Leptin Is Reduced in Lean Subjects With Type 2 Diabetes in Bangladesh
- Mohammed Abu Sayeed, MBBS, DCM, MD, PHD1,
- Abul Kalam Azad Khan, MBBS, FCPS, PHD1,
- Hajera Mahtab, MBCHB, DTM&H, FCPS, FRCP1,
- Khandaker Abdul Ahsan, MBBS1,
- Akhtar Banu, MBBS, MSC, PHD1,
- Parvin Akter Khanam, MSC1 and
- Bo Ahrén, MD, PHD2
- 1Bangladesh Institute of Research and Rehabilitation in Diabetes, Endocrine and Metabolic Disorders (BIRDEM), Dhaka, Bangladesh
- 2Department of Medicine, Lund University, Lund, Sweden
Although leptin levels are increased in obesity (1), obese subjects with type 2 diabetes display reduced leptin (2–4), which may be due to altered fat distribution (5). This study examined whether leptin levels are also reduced in lean subjects with type 2 diabetes.
Fifty nonobese Bangladeshi women with type 2 diabetes (aged 37.2 ± 1.3 years) were selected randomly from the Bangladesh Institute of Research and Rehabilitation in Diabetes, Endocrine and Metabolic Disorders (BIRDEM) outpatient department (28 were on diet and exercise, and 22 were on oral hypoglycemic agents; HbA1c 9.6 ± 0.8%). A total of 50 nondiabetic age- and BMI-matched health professional women (aged 33.4 ± 1.9 years) served as control subjects. Circulating leptin (RIA; Linco, St. Charles, MO), BMI, waist-to-hip ratio (WHR), and mid-arm circumference (MAC) were measured. A 75-g oral glucose tolerance test (OGTT) was undertaken with measurements of glucose and insulin (radioimmunoassay).
Diabetic subjects had lower leptin (11.1 ± 1.6 vs. 16.2 ± 1.9 ng/ml, P < 0.001), higher WHR (0.86 ± 0.02 vs. 0.84 ± 0.01; P = 0.034), and lower MAC (23.7 ± 0.4 vs. 25.4 ± 0.7 cm; P < 0.001) than nondiabetic subjects, without any difference in BMI (22.8 ± 0.4 vs. 23.0 ± 0.6 kg/m2). Leptin correlated to MAC (r = 0.46, P < 0.001) but not to WHR (r = 0.01). Although fasting insulin did not differ between the groups (84.2 ± 16.6 vs. 92.7 ± 34.2 pmol/l), the 60-min insulin levels during the OGTT were lower in the diabetic subjects (209 ± 22 vs. 467 ± 38 pmol/l, P < 0.001) in spite of higher 60-min glucose levels in the diabetic subjects (14.2 ± 4.8 vs. 6.8 ± 2.1 mmol/l; P < 0.001). In the diabetic subjects, leptin correlated significantly to fasting insulin independent of BMI (r = 0.65, P = 0.007).
This shows that lean diabetic subjects also exhibit low leptin levels, as previously observed for moderately obese diabetic subjects (2–4). The lower leptin levels in diabetes might be explained by altered fat distribution, since we observed higher WHR and lower MAC in the diabetic subjects. This is consistent with a higher leptin secretion from subcutaneous fat tissue than from intraabdominal fat tissue (6). Other possibilities also exist, such as the low insulin or different caloric intake, or the degree of physical activity, which was not determined in this study. The lower leptin might be of importance for accumulation of cellular lipids that is associated with diabetes (7).
We thank Sida, Stockholm, Sweden, for financial help; BIRDEM for logistic support; and Dr. M. Sawkat Hassan and Lilian Bengtsson for conducting lab investigations.
Address correspondence to Dr. Bo Ahrén, Department of Medicine, B11 BMC, SE-221 84 Lund, Sweden. E-mail:.
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