PMID- 12841357
OWN - NLM
STAT- MEDLINE
DCOM- 20040301
LR  - 20220409
IS  - 0300-8177 (Print)
IS  - 0300-8177 (Linking)
VI  - 246
IP  - 1-2
DP  - 2003 Apr
TI  - High levels of palmitic acid lead to insulin resistance due to changes in the 
      level of phosphorylation of the insulin receptor and insulin receptor 
      substrate-1.
PG  - 155-62
AB  - Insulin resistance is defined as the decrease in the glucose disposal in response 
      to insulin by the target tissues. High concentrations of nonesterified fatty 
      acids (NEFA) in plasma have been implicated with many insulin resistance states. 
      We evaluated several aspects of the insulin resistance induced by palmitic acid 
      in rats and found that after treatment with 0.09 g/kg of palmitic acid there is a 
      delay in the curve of tolerance to glucose. We measured the changes in protein 
      phosphorylation in samples from abdominus rectus muscle and there was a decrease 
      of 64 and 75% in the levels of phosphorylation in tyrosine of the insulin 
      receptor and insulin receptor substrate-1, respectively. This diminution in the 
      tyrosine phosphorylation is consistent with a decrease in the main pathway known 
      to be activated after insulin treatment, the mitogen activated protein kinases 
      (MAPKs). If the animals were treated with inhibitors of PKC, like sphingosine, 
      there was a prevention of the effect of palmitic acid determined at the level of 
      tyrosine phosphorylation. According with this result, we found an increase in the 
      phosphorylations in serine of the insulin receptor after the treatment with 
      palmitate. These results suggest that PKC has a role as negative regulator (by 
      phosphorylation in serine) of the insulin receptors activation in the insulin 
      resistance induced by palmitic acid.
FAU - Reynoso, Rosalia
AU  - Reynoso R
AD  - Departamento de Bioquimica, Centro de Investigacion y de Estudios Avanzados del 
      IPN, Mexico.
FAU - Salgado, Luis M
AU  - Salgado LM
FAU - Calderon, Victor
AU  - Calderon V
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
PL  - Netherlands
TA  - Mol Cell Biochem
JT  - Molecular and cellular biochemistry
JID - 0364456
RN  - 0 (Enzyme Inhibitors)
RN  - 0 (Insulin Receptor Substrate Proteins)
RN  - 0 (Irs1 protein, rat)
RN  - 0 (Phosphoproteins)
RN  - 2V16EO95H1 (Palmitic Acid)
RN  - 42HK56048U (Tyrosine)
RN  - 452VLY9402 (Serine)
RN  - EC 2.7.10.1 (Receptor, Insulin)
RN  - EC 2.7.11.13 (Protein Kinase C)
RN  - NGZ37HRE42 (Sphingosine)
SB  - IM
MH  - Animals
MH  - Enzyme Inhibitors/pharmacology
MH  - Insulin Receptor Substrate Proteins
MH  - *Insulin Resistance
MH  - MAP Kinase Signaling System
MH  - Male
MH  - Muscle, Skeletal/drug effects/metabolism
MH  - Palmitic Acid/*pharmacology
MH  - Phosphoproteins/chemistry/*metabolism
MH  - Phosphorylation
MH  - Protein Kinase C/antagonists & inhibitors/metabolism
MH  - Rats
MH  - Rats, Wistar
MH  - Receptor, Insulin/chemistry/*metabolism
MH  - Serine/chemistry
MH  - Sphingosine/pharmacology
MH  - Tyrosine/chemistry
EDAT- 2003/07/05 05:00
MHDA- 2004/03/03 05:00
CRDT- 2003/07/05 05:00
PHST- 2003/07/05 05:00 [pubmed]
PHST- 2004/03/03 05:00 [medline]
PHST- 2003/07/05 05:00 [entrez]
PST - ppublish
SO  - Mol Cell Biochem. 2003 Apr;246(1-2):155-62.