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 insulin resistance  



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Author12 Posts
  #1

what of the following responsible for insulin resistance
a. high LDL
b. low HDL
c. high free fatty acids.
what other substances have same mode of action on insulin resistance




  #2

High LDL, Low HDL, High TGs. FBS > 120mg/dl, Obesity, Impaired Glucose Tolerance,


  #3

to me 007
Why u will see low HDL in insulin resistance. Can u explain?


  #4

high LDL ?? one best answer, right ?


  #5

the q is :
What of the following responsible for insulin resistance?

a. high LDL
b. low HDL
c. high free fatty acids


  #6

Excess of IGF-1 ( other substances) GLucocorticoids


  #7

glucagon excess, long term gloco cortic and cortisol excess------------> sec DM


  #8

In Ganong book if I understand it right it says that one of the hypothesis is that free fatty acid act as a signal to increase insuline resistence in muscle and liver.
Other possibilities are proteines and peptides secreted by fat cells.

Is it C) ?




  #9

Free fatty acid-induced insulin resistance is associated with activation of protein kinase C theta and alterations in the insulin signaling cascade

ME Griffin, MJ Marcucci, GW Cline, K Bell, N Barucci, D Lee, LJ Goodyear, EW Kraegen, MF White and GI Shulman
Department of Internal Medicine, Yale University School of Medicine, New Haven, Connecticut 06520-8020, USA.

To examine the mechanism by which free fatty acids (FFAs) induce insulin resistance in vivo, awake chronically catheterized rats underwent a hyperinsulinemic-euglycemic clamp with or without a 5-h preinfusion of lipid/heparin to raise plasma FFA concentrations. Increased plasma FFAs resulted in insulin resistance as reflected by a approximately 35% reduction in the glucose infusion rate (P < 0.05 vs. control). The insulin resistance was associated with a 40-50% reduction in 13C nuclear magnetic resonance (NMR)-determined rates of muscle glycogen synthesis (P < 0.01 vs. control) and muscle glucose oxidation (P < 0.01 vs. control), which in turn could be attributed to a approximately 25% reduction in glucose transport activity as assessed by 2-[1,2-3H]deoxyglucose uptake in vivo (P < 0.05 vs. control). This lipid-induced decrease in insulin-stimulated muscle glucose metabolism was associated with 1) a approximately 50% reduction in insulin-stimulated insulin receptor substrate (IRS)-1-associated phosphatidylinositol (PI) 3-kinase activity (P < 0.05 vs. control), 2) a blunting in insulin-stimulated IRS-1 tyrosine phosphorylation (P < 0.05, lipid-infused versus glycerol-infused), and 3) a four-fold increase in membrane-bound, or active, protein kinase C (PKC) theta (P < 0.05 vs. control). We conclude that acute elevations of plasma FFA levels for 5 h induce skeletal muscle insulin resistance in vivo via a reduction in insulin-stimulated muscle glycogen synthesis and glucose oxidation that can be attributed to reduced glucose transport activity. These changes are associated with abnormalities in the insulin signaling cascade and may be mediated by FFA activation of PKC theta.


  #10

epica wrote:
Free fatty acid-induced insulin resistance is associated with activation of protein kinase C theta and alterations in the insulin signaling cascade

ME Griffin, MJ Marcucci, GW Cline, K Bell, N Barucci, D Lee, LJ Goodyear, EW Kraegen, MF White and GI Shulman
Department of Internal Medicine, Yale University School of Medicine, New Haven, Connecticut 06520-8020, USA.




Cool coolcool



  #11

Yes, this is the ans for ME 007 Q (UW)
We conclude that acute elevations of PLASMA FA for 5 h induce skeletal muscle insulin resistance in vivo via a reduction in insulin-stimulated muscle glycogen synthesis and glucose oxidation that can be attributed to reduced glucose transport activity. These changes are associated with abnormalities in the insulin signaling cascade and may be mediated by FFA activation of PKC theta.


  #12

To me 007.
Please give your ans and explanat to all your Q that u posted.
Thanks





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