PMID- 30311584
OWN - NLM
STAT- MEDLINE
DCOM- 20190912
LR  - 20190912
IS  - 1045-4403 (Print)
IS  - 1045-4403 (Linking)
VI  - 28
IP  - 4
DP  - 2018
TI  - A Putative Association of Interleukin-1beta Promoter Polymorphisms and IL-1beta Levels 
      in Saudi Diabetic Patients.
PG  - 349-356
LID - 10.1615/CritRevEukaryotGeneExpr.2018025757 [doi]
AB  - Type 2 diabetes mellitus (T2DM) is a well-known endocrine disorder affecting a 
      significant number of individuals across the globe. Risk factors such as 
      inflammation, obesity, high blood glucose level, cardiovascular disease, and 
      genetic alteration are believed to be the reason for T2DM onset. The current 
      study was intended to envisage the possible association between polymorphisms in 
      the interleukin-1beta (IL-1beta) promoter and IL-1beta serum levels in Saudi T2DM 
      patients. Biochemical parameters such as fasting blood glucose (FBS), percentage 
      glycosylated hemoglobin (HbAic), and lipid profile were measured 
      spectrophotometrically. Serum insulin levels were measured using an 
      immunochemistry analyzer. The commercial enzyme-linked immune assay (ELISA) kit 
      was used to estimate the level of IL-1beta in the serum samples. The Sanger 
      sequencing method was adopted to determine single-nucleotide polymorphisms (SNPs) 
      in the IL-1beta promoter. We observed a significant (P < 0.001) elevation in FBS, 
      Hb1Ac, insulin, and low-density lipoprotein cholesterol in T2DM patients compared 
      with control individuals. Similarly, IL-1beta level were found to be increased by 
      221% in T2DM patients compared with controls. A nonsignificant genotypic 
      association was observed in the IL-1beta gene at the -511C/T and -31C/T positions in 
      T2DM patients compared with control individuals. However, a significant 
      association (P < 0.05) was observed at the allelic level. Further studies on 
      larger sample sizes are recommended to establish the exact role of IL-1beta 
      polymorphism in the pathogenesis of T2DM and its genetic risk.
FAU - Tabrez, Shams
AU  - Tabrez S
AD  - King Fahd Medical Research Center, King Abdulaziz University, Jeddah, Saudi 
      Arabia.
FAU - Ashraf, Ghulam Md
AU  - Ashraf GM
AD  - King Fahd Medical Research Center, King Abdulaziz University, Jeddah, Saudi 
      Arabia.
FAU - Hindawi, Salwa
AU  - Hindawi S
AD  - Department of Hematology, Faculty of Medicine, King Abdulaziz University 
      Hospital, Jeddah, Saudi Arabia.
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
PL  - United States
TA  - Crit Rev Eukaryot Gene Expr
JT  - Critical reviews in eukaryotic gene expression
JID - 9007261
RN  - 0 (IL1B protein, human)
RN  - 0 (Interleukin-1beta)
SB  - IM
MH  - Arabs/genetics
MH  - Case-Control Studies
MH  - Diabetes Mellitus, Type 2/blood/*genetics
MH  - Female
MH  - Gene Frequency
MH  - Humans
MH  - Interleukin-1beta/*blood/*genetics
MH  - Male
MH  - Middle Aged
MH  - Polymorphism, Single Nucleotide
MH  - *Promoter Regions, Genetic
MH  - Saudi Arabia
EDAT- 2018/10/13 06:00
MHDA- 2019/09/13 06:00
CRDT- 2018/10/13 06:00
PHST- 2018/10/13 06:00 [entrez]
PHST- 2018/10/13 06:00 [pubmed]
PHST- 2019/09/13 06:00 [medline]
AID - 0a9875bd7f54033e,1e6c9c7479cb501f [pii]
AID - 10.1615/CritRevEukaryotGeneExpr.2018025757 [doi]
PST - ppublish
SO  - Crit Rev Eukaryot Gene Expr. 2018;28(4):349-356. doi: 
      10.1615/CritRevEukaryotGeneExpr.2018025757.