Obesity as an Inflammatory Agent Can Cause Cellular Changes in Human Milk due to the Actions of the Adipokines Leptin and Adiponectin

Abstract

Adiponectin and leptin play roles in the hunger response, and they can induce the inflammatory process as the initial mechanism of the innate immune response. It is possible for alterations in the levels of these adipokines to compromise the functional activity of human colostrum phagocytes. Therefore, the objective of this study is to analyze the effects of adiponectin and leptin on colostrum mononuclear (MN) cells. Colostrum was collected from 80 healthy donors, who were divided into two groups: the control group and the high body mass index (BMI) group. MN cells were used to analyze phagocytosis by flow cytometry, and reactive oxygen species (ROS), intracellular calcium, and apoptosis were assessed by fluorimetry using a microplate reader. Adipokines restored the levels of phagocytosis to the high BMI group (p < 0.05), with a mechanism that is action-dependent on the release of ROS and intracellular calcium. However, adiponectin and leptin simultaneously contributed to better microbicidal activity, thus reflecting an increase in the apoptosis level (p < 0.05) in the high BMI group. Probably, the maintenance of the balance between adiponectin and leptin levels enhances the protection and decreases the indices of neonatal infection in the breastfeeding infants of women with high BMI values. Therefore, policies that support pre-gestational weight control should be encouraged.

Keywords: adiponectin; body mass index; colostrum; leptin; obesity; overweight; oxidative stress; phagocytes.

Figure 1

Effects of adiponectin and leptin on phagocytosis by colostrum mononuclear (MN) cells from women with normal BMI and high BMI values. Phagocytosis Index (%) values were determined by the assessment of pHRodo™ Green zymosan in MN cells from human colostrum. The results are presented as mean ± SD (n = 10 per group). They were assessed by ANOVA and Tukey’s Test. * Statistical difference between colostrum cells incubated with 119 medium and hormones within groups (p < 0.05). ^# Statistical difference among groups with the same treatment and samples (p < 0.05).

Figure 2

The effects of adiponectin and leptin on the oxidative burst of colostrum mononuclear cells from women with normal BMI and high BMI values incubated with Zymosan A from Saccharomyces cerevisiae. Reactive oxygen species were released by colostrum mononuclear phagocytes. The results are presented as mean ± SD (n = 10 per group) and assessed by ANOVA and Tukey’s Test. * Statistical difference between colostrum cells incubated with 199 medium and hormones within groups (p < 0.05). ^# Statistical difference among groups with the same treatment and sample (p < 0.05).

Figure 3

The effects of adiponectin and leptin on the release of intracellular calcium by colostrum mononuclear phagocytes from women with normal BMI and high BMI values incubated with Zymosan A from Saccharomyces cerevisiae. Intracellular calcium release was performed with Fluo-3AM (n = 10). The results are presented as the mean ± SD (n = 10 per group). They were assessed by ANOVA and Tukey’s Test. * Statistical difference between colostrum cells incubated with 119 medium and hormones within groups (p < 0.05). ^# Statistical difference among groups with the same treatment and sample (p < 0.05).

Figure 4

The effects of adiponectin and leptin on the apoptosis index of colostrum mononuclear phagocytes from women with normal BMI and high BMI values incubated with Zymosan A from Saccharomyces cerevisiae. The apoptosis assay was performed by Annexin V-fluorescein isothiocyanate (FITC) staining (n = 10). The results are presented as mean ± SD. They were assessed by ANOVA and Tukey’s test. * Statistical difference between colostrum cells incubated with 119 medium and hormones within groups (p < 0.05). ^# Statistical difference among groups with the same treatment and sample (p < 0.05).