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Am J Physiol Endocrinol Metab (June 18, 2002). doi:10.1152/ajpendo.00105.2002
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Articles in PresS, published online ahead of print June 18, 2002
Am J Physiol Endocrinol Metab, 10.1152/ajpendo.00105.2002
Submitted on March 8, 2002
Accepted on June 7, 2002

Behavioral, Metabolic, and Molecular Correlates of Lower Insulin Sensitivity in Mexican Americans

Richard C. Ho1, Kevin P. Davy2, Matthew S. Hickey2, Scott A. Summers3, and Christopher L. Melby1*

1 Food Science and Human Nutrition, Colorado State University, Fort Collins, CO, USA
2 Health and Exercise Science, Colorado State University, Fort Collins, CO, USA
3 Biochemistry and Molecular Biology, Colorado State University, Fort Collins, CO, none

* To whom correspondence should be addressed. E-mail: melby{at}cahs.colostate.edu.

We determined whether lower insulin sensitivity persists in young, nonobese, nondiabetic Mexican American (MA; n=13; 27.0 ± 2.0 yrs; BMI=23.0 ± 0.7) compared to non-Hispanic White (NHW; n=13; 24.8 ± 1.5 yrs; BMI=22.8 ± 0.6) males and females after accounting for cardiorespiratory fitness (VO2max), abdominal fat distribution (CT scans), dietary intake (4-day records) and skeletal muscle insulin signaling protein abundance from muscle biopsies (western blot analysis). MA were significantly less insulin sensitive compared to their NHW counterparts when estimated by homeostatic model assessment of insulin resistance (HOMA-IR) (MA: 1.53 ± 0.22 vs. NHW: 0.87 ± 0.16, p<0.05) and the revised quantitative insulin sensitivity check index (revised QUICKI) (MA: 0.45 ± 0.08 vs. NHW: 0.58 ± 0.19, p=0.05). However, skeletal muscle protein abundance of insulin receptor ß subunit (IRß), phosphatidylinositol 3-kinase (PI3K) p85 subunit, Akt1, Akt2 and GLUT4 were not significantly different. Differences in indices of insulin sensitivity lost significance after accounting for percent dietary intake of palmitic acid, palmitoleic acid and skeletal muscle protein abundance of IRß. We conclude that differences in insulin sensitivity between nonobese, nondiabetic MA and NHW persist after accounting for effects of chronic and acute exercise, and total and abdominal fat distribution. These differences may be mediated, in part, by dietary fat intake.






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