Is Altered Body Fat Distribution Responsible for Reduced Pulmonary Function in Obese Type 2 Diabetic Adult Women? Free

Most patients with type 2 diabetes are overweight (1), and their fat-distribution pattern shows more truncal and less peripheral subcutaneous fat. Particularly, adult women with type 2 diabetes have been reported to have significantly reduced lower-body fat compared with normoglycemic women matched for age and BMI (2). With regard to the association between diabetes and pulmonary function, only a few studies have described pulmonary function in subjects with type 2 diabetes, and their results are conflicting. Lange et al. (3) reported reductions in forced vital capacity (FVC) and forced expiratory volume in one second (FEV1) among type 2 diabetic patients of different ages. The Rancho Bernardo Study (4), on the other hand, found no relationship between type 2 diabetes and pulmonary function in normal-weight adults.

The effects of obesity on ventilatory parameters may depend on both the distribution and size of excess adipose tissue, and may also change according to the specific pattern of body fat deposition. In fact, decreased ventilatory parameters have been reported to be associated with the accumulation of fat in the abdominal region, which impedes the descent of the diaphragm into the abdominal cavity. Dual-energy X-ray absorptiometry (DEXA) is an accurate and precise method of measuring body composition (i.e., fat mass and lean body mass). When measuring body fat distribution by DEXA, it has been shown that a decrease in the upper-body fat of obese subjects, without any decrease in upper–lean body mass, is associated with improvements in ventilatory function (5). Although the role of central obesity in ventilatory impairment is well known, few studies have evaluated this association among individuals with type 2 diabetes. Our objective was to evaluate this association between pulmonary dysfunctional restrictive pattern and body fat distribution, as measured by DEXA, and anthropometry in type 2 diabetes obese women.

We recruited seven nonsmoking mildly obese adult women affected with type 2 diabetes (mean age 50.29 ± 2.87 years) and seven normoglycemic nonsmoking women matched for age and BMI. After physical examination, patients with respiratory symptoms, lung diseases, FEV1/FVC <76% of the predicted value, or limited joint mobility were excluded. Dynamic spirometric tests were performed for all participants according to the guidelines of the American Thoracic Society. Maximum voluntary ventilation (MVV) was determined by fast deep breathing for 12 s. Total fat mass, total lean body mass (LBMtot), trunk fat mass (FMtrunk), and trunk lean body mass (LBMtrunk) were measured using DEXA.

Dynamic respiratory indexes FVC, VC, and FEV1 in the type 2 diabetes women had significantly lower (P ≤ 0.05) values (2.68 ± 0.30, 2.59 ± 0.40, and 2.17 ± 0.20 l, respectively) compared with control subjects (3.23 ± 0.30, 3.15 ± 0.46, and 2.59 ± 0.31 l, respectively). This finding is compatible with results from the Copenhagen Heart Study (4) and is also consistent with studies that reported significantly reduced pulmonary function among middle-aged men with type 2 diabete subjects (6). We found no significant difference between type 2 diabetic women and control subjects in terms of fat distribution, specifically, in FMtrunk (a measure of central obesity), which can be associated with the significant low pulmonary respiratory parameters (FVC and FEV1) of type 2 diabetic women. Nevertheless, we recently observed a significant correlation between FMtrunk and poor respiratory function among obese subjects (5).

The overall absence in obese type 2 diabetic women of an association between reduced pulmonary function and body fat mass (total and segmental) suggests that this abnormality in respiratory pattern may derive from nonenzymatic glycosylation of collagen proteins. If accumulation of cross-linked collagen occurs in the lungs of type 2 diabetic patients, functional changes resembling mild interstitial fibrosis may follow (7). The patients in our study had been recently diagnosed with type 2 diabetes, which is in line with the results of Lange et al. (3). Furthermore, among our patients, diabetes was decompensated, as confirmed by the mean fasting plasma glucose (206.80 ± 45.51 mg/dl). Thus, it can be hypothesized that the excessive decrease in ventilatory function among obese women who recently developed type 2 diabetes may be due to cross-linking of pulmonary collagen; however, this hypothesis would need to be tested by measuring the diffusing capacity of the lung for carbon monoxide.

The MVV was also significantly lower (P ≤ 0.05) in type 2 diabetic women (71.92 ± 12.32 l/min vs. 93.32 ± 17.11 l/min for control subjects), as was peak expiratory flow (PEF) (4.31 ± 0.60 l/s for type 2 diabetic women vs. 5.82 ± 0.43 l/s for control subjects; P = 0.0003). This finding may be associated with diabetes-related peripheral neuropathy developed during the asymptomatic preclinical phase of the disease. Among the newly diagnosed patients of the U.K. Prospective Diabetes Study Group, involvement of the peripheral nervous system was common, and 5% of these people had impaired reflexes and 7% had abnormal vibration threshold (8). Therefore, decreases in MVV can be viewed as an early abnormality that precedes symptomatic neuropathy. Similarly, the decreased PEF among type 2 diabetic women in our study, as compared with control subjects, may also be related to muscloskeletal etiology. It is also worth noting that MVV and PEF are reduced in patients with muscular diseases. The finding that total and/or segmental lean body mass (LBMtot and LBMtrunk) measurements were similar in both study groups excludes the possibility of muscle depletion but not of muscle dysfunction, which might have been responsible for the abnormalities in FVC, FEV1, PEF, and MVV.

Finally, we deduce that pulmonary dysfunction is not associated with body fat distribution, specifically with truncal fat mass deposition. We further postulate that the diffusing capacity of the lung for carbon monoxide and respiratory muscle function in obese women with type 2 diabetes may explain the relationship between pulmonary dysfunction and body composition (fat mass distribution and lean function).