PMID- 20526383
OWN - NLM
STAT- MEDLINE
DCOM- 20100726
LR  - 20220719
IS  - 1226-3303 (Print)
IS  - 2005-6648 (Electronic)
IS  - 1226-3303 (Linking)
VI  - 25
IP  - 2
DP  - 2010 Jun
TI  - Molecular mechanism of insulin resistance in obesity and type 2 diabetes.
PG  - 119-29
LID - 10.3904/kjim.2010.25.2.119 [doi]
AB  - Insulin resistance is a major risk factor for developing type 2 diabetes caused 
      by the inability of insulin-target tissues to respond properly to insulin, and 
      contributes to the morbidity of obesity. Insulin action involves a series of 
      signaling cascades initiated by insulin binding to its receptor, eliciting 
      receptor autophosphorylation and activation of the receptor tyrosine kinase, 
      resulting in tyrosine phosphorylation of insulin receptor substrates (IRSs). 
      Phosphorylation of IRSs leads to activation of phosphatidylinositol 3-kinase 
      (PI3K) and, subsequently, to activation of Akt and its downstream mediator AS160, 
      all of which are important steps for stimulating glucose transport induced by 
      insulin. Although the mechanisms underlying insulin resistance are not completely 
      understood in skeletal muscle, it is thought to result, at least in part, from 
      impaired insulin-dependent PI3K activation and downstream signaling. This review 
      focuses on the molecular basis of skeletal muscle insulin resistance in obesity 
      and type 2 diabetes. In addition, the effects of insulin-sensitizing agent 
      treatment and lifestyle intervention of human insulin-resistant subjects on 
      insulin signaling cascade are discussed. Furthermore, the role of Rho-kinase, a 
      newly identified regulator of insulin action in insulin control of metabolism, is 
      addressed.
FAU - Choi, Kangduk
AU  - Choi K
AD  - Division of Endocrinology, Diabetes and Metabolism, Beth Israel Deaconess Medical 
      Center and Harvard Medical School, Boston, MA 02115, USA.
FAU - Kim, Young-Bum
AU  - Kim YB
LA  - eng
PT  - Journal Article
PT  - Review
DEP - 20100601
PL  - Korea (South)
TA  - Korean J Intern Med
JT  - The Korean journal of internal medicine
JID - 8712418
RN  - 0 (Blood Glucose)
RN  - 0 (Insulin)
SB  - IM
MH  - Blood Glucose/*metabolism
MH  - Diabetes Mellitus, Type 2/*metabolism
MH  - Humans
MH  - Insulin/metabolism
MH  - Insulin Resistance/*physiology
MH  - Obesity, Abdominal/*metabolism
MH  - Signal Transduction/physiology
PMC - PMC2880683
OTO - NOTNLM
OT  - Glucose transport
OT  - Insulin resistance
OT  - Skeletal muscle
OT  - Type 2 diabetes
COIS- No potential conflict of interest relevant to this article was reported.
EDAT- 2010/06/09 06:00
MHDA- 2010/07/27 06:00
PMCR- 2010/06/01
CRDT- 2010/06/08 06:00
PHST- 2010/06/08 06:00 [entrez]
PHST- 2010/06/09 06:00 [pubmed]
PHST- 2010/07/27 06:00 [medline]
PHST- 2010/06/01 00:00 [pmc-release]
AID - 10.3904/kjim.2010.25.2.119 [doi]
PST - ppublish
SO  - Korean J Intern Med. 2010 Jun;25(2):119-29. doi: 10.3904/kjim.2010.25.2.119. Epub 
      2010 Jun 1.