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Diabetes, Vol 46, Issue 11 1822-1828, Copyright © 1997 by American Diabetes Association
Evidence of an increased number of type IIb muscle fibers in insulin-resistant first-degree relatives of patients with NIDDM
B Nyholm, Z Qu, A Kaal, SB Pedersen, CH Gravholt, JL Andersen, B Saltin and O Schmitz
Department of Medicine (Endocrinology and Diabetes), Institute for Experimental Clinical Research, University of Aarhus, Denmark.
Insulin resistance is a common feature in first-degree relatives of NIDDM
patients. To explore the mechanism(s) behind this condition in more detail,
a percutaneous muscle biopsy (vastus lateralis) was performed in 25
first-degree relatives of NIDDM patients and 21 control subjects to examine
muscle fiber composition and capillary density. Insulin-stimulated glucose
disposal (Rd) was determined employing a hyperinsulinemic-(insulin infusion
rate 0.6 mU x kg[-1] x min[-1]) euglycemic clamp. Rd (5.76 +/- 0.35 vs.
8.06 +/- 0.36 mg x kg lean body weight [LBW]-1 x min[-], P < 0.001) and
estimated VO2max (49.3 +/- 2.8 vs. 57.2 +/- 3.5 mg x kg LBW[-1] x min[-1],
0.05 < P < 0.10) were decreased in the relatives. The number of type
IIb fibers (29.5 +/- 2.5 vs. 21.0 +/- 2.8%, P < 0.05) was increased in
the relatives, whereas no significant differences were found in other fiber
types or capillary density between the groups. Correlations were observed
between number of type I fibers (positive), number of type IIb fibers
(negative), and capillary density (positive) versus Rd as well as estimated
VO2max (P < 0.05). In a multiple linear regression analysis with Rd as a
dependent variable, estimated VO2max, family history of NIDDM, and number
of type IIb fibers (P < 0.001, r2 = 0.64) significantly determined the
level of Rd, whereas capillary density did not. In conclusion,
insulin-resistant first-degree relatives of NIDDM patients are
characterized by an increased number of type IIb muscle fibers. Whether
this finding reflects a reduced physical activity level and fitness in the
relatives or is of primary genetic origin remains to be determined.

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Copyright © 1997 by the American Diabetes Association.
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