Copyright © 2004 by the Johns Hopkins Bloomberg School of Public Health
LETTERS TO THE EDITOR |
THREE AUTHORS REPLY
1 Department of Preventive Medicine, University of Tennessee Health Science Center, Memphis, TN 38163
2 Department of Nutrition, Harvard School of Public Health, Boston, MA 02115
3 Department of Human Nutrition and Division of Epidemiology and Biostatistics, University of Illinois at Chicago, Chicago, IL 60612
4 Department of Epidemiology, Harvard School of Public Health, Boston, MA 02115
5 Channing Laboratory, Department of Medicine, Brigham and Womens Hospital and Harvard Medical School, Boston, MA 02115
We thank Snijder et al. (1) for their insightful comments regarding our article (2). They direct our attention to an additional potential explanation for the association we observed between smaller hip circumference and increased risk of type 2 diabetes mellitus. In particular, they argue that the hazards posed by a smaller hip circumference may be attributed to a reduction in leg fat mass in addition to peripheral muscle wasting.
We agree that there is mounting evidence to support such associations and that the leg fat depot, unlike the truncal fat depot, may confer protection against metabolic disturbances due to regional differences in the regulation of lipolysis (3) as well as to variation in adipokine secretion and function deriving from these depots (4). However, the studies that linked baseline leg fat depot to a more favorable metabolic profile were cross-sectional (46). These studies did not quantify the relative degree of change in the fat versus fat-free depots at particular circumference sites in the same population, which may more strongly explain changes in diabetes risk. It is in the context of our original study aims that these questions are important, since we examined how 9-year changes in circumference predicted subsequent 4-year risk (2).
To our knowledge, one prospective study to date has documented the relation of magnitude of change in appendicular and trunk circumferences to regional changes in fat and fat-free tissue (7). In that study, mean thigh circumference significantly decreased by 2.4 cm (standard deviation, 2.9) among men and 4.5 cm (standard deviation, 4.4) among women over an average of 9.4 years. With the use of computed tomography in a subset of men, the investigators determined that the decline in thigh area was explained entirely by the decrease in muscle area, whereas subcutaneous fat area remained unchanged (7). Such findings support the greater emphasis we placed on diminishing peripheral muscle mass versus declining leg fat in explaining the decrease in hip circumference over time among the men. The fact that skeletal muscle is the main target organ and site of insulin resistance (8), coupled with the high degree to which gluteal/femoral muscle mass accounts for total skeletal muscle, supports the hypothesis of an independent role of peripheral muscle atrophy in the progression to diabetes, which we and other investigators have postulated (8, 9).
Further data are needed to assess whether the reduction in hip girth signifies a predominant loss of muscle mass and whether it may serve as an independent correlate of insulin resistance in predicting diabetes risk. Moreover, whether the quality of muscle mass affects insulin resistance, with respect to changes in fiber type and/or increased infiltration of intramuscular fat mass, is unknown. In the meantime, our data provide further support for recommending regular physical activity and avoidance of excess energy intake, which helps in maintaining muscle mass and avoiding gain in waist circumference, as strategies for preventing type 2 diabetes.
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