Type 2 - therapy
Female
Glucose
Glucose Transporter Type 4 - metabolism
Homeostasis
Humanities and Social Sciences
Humans
Insulin
Insulin - metabolism
Insulin resistance
Macrophages - metabolism
Mesenchymal Stem Cell Transplantation
Mesenchymal stem cells
Mesenchymal Stem Cells - cytology
Metabolic disorders
Metabolic syndrome
Models, Biological
multidisciplinary
Obesity - complications
Palmitic acid
Peripheral blood
Phosphatidylinositol 3-Kinases - metabolism
Placenta
Placenta - cytology
Pregnancy
Protein Transport
Proto-Oncogene Proteins c-akt - metabolism
Rats
Risk factors
Science
Science (multidisciplinary)
Signal Transduction
Stem cells
Therapeutic applications
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Title The promise(s) of mesenchymal stem cell therapy in averting preclinical diabetes: lessons from in vivo and in vitro model systems
URI https://link.springer.com/article/10.1038/s41598-021-96121-0
https://www.ncbi.nlm.nih.gov/pubmed/34417511
https://www.proquest.com/docview/2563062979
https://www.proquest.com/docview/2563421392
https://pubmed.ncbi.nlm.nih.gov/PMC8379204
https://doaj.org/article/0ddcc500f44e4b2686b49fe7751e74e2
Volume 11
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