We observed a significant positive association between MUAC and MetS in a large-scale population study. Furthermore, we found that MUAC is strongly correlated with waist circumference, lipid parameters, blood pressure, and insulin, which indicated that abnormal local fat depot is a potential screening index for identifying metabolic disorders.
BMI and waist circumference are common screening measures for identifying individuals with abnormal distribution of body fat. Nevertheless, BMI cannot provide accurate information about the local distribution of body fat and it is difficult to obtain height and weight for patients who cannot stand. As for waist circumference, the deficiency of daily application lies in the big difference between preprandial and postprandial measurements. In view of the above reasons, MUAC began to show diagnostic value for assessing nutritional status. Compared to other anthropometric measurements, MUAC is not only easier to obtain, but also has other advantages such as being more accurate, convenient, and low-cost. Small MUAC has shown excellent performance in assessing malnutrition and predicting mortality both in children and older individuals[18, 19]. More recently, large MUAC has been recognized as a valid tool for detecting overweight and obesity in children and adolescents[20, 21]. However, the study about whether MUAC is associated with obesity-related metabolic abnormality, such as MetS, is scarce. Currently, we found that MUAC, as a proxy of upper-body subcutaneous adipose, was positively associated with MetS. Moreover, consistent with previous studies, we found large MUAC also tightly correlated with central obesity, elevated blood pressure, and low HDL cholesterol.
The abnormal accumulation of fat affects adipose tissue metabolic capacities, endocrine, and immune function and leads to altered production of lipid mediators, adipokines, pro- or anti-inflammatory cytokines, and impaired signaling pathways that contribute to obesity-related metabolic abnormality. Obesity increases the flux of fatty acids from adipose tissue to peripheral tissues. The increase in FFAs derived from adipose tissue is mainly mediated by the resistance of adipose tissue to the anti-lipolytic action of insulin. There is compelling evidence that abnormally increased visceral fat is a maker of excessive systemic FFAs release, but it is worth noting that it is upper-body subcutaneous fat released the majority of FFAs. Large MUAC means excessive subcutaneous fat accumulation, which contributes a greater portion of the fatty acids released into the circulation. Circulating FFAs is a crucial mediator in the development of metabolic disorders. Elevated plasma FFAs induce insulin resistance, inflammation, and increase the synthesis and ectopic deposition of triglycerides[28-31]. Concomitantly, excessive FFAs also affect glucose metabolism by inhibiting glucose uptake, oxidation, glycogen synthesis, and increasing output hepatic glucose. Additionally, increased FFAs can trigger oxidative stress which is an early instigator of MetS, and endoplasmic reticulum stress which intersects with many different inflammatory and stress signaling pathways by unfolded protein response[34-36]. The excess FFAs release derived from excess accumulation of arm subcutaneous adipose might be a potential mechanism to partly explain the correlation between MUAC and MetS.
Moreover, the adipose tissue is not only a depot of excess energy but also a highly active metabolic endocrine organ that secretes numerous biologically active molecules, which are collectively termed adipokines. When adipose tissue expands, the capacity of adipocytes to function as endocrine cells and secrete various adipokines is altered in individuals with obesity and MetS[33, 38]. These abnormal levels of adipokine are linked to insulin resistance, impaired triglyceride storage and increased fatty acids in circulation. Furthermore, as fat accumulation, substantial infiltration of immune cells occurs, and there is a specific crown-like disposition of macrophages around single necrotic adipocytes in obese people and subjects with MetS. Subsequently, proinflammatory pathways were activated, and certain proinflammatory cytokines and chemokines were overflowed that result in low-grade inflammation and insulin resistance[22, 38]. In line with the previous study, our findings also observed that MUAC is positively correlated with CRP. Overall, adipose dysfunctions, inflammation, and stress linking mid-upper arm obesity to insulin resistance and MetS.
To our knowledge, this is the first study to evaluate the association between MUAC and Mets among large-scale middle‐aged and older people. The major strength of this study is the analysis based on a large sample. Potential covariates were strictly controlled in the analysis, so as to eliminated the possibility of residual confounding effects.
This study has several limitations. For one thing, we did not measure the tissue composition of the mid-upper arm. The use of MUAC to evaluate the mid-upper arm subcutaneous fat was a convenient and practical way but was unable to quantify the fat accumulation. Therefore, the amount and size of subcutaneous adipocyte and muscle fat are not clear. For another, due to the present study is a cross-sectional analysis, we cannot draw the causality from our findings. Additionally, it is still unclear whether our findings in middle‐aged/older Chinese subjects can be generalized to younger populations or individuals of other ethnicities.
In brief, our study observed that MUAC is positively associated with MetS even after adjustment for potential covariates. These findings provide a novel insight into the association between upper-body obesity and MetS, and a potential screening tool for identifying individuals with MetS. Further researches are necessary to explore the underlying pathophysiological mechanism of the relationship between mid-upper arm subcutaneous fat and MetS.