Diabetes 51:915-920, 2002
© 2002 by the American Diabetes Association, Inc.
Independent Regulation of In Vivo Insulin Action on Glucose Versus K+ Uptake by Dietary Fat and K+ Content
Cheol S. Choi,
Felix N. Lee,
Alicia A. McDonough, and
Jang H. Youn
From the Department of Physiology and Biophysics, University of Southern California Keck School of Medicine, Los Angeles, California
Insulin stimulates both glucose and K+ uptake, and high-fat feeding is known to decrease insulin-stimulated glucose uptake. The purpose of this study was to examine whether insulins actions on glucose and K+ uptake are similarly decreased by a high-fat diet. Wistar rats were fed a standard control (12.2% fat; n = 6) or high-fat (66.5% fat; n = 13) diet for 15 days. Because K+ content was 1% in the control and 0.5% in the high-fat diet and because the rats ate less of the high-fat diet, we also compared the high-fat diet with 0.5% K+ (HFD; n = 7) to a high-fat diet supplemented with 1.5% K+ (HFD+K; n = 6). K+ intake was matched between the control and HFD+K groups (246 ± 8 vs. 224 ± 2 mg/day), but was lower in the HFD group (78 ± 10 mg/day; P < 0.05). Insulin-stimulated glucose and K+ uptake were determined by hyperinsulinemic (5 mU · kg-1 · min-1) glucose and K+ clamps. The HFD depressed both insulin-stimulated glucose uptake compared to the control (133 ± 5 vs. 166 ± 7 µmol · kg-1 · min-1; P < 0.05) and K+ uptake (5.5 ± 0.9 vs. 8.9 ± 1.0 µmol · kg-1 · min-1; P < 0.05) compared to the control. However, insulin-stimulated K+ uptake was unchanged in the HFD+K versus in the control group (10.0 ± 0.6 vs. 8.9 ± 1.0 µmol · kg-1 · min-1; P > 0.05), whereas insulin-stimulated glucose uptake in the HFD+K group was decreased to a rate (137 ± 9 µmol · kg-1 · min-1), similar to that of the HFD group. We concluded that the decrease in insulin-stimulated K+ uptake during high-fat feeding was a result of decreased K+ intake, and that insulins actions on glucose uptake and K+ uptake are independently regulated by dietary fat and K+ content, respectively.

CiteULike Del.icio.us Digg Reddit Technorati What's this?
This article has been cited by other articles:

|
 |

|
 |
 
F. N. Lee, G. Oh, A. A. McDonough, and J. H. Youn
Evidence for gut factor in K+ homeostasis
Am J Physiol Renal Physiol,
August 1, 2007;
293(2):
F541 - F547.
[Abstract]
[Full Text]
[PDF]
|
 |
|

|
 |

|
 |
 
P. Chen, J. P. Guzman, P. K. K. Leong, L. E. Yang, A. Perianayagam, E. Babilonia, J. S. Ho, J. H. Youn, W. H. Wang, and A. A. McDonough
Modest dietary K+ restriction provokes insulin resistance of cellular K+ uptake and phosphorylation of renal outer medulla K+ channel without fall in plasma K+ concentration
Am J Physiol Cell Physiol,
May 1, 2006;
290(5):
C1355 - C1363.
[Abstract]
[Full Text]
[PDF]
|
 |
|

|
 |

|
 |
 
C. Demigne, H. Sabboh, C. Remesy, and P. Meneton
Protective Effects of High Dietary Potassium: Nutritional and Metabolic Aspects
J. Nutr.,
November 1, 2004;
134(11):
2903 - 2906.
[Abstract]
[Full Text]
[PDF]
|
 |
|

|
 |

|
 |
 
M. S. Rhee, A. Perianayagam, P. Chen, J. H. Youn, and A. A. McDonough
Dexamethasone treatment causes resistance to insulin-stimulated cellular potassium uptake in the rat
Am J Physiol Cell Physiol,
November 1, 2004;
287(5):
C1229 - C1237.
[Abstract]
[Full Text]
[PDF]
|
 |
|
Copyright © 2002 by the American Diabetes Association.
|
|
| |
|