PMID- 28569437
OWN - NLM
STAT- MEDLINE
DCOM- 20180601
LR  - 20220409
IS  - 1097-4644 (Electronic)
IS  - 0730-2312 (Linking)
VI  - 119
IP  - 1
DP  - 2018 Jan
TI  - Tumor Necrosis Factor-Alpha: Role in Development of Insulin Resistance and 
      Pathogenesis of Type 2 Diabetes Mellitus.
PG  - 105-110
LID - 10.1002/jcb.26174 [doi]
AB  - Pathogenesis of type 2 diabetes mellitus (T2DM) and development of insulin 
      resistance are characterized by multi-stimuli factors notably glucolipotoxicity, 
      generation of reactive oxygen species (ROS), epigenetic factors, activation of 
      various transcriptional mediated pathways along with the augmented levels of 
      various pro-inflammatory cytokines. Among the various pro-inflammatory cytokines, 
      tumor necrosis factor-alpha (TNF-alpha) is one the most important pro-inflammatory 
      mediator that is critically involved in the development of insulin resistance and 
      pathogenesis of T2DM. TNF-alpha is mainly produced in adipocytes and/or peripheral 
      tissues, and induces tissue-specific inflammation through the involvement of 
      generation of ROS and activation of various transcriptional mediated pathways. 
      The raised level of TNF-alpha induces insulin resistance in adipocytes and peripheral 
      tissues by impairing the insulin signaling through serine phosphorylation that 
      leads to the development of T2DM. Anti-TNF-alpha treatment strategies have been 
      developed to reduce the incidence of insulin resistance and development of T2DM. 
      In this article, we have briefly described how TNF-alpha plays crucial role to induce 
      insulin resistance and pathogenesis of T2DM. To block the inflammatory responses 
      by blocking TNF-alpha and TNF-alpha signaling may be an effective strategy for the 
      treatment of insulin resistance and T2DM. J. Cell. Biochem. 119: 105-110, 2018. (c) 
      2017 Wiley Periodicals, Inc.
CI  - (c) 2017 Wiley Periodicals, Inc.
FAU - Akash, Muhammad Sajid Hamid
AU  - Akash MSH
AUID- ORCID: 0000-0002-9446-5233
AD  - Department of Pharmaceutical Chemistry, Government College University, 
      Faisalabad, Pakistan.
FAU - Rehman, Kanwal
AU  - Rehman K
AD  - Institute of Pharmacy, Physiology and Pharmacology, University of Agriculture, 
      Faisalabad, Pakistan.
FAU - Liaqat, Aamira
AU  - Liaqat A
AD  - Department of Pharmaceutical Chemistry, Government College University, 
      Faisalabad, Pakistan.
AD  - Department of Biochemistry, Government College University, Faisalabad, Pakistan.
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
PT  - Review
DEP - 20170622
PL  - United States
TA  - J Cell Biochem
JT  - Journal of cellular biochemistry
JID - 8205768
RN  - 0 (Tumor Necrosis Factor-alpha)
SB  - IM
MH  - Animals
MH  - Diabetes Mellitus, Type 2/*etiology
MH  - Humans
MH  - *Insulin Resistance
MH  - Tumor Necrosis Factor-alpha/antagonists & inhibitors/*physiology
OTO - NOTNLM
OT  - INSULIN RESISTANCE
OT  - PRO-INFLAMMATORY CYTOKINES
OT  - TNF-alpha
OT  - TYPE 2 DIABETES MELLITUS
EDAT- 2017/06/02 06:00
MHDA- 2018/06/02 06:00
CRDT- 2017/06/02 06:00
PHST- 2017/04/07 00:00 [received]
PHST- 2017/05/31 00:00 [accepted]
PHST- 2017/06/02 06:00 [pubmed]
PHST- 2018/06/02 06:00 [medline]
PHST- 2017/06/02 06:00 [entrez]
AID - 10.1002/jcb.26174 [doi]
PST - ppublish
SO  - J Cell Biochem. 2018 Jan;119(1):105-110. doi: 10.1002/jcb.26174. Epub 2017 Jun 
      22.