Background. Serum levels of the mannose-binding lectin (MBL), which is an activator of the complement system, have been considered as a pathogenic factor in a broad range of diseases, and means of modulating MBL are therefore being evaluated. In this study we examine the effects of weight loss on MBL levels, and in continuation of this if MBL is synthesized in human adipose tissue. Methods. 36 nondiabetic obese subjects received a very low-calorie diet (VLCD) of 800 kcal/day for 8 weeks. Blood samples were collected at baseline and after VLCD. Furthermore, we measured MBL mRNA levels by the real-time RT-PCR on human adipose tissue compared to liver tissue. Results. The mean body weight was reduced from ？kg to ？kg, . Median MBL at baseline was 746？μg/L (IQR 316–1190) versus 892？μg/L (IQR 336–1511) after 8 weeks, . No correlations were found between weight loss and changes in MBL ( , ). MBL real-time RT-PCR showed no expression of mRNA in adipose tissue, but as expected a good expression in liver tissue was seen. Conclusions. MBL levels are not affected by weight loss and MBL is not synthesized in human adipose tissue. 1. Introduction Mannose-binding lectin (MBL) is a serum protein known to be synthesized by hepatocytes. MBL exerts an important role in the innate immune system, where it upon binding to carbohydrate patterns of microorganisms activates the lectin pathway of the complement system through MBL-associated serine protease 1, 2, and 3 [1, 2]. This leads to recruitment of inflammatory cells, opsonization, and formation of the membrane attack complex [3], which causes destruction of the microorganisms. Serum MBL level is dependent on genotype and, because of commonly occurring polymorphisms in the MBL encoding gene MBL2, the interindividually expressed serum level of MBL ranges from a few μg/L to several thousand μg/L. In healthy subjects approximately 56% have a high MBL encoding genotype (homozygote wild type), 40% have an intermediate MBL encoding genotype (mutation in one allele), and 4% have a low MBL encoding genotype (mutations in both alleles), the latter being functionally deficient in MBL [4], the most common immunodeficiency described. Several clinical studies have shown low MBL levels to be associated with increased susceptibility or to poor outcome of infections. This lack of defense against invading microorganisms may be important especially in certain situations, for example, in infants with an immature immune system [5–7] and in adults with a compromised immune system [8, 9], as the immune system normally features a degree of
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