Is insulin resistance in the spontaneously hypertensive rat related to changes in protein kinase C in skeletal muscle?
The mechanism of insulin resistance in the spontaneously hypertensive rat (SHR) has not been clearly identified, but protein kinase C (PKC) has been implicated as a mechanism of insulin resistance in obesity and diabetes mellitus and in a diet-induced (fructose-fed) model of insulin resistance and hypertension. This study compared PKC enzyme activity (cytosol and particulate fractions) and expression of the muscle-specific isoform, PKC-theta (Western blotting), in red (soleus) and white (tensor fascia latae) hindlimb muscles from SHR (n = 12) and WKY (n = 12) rats. SHRs were hypertensive and insulin resistant, as shown by higher insulin (188 +/- 34 v 169 +/- 22 pmol/L), triglycerides (1.65 +/- 0.07 v 1.38 +/- 0.06 mmol/L), and nonesterified fatty acids (0.99 +/- 0.05 v 0.78 +/- 0.04 mmol/L) concentrations. PKC activity was significantly greater in the membrane fraction, compared with the cytosol, but there were no significant differences either in PKC activity or subcellular distribution, or expression of PKC-theta, between the two strains. Thus, insulin resistance in the SHR (in contrast to the fructose-fed dietary model of insulin resistance and hypertension) is not related to changes in PKC signaling or expression of PKC-theta in skeletal muscle.
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Department of Pharmacology, University of Sydney, and The Endocrinology Institute, Royal Prince Alfred Hospital, NSW, Australia.
Donnelly
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D000818:Animals; D006973:Hypertension / Q000201:enzymology* / Q000503:physiopathology; D007333:Insulin Resistance; D007527:Isoenzymes / Q000378:metabolism; D008297:Male; D018482:Muscle, Skeletal / Q000201:enzymology*; D011493:Protein Kinase C / Q000378:metabolism*; D051381:Rats; D011918:Rats, Inbred SHR / Q000378:metabolism / Q000502:physiology*; D011921:Rats, Inbred WKY; D014018:Tissue Distribution
D007527:Isoenzymes; D011493:Protein Kinase C