PMID- 30356719
OWN - NLM
STAT- PubMed-not-MEDLINE
LR  - 20191120
IS  - 1664-2392 (Print)
IS  - 1664-2392 (Electronic)
IS  - 1664-2392 (Linking)
VI  - 9
DP  - 2018
TI  - Differential Expression of Human Peripheral Mononuclear Cells Phenotype Markers 
      in Type 2 Diabetic Patients and Type 2 Diabetic Patients on Metformin.
PG  - 537
LID - 10.3389/fendo.2018.00537 [doi]
LID - 537
AB  - Background: Although peripheral blood mononuclear cells (PBMC) have been 
      demonstrated to be in a pro-inflammatory state in obesity and type 2 Diabetes 
      Mellitus (T2DM), characterization of circulating PBMC phenotypes in the obese and 
      T2DM and the effect of Metformin on these phenotypes in humans is still 
      ill-defined and remains to be determined. Methods: Thirty normal healthy adult 
      volunteers of normal weight, 30 obese subjects, 20 obese newly diagnosed 
      diabetics and 30 obese diabetics on Metformin were recruited for the study. 
      Fasting blood samples were collected and PBMC were isolated from whole blood. 
      Polarization markers (CD86, IL-6, TNFalpha, iNOS, CD36, CD11c, CD169, CD206, CD163, 
      CD68, CD11b, CD16, and CD14) were measured by RT-qPCR. Gene expression fold 
      changes were calculated using the 2(-DeltaDeltaCT) method for RT-qPCR. Results: Obesity 
      and T2DM are associated an increased CD68 marker in PBMC. mRNA expression of 
      CD11b, CD11c, CD169, and CD163 were significantly reduced in PBMC from T2DM 
      subjects whereas CD11c was significantly inhibited in PBMC from obese subjects. 
      On the other hand, macrophage M1-like phenotype was observed in T2DM circulation 
      as demonstrated by increased mRNA expression of CD16, IL-6, iNOS, TNFalpha, and CD36. 
      There were no significant changes in CD14 and CD86 in the obese and T2DM when 
      compared to the lean subjects. Metformin treatment in T2DM reverted CD11c, CD169, 
      IL-6, iNOS, TNFalpha, and CD36 to levels comparable to lean subjects. CD206 mRNA 
      expression was significantly upregulated in PBMC of T2DM while Metformin 
      treatment inhibited CD206 expression levels. Conclusions: These data support the 
      notion that PBMC in circulation in T2DM express different pattern of phenotypic 
      markers than the patterns typically present in M1 and M2 like cells. These 
      phenotypic markers could be representative of metabolically activated macrophages 
      (MMe)-like cells. Metformin, on the other hand, reduces MMe-like cells in 
      circulation.
FAU - Al Dubayee, Mohammed S
AU  - Al Dubayee MS
AD  - College of Medicine, King Saud bin Abdulaziz University for Health Sciences, 
      Riyadh, Saudi Arabia.
AD  - King Abdullah Specialized Children Hospital, Ministry of National Guard Health 
      Affairs, Riyadh, Saudi Arabia.
FAU - Alayed, Hind
AU  - Alayed H
AD  - College of Medicine, King Saud bin Abdulaziz University for Health Sciences, 
      Riyadh, Saudi Arabia.
FAU - Almansour, Rana
AU  - Almansour R
AD  - College of Medicine, King Saud bin Abdulaziz University for Health Sciences, 
      Riyadh, Saudi Arabia.
FAU - Alqaoud, Nora
AU  - Alqaoud N
AD  - College of Medicine, King Saud bin Abdulaziz University for Health Sciences, 
      Riyadh, Saudi Arabia.
FAU - Alnamlah, Rahaf
AU  - Alnamlah R
AD  - College of Medicine, King Saud bin Abdulaziz University for Health Sciences, 
      Riyadh, Saudi Arabia.
FAU - Obeid, Dana
AU  - Obeid D
AD  - College of Medicine, King Saud bin Abdulaziz University for Health Sciences, 
      Riyadh, Saudi Arabia.
FAU - Alshahrani, Awad
AU  - Alshahrani A
AD  - College of Medicine, King Saud bin Abdulaziz University for Health Sciences, 
      Riyadh, Saudi Arabia.
FAU - Zahra, Mahmoud M
AU  - Zahra MM
AD  - College of Medicine, King Saud bin Abdulaziz University for Health Sciences, 
      Riyadh, Saudi Arabia.
FAU - Nasr, Amre
AU  - Nasr A
AD  - College of Medicine, King Saud bin Abdulaziz University for Health Sciences, 
      Riyadh, Saudi Arabia.
FAU - Al-Bawab, Ahmad
AU  - Al-Bawab A
AD  - College of Medicine, King Saud bin Abdulaziz University for Health Sciences, 
      Riyadh, Saudi Arabia.
FAU - Aljada, Ahmad
AU  - Aljada A
AD  - College of Medicine, King Saud bin Abdulaziz University for Health Sciences, 
      Riyadh, Saudi Arabia.
AD  - King Abdullah International Medical Research Center, Riyadh, Saudi Arabia.
LA  - eng
PT  - Journal Article
DEP - 20181009
PL  - Switzerland
TA  - Front Endocrinol (Lausanne)
JT  - Frontiers in endocrinology
JID - 101555782
PMC - PMC6189318
OTO - NOTNLM
OT  - atherosclerosis
OT  - inflammation
OT  - metabolic syndrome
OT  - metabolically-activated macrophages
OT  - monocyte subtypes
EDAT- 2018/10/26 06:00
MHDA- 2018/10/26 06:01
PMCR- 2018/01/01
CRDT- 2018/10/26 06:00
PHST- 2017/10/28 00:00 [received]
PHST- 2018/08/23 00:00 [accepted]
PHST- 2018/10/26 06:00 [entrez]
PHST- 2018/10/26 06:00 [pubmed]
PHST- 2018/10/26 06:01 [medline]
PHST- 2018/01/01 00:00 [pmc-release]
AID - 10.3389/fendo.2018.00537 [doi]
PST - epublish
SO  - Front Endocrinol (Lausanne). 2018 Oct 9;9:537. doi: 10.3389/fendo.2018.00537. 
      eCollection 2018.