The major findings of this study are 1) the subjects with reduced lung function as measured with FVC (% predicted) and FEV1 (% predicted) had higher incidence of type 2 diabetes, independent of other confounding factors including age, BMI, education, smoking, exercise, alcohol and HOMA-IR; and 2) in non-obese subjects with BMI <25, decreased FVC (% predicted) and FEV1 (% predicted) were also inversely and significantly correlated with the incidence of type 2 diabetes. Our findings are generally consistent with previous studies that reported a significant association between reduced lung function and type 2 diabetes [8–10, 20, 21].
Previous studies have reported that the risk of being relatively insulin resistant, as measured by HOMA-IR, significantly increased as lung function decreased [7, 9, 21]. In the Normative Aging Study, 1,050 non-diabetic male subjects were followed over 20 years. Lower FVC, FEV1, and maximal mid-expiratory flow rate at baseline were significantly associated with risk of hyperinsulinemia and estimated insulin resistance . Some epidemiologic and clinical studies have found that decreased lung function is associated with type 2 diabetes, independent of obesity [8–10, 21–23]. In Asia, a number of studies have reported relationships between lung function and type 2 diabetes, insulin resistance and metabolic syndrome (MS) [12–15, 24, 25]. Although studies were limited by their cross-sectional design or small cohorts, they suggested that FVC and FEV1 could be predictive markers of incident type 2 diabetes or MS in Asian populations. Recently, The Strong Heart Study reported that reduced lung function is independently associated with diabetes, and impaired lung function presents before the development of diabetes in American Indians .
Type 2 diabetes is associated with insulin resistance and glucose tolerance, which could originate from visceral obesity . Yeh et al. found that abdominal obesity is a significant factor affecting type 2 diabetes, MS, and pulmonary function test results . Another study by Jung et al.  reported that nonalcoholic fatty liver disease, a well-known marker for insulin resistance and MS, was associated with reduced pulmonary function. In our study, subjects in the diabetes group had a significantly higher BMI and lower FVC and FEV1 (L) at baseline compared to those in the non-diabetes group. In addition, ventilatory function is partially determined by respiratory muscle strength, which may be compromised in obese subjects .
The association between diminished lung function and type 2 diabetes may be explained according to a common inflammatory process . Obesity and metabolic syndrome are associated with elevated systemic inflammatory markers and adipocytokines . Alternatively, the induction of increased oxidative activity, intracellular NF-kB and inflammatory mediators could also result in chronic hyperglycemia and an increase in collagen molecule synthesis and cross-linking via the acceleration of advanced glycation end-products, ultimately negatively influencing lung function . Moreover, previous studies have indicated that proinflammatory cytokines such as C-reactive protein (CRP), fibrinogen and IL-6 may play a role in the pathogenesis of type 2 diabetes [10, 13, 15, 23], although a recent study showed no association of glucose control with hs-CRP . However, we could not address the association between inflammation and type 2 diabetes because most study subjects did not have available measurements of inflammatory markers such as CRP and IL-6.
We note that our study had some limitations. First, there is the possibility of selection bias because most participants were residents of an urban community, all subjects were of Korean descent, from one university hospital, and there were no women in this study. Therefore, the results of this study cannot be generalized to the worldwide population. Second, incident type 2 diabetes was defined based only on fasting glucose level or a self-reported medical history of type 2 diabetes, and no oral glucose tolerance tests were performed. Thus, the incidence of type 2 diabetes may have been underestimated in this study. Third, risk of diabetes may have been influenced by early life style factors which was not investigated in this study. Therefore, future studies including birth cohort analysis are needed to clarify the cause-effect link between reduced lung function and risk of developing diabetes. Finally, our data consisted of only baseline and five-year follow-up time points. The outcome was considered the presence of type 2 diabetes at five years. Thus, logistic regression was used for analysis instead of a Cox regression model. However, our study had the advantage of including a relatively large total number of subjects over a relatively long follow-up period.