Letter: Association of Thigh Muscle Mass with Insulin Resistance and Incident Type 2 Diabetes Mellitus in Japanese Americans (Diabetes Metab J 2018;42:488–95)

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Diabetes Metab J. 2019;43(1):123-124
Publication date (electronic) : 2019 February 19
doi : https://doi.org/10.4093/dmj.2019.0026
Department of Internal Medicine, Keimyung University School of Medicine, Daegu, Korea.
Corresponding author: Hye Soon Kim. Department of Internal Medicine, Keimyung University Dongsan Medical Center, Keimyung University School of Medicine, 56 Dalseong-ro, Jung-gu, Daegu 41931, Korea. hsk12@dsmc.or.kr

Skeletal muscle is a major tissue responsible for the majority of insulin-stimulated glucose uptake in the body [1]. Muscle quantity and quality are regarded to play an important role in the development of type 2 diabetes mellitus (T2DM), as well as related metabolic disorders. Previous studies have demonstrated the cross-sectional associations between low muscle mass and strength, and insulin resistance and prevalent diabetes [234]. Recently, however, a few prospective studies have been conducted focusing on confirming the causality and suggested that low muscle mass and strength are potential risk factors for the development of diabetes, although there are some conflicting results [567].

In this issue, Han et al. [8] investigated the association of thigh muscle mass measured by computed tomography (CT) with insulin resistance and incident T2DM over a 10-year follow-up in a Japanese American cohort. The mean age of study participants was 51.6 years. Among 399 participants, 22.1% developed diabetes. The authors showed that the thigh muscle area measured by CT was inversely associated with future insulin resistance after adjustment for covariates including total abdominal fat area and thigh subcutaneous fat area. In addition, they found that greater thigh muscle area was associated with lower risk of incident T2DM for subjects with lower levels of body mass index (BMI), but this association was not seen in those with higher BMI levels. This clearly shows that greater thigh muscle area predicts a lower risk of incident T2DM for lean individuals. It would have been more valuable if the authors measured the thigh intramuscular or intermuscular fat content, which is significantly associated with insulin resistance [9]. Also, we would like to ask if the authors investigated the relationship between abdominal fat distribution and thigh muscle mass, as well as incident T2DM. Nevertheless, these findings are meaningful as they are because the results are based on a well-designed cohort with a long-term follow-up period, and it extends prior findings by showing consistent results with the earlier Health ABC study. There also was an inverse association between abdominal muscle and thigh muscle area, and incident diabetes in normal-weight women in the Health ABC study of elderly Caucasian and African Americans. However, this finding was difficult to generalize, because the study participants were older than 70 years and the results varied by sex [6].

It is interesting to note that BMI acts as an effect modifier in the association between muscle mass and T2DM risk. Previous studies also showed diminution of the inverse association between muscle and T2DM risk at higher BMI levels [56]. The underlying mechanism is unclear, but there has been speculations that the harmful effects of excess adiposity overpowered the benefits of muscle for obese individuals [8]. This finding suggests that muscle mass could play a stronger role in metabolic health in those without excess adiposity, which may be related to normal weight-obesity. In addition, particularly for normal weight individuals, the need to increase muscle mass should be emphasized. To establish this view, further research is needed to determine whether increasing muscle mass could prevent diabetes and whether the effect varies with BMI.


CONFLICTS OF INTEREST: No potential conflict of interest relevant to this article was reported.


1. Mizgier ML, Casas M, Contreras-Ferrat A, Llanos P, Galgani JE. Potential role of skeletal muscle glucose metabolism on the regulation of insulin secretion. Obes Rev 2014;15:587–597. 24618283.
2. Srikanthan P, Karlamangla AS. Relative muscle mass is inversely associated with insulin resistance and prediabetes. Findings from the Third National Health and Nutrition Examination Survey. J Clin Endocrinol Metab 2011;96:2898–2903. 21778224.
3. Larsen BA, Allison MA, Laughlin GA, Araneta MR, Barrett-Connor E, Wooten WJ, Saad SD, Wassel CL. The association between abdominal muscle and type II diabetes across weight categories in diverse post-menopausal women. J Clin Endocrinol Metab 2015;100:E105–E109. 25250636.
4. Grontved A, Pan A, Mekary RA, Stampfer M, Willett WC, Manson JE, Hu FB. Muscle-strengthening and conditioning activities and risk of type 2 diabetes: a prospective study in two cohorts of US women. PLoS Med 2014;11e1001587. 24453948.
5. Wander PL, Boyko EJ, Leonetti DL, McNeely MJ, Kahn SE, Fujimoto WY. Greater hand-grip strength predicts a lower risk of developing type 2 diabetes over 10 years in leaner Japanese Americans. Diabetes Res Clin Pract 2011;92:261–264. 21281974.
6. Larsen BA, Wassel CL, Kritchevsky SB, Strotmeyer ES, Criqui MH, Kanaya AM, Fried LF, Schwartz AV, Harris TB, Ix JH. Health ABC Study. Association of muscle mass, area, and strength with incident diabetes in older adults: The Health ABC Study. J Clin Endocrinol Metab 2016;101:1847–1855. 26930180.
7. Son JW, Lee SS, Kim SR, Yoo SJ, Cha BY, Son HY, Cho NH. Low muscle mass and risk of type 2 diabetes in middle-aged and older adults: findings from the KoGES. Diabetologia 2017;60:865–872. 28102434.
8. Han SJ, Boyko EJ, Kim SK, Fujimoto WY, Kahn SE, Leonetti DL. Association of thigh muscle mass with insulin resistance and incident type 2 diabetes mwellitus in Japanese Americans. Diabetes Metab J 2018;42:488–495. 30302961.
9. Goodpaster BH, Thaete FL, Kelley DE. Thigh adipose tissue distribution is associated with insulin resistance in obesity and in type 2 diabetes mellitus. Am J Clin Nutr 2000;71:885–892. 10731493.

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