PMID- 32125563
OWN - NLM
STAT- MEDLINE
DCOM- 20210927
LR  - 20210927
IS  - 1573-2606 (Electronic)
IS  - 1389-9155 (Linking)
VI  - 21
IP  - 4
DP  - 2020 Dec
TI  - Current perspectives of oleic acid: Regulation of molecular pathways in 
      mitochondrial and endothelial functioning against insulin resistance and 
      diabetes.
PG  - 631-643
LID - 10.1007/s11154-020-09549-6 [doi]
AB  - Insulin resistance (IR) and type 2 diabetes mellitus (T2DM) is a leading cause of 
      deaths due to metabolic disorders in recent years. Molecular mechanisms involved 
      in the initiation and development of IR and T2DM are multiples. The major factors 
      include mitochondrial dysfunction which may cause incomplete fatty acid oxidation 
      (FAO). Oleic acid upregulates the expression of genes causing FAO by 
      deacetylation of PGC1alpha by PKA-dependent activation of SIRT1-PGC1alpha complex. 
      Another potent factor for the development of IR and T2DM is endothelial 
      dysfunction as damaged endothelium causes increased release of inflammatory 
      mediators such as TNF-alpha, IL-6, IL-1beta, sVCAM, sICAM, E-selectin and other 
      proinflammatory cytokines. While, on the other hand, oleic acid has the ability 
      to regulate E-selectin, and sICAM expression. Rest of the risk factors may 
      include inflammation, beta-cell dysfunction, oxidative stress, hormonal imbalance, 
      apoptosis, and enzyme dysregulation. Here, we have highlighted how oleic acid 
      regulates underlying causatives factors and hence, keeps surpassing effect in 
      prevention and treatment of IR and T2DM. However, the percentage contribution of 
      these factors in combating IR and ultimately averting T2DM is still debatable. 
      Thus, because of its exceptional protective effect, it can be considered as an 
      improved therapeutic agent in prophylaxis and/or treatment of IR and T2DM.
FAU - Rehman, Kanwal
AU  - Rehman K
AUID- ORCID: 0000-0001-7873-6681
AD  - Department of Pharmacy, University of Agriculture, Faisalabad, Pakistan. 
      kanwal.akash@uaf.edu.pk.
FAU - Haider, Kamran
AU  - Haider K
AD  - Department of Pharmacy, University of Agriculture, Faisalabad, Pakistan.
FAU - Jabeen, Komal
AU  - Jabeen K
AD  - Department of Pharmacy, University of Agriculture, Faisalabad, Pakistan.
AD  - Institute of Physiology and Pharmacology, University of Agriculture, Faisalabad, 
      Pakistan.
FAU - Akash, Muhammad Sajid Hamid
AU  - Akash MSH
AD  - Department of Pharmaceutical Chemistry, Government College University, 
      Faisalabad, Pakistan. sajidakash@gcuf.edu.pk.
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
PT  - Review
PL  - Germany
TA  - Rev Endocr Metab Disord
JT  - Reviews in endocrine & metabolic disorders
JID - 100940588
RN  - 2UMI9U37CP (Oleic Acid)
SB  - IM
MH  - *Diabetes Mellitus, Type 2/drug therapy/immunology/metabolism/physiopathology
MH  - *Endothelium, Vascular/drug effects/immunology/metabolism/physiopathology
MH  - Humans
MH  - *Insulin Resistance
MH  - *Mitochondria/drug effects/metabolism
MH  - Oleic Acid/*pharmacology/*physiology
OTO - NOTNLM
OT  - Inflammatory responses
OT  - Insulin resistance
OT  - Mitochondrial dysfunction
OT  - Oleic acid
EDAT- 2020/03/04 06:00
MHDA- 2021/09/28 06:00
CRDT- 2020/03/04 06:00
PHST- 2020/03/04 06:00 [pubmed]
PHST- 2021/09/28 06:00 [medline]
PHST- 2020/03/04 06:00 [entrez]
AID - 10.1007/s11154-020-09549-6 [pii]
AID - 10.1007/s11154-020-09549-6 [doi]
PST - ppublish
SO  - Rev Endocr Metab Disord. 2020 Dec;21(4):631-643. doi: 10.1007/s11154-020-09549-6.