In:
American Journal of Physiology-Endocrinology and Metabolism, American Physiological Society, Vol. 293, No. 1 ( 2007-07), p. E264-E269
Abstract:
Suppression of lipid oxidation (L ox ) by insulin is impaired in obesity and type 2 diabetes mellitus (T2DM). Here we tested whether high L ox represents a primary or acquired characteristic in the pathogenesis of T2DM. Hood-indirect calorimetry was performed under postabsorptive conditions and during a two-step hyperinsulinemic euglycemic clamp (insulin infusion rates in mU·m −2 ·min −1 : 40 low and 400 high) in 465 Pima Indians: 317 with normal glucose tolerance (NGT), 117 with impaired glucose tolerance (IGT), and 31 with T2DM. The predictive effect of net lipid oxidation (L ox ) on development of T2DM was assessed in 296 subjects (51 of whom developed T2DM), whereas the predictive effect of L ox on followup changes in insulin-mediated glucose disposal (M) and acute insulin response (AIR) was studied in 190 subjects with NGT at baseline. Cross-sectionally, after adjustment for age, sex, body fat (BF), and M low, L ox low was increased in T2DM compared with NGT and IGT subjects ( P 〈 0.05). Prospectively, after adjustment for followup duration, age, sex, BF, M, and AIR, increased clamp L ox predicted T2DM [hazard rate ratios (95% CI): L ox low, 1.5 (1.1, 2.0), P 〈 0.01; L ox high, 1.3 (1.0, 1.8), P = 0.05]. High L ox low at baseline was also associated with subsequent worsening of M low ( P = 0.04). These data indicate that the inability of insulin to suppress L ox may represent an early risk marker for insulin resistance and T2DM that is independent of adiposity, acute insulin secretion, and insulin action on glucose uptake.
Type of Medium:
Online Resource
ISSN:
0193-1849
,
1522-1555
DOI:
10.1152/ajpendo.00662.2006
Language:
English
Publisher:
American Physiological Society
Publication Date:
2007
detail.hit.zdb_id:
1477331-4
SSG:
12
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