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

Morais, Tassiane Cristina; Abreu, Luíz Carlos de; Quental, Ocilma Barros de; Pessoa, Rafael Souza; Fujimori, Mahmi; Daboin, Blanca Elena Guerrero; França, Eduardo Luzía; Honório-França, Adenilda Cristina

doi:10.3390/cells8060519

Cited by 15 publications

(23 citation statements)

References 55 publications

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“…This is consistent with the finding that leptin can reduce oxidative stress and decrease apoptosis in other cells (Balasubramaniyan et al, 2007;Kaeidi et al, 2019). Morais et al (2019) have shown that leptin can activate the classical nuclear factor-κB pathway, which can regulate the genes responsible for ROS production.…”

Section: Discussionsupporting

confidence: 91%

Leptin attenuates hypoxia‐induced apoptosis in human periodontal ligament cells via the reactive oxygen species–hypoxia‐inducible factor‐1α pathway

Gao

Zhu

Zhao

et al. 2021

Experimental Physiology

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Hypoxia-induced apoptosis of human periodontal ligament cells (hPDLCs) is an important contributor to the progression of various periodontal diseases. Although leptin has been shown to protect connective tissue cells against hypoxia-induced injury, whether it might do so by attenuating hypoxia-induced apoptosis in hPDLCs remains unclear. Here, using CoCl 2 treatment, we simulated hypoxic conditions in hPDLCs and explored whether apoptosis and reactive oxygen species (ROS) levels were related to hypoxia. After small interfering RNA (siRNA) inhibition of leptin and hypoxia-inducible factor-1α (HIF-1α), the levels of apoptosis, ROS and leptin expression were measured.We showed that in CoCl 2 -treated hPDLCs, significantly higher cell apoptosis rates and ROS accumulation were observed. Cobalt chloride also increased leptin and HIF-1α expression in hPDLCs. Further investigation of the pathway demonstrated that inhibition of ROS attenuated hypoxia-induced cell apoptosis and leptin expression, whereas siRNA inhibition of leptin aggravated hypoxia-induced cell apoptosis and ROS accumulation. Hypoxia induces cell apoptosis and leptin expression in hPDLCs through the induction of ROS and HIF-1α pathways, and leptin shows feedback inhibition on ROS-mediated apoptosis in hPDLCs. These findings suggest a new application of leptin for hypoxic damage in periodontal diseases.

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Section: Discussionsupporting

confidence: 91%

Leptin attenuates hypoxia‐induced apoptosis in human periodontal ligament cells via the reactive oxygen species–hypoxia‐inducible factor‐1α pathway

Gao

Zhu

Zhao

et al. 2021

Experimental Physiology

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“…Obesity and diabetes are related to a higher incidence and severity of infectious diseases and involve different cells and immune mechanisms [ 41 ]. In addition, the immunological factors observed cause alterations in the percentage and function of cell, cytokine, antibody, and adipokine levels [ 18 , 42 , 43 ], suggesting changes in inflammatory mediators [ 44 ].…”

Section: Discussionmentioning

confidence: 99%

Resistin Modulates the Functional Activity of Colostral Macrophages from Mothers with Obesity and Diabetes

et al. 2022

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Background: Obesity and diabetes are major public health problems. Resistin is an adipokine that links the two diseases. There are few reports regarding colostrum cells and resistin from mothers with obesity and diabetes. Thus, this study aimed to determine the functional activity of macrophages present in the breast milk and colostrum of diabetic mothers with obesity and the effects of resistin on these cells. Methods: The women were divided according to BMI and glycemic status into normal weight non-diabetic, obese non-diabetic, normal weight type 2 diabetic, or obese type 2 diabetic groups. ELISA determined the resistin in colostrum. The cell subsets and apoptosis were determined by flow cytometry and the functional activity of cells by fluorescence microscopy. Results: The resistin levels were higher in the colostrum from diabetic mothers with obesity. The frequencies of CD14+ cells and cells expressing CD95+, independent of resistin treatment, were higher in the colostrum from diabetic mothers with obesity. The frequency of cells expressing CD14+CD95+ was higher in cells not treated with resistin in the colostrum from diabetic mothers with obesity. Apoptosis, irrespective of the presence of resistin, increased, whereas microbicidal activity decreased in cells from diabetic mothers with obesity. Conclusion: The data suggest that hyperglycemia associated with low-grade inflammation caused by obesity affects the percentage of cells expressing CD14+CD95+, death by apoptosis, and microbicidal indices; meanwhile, resistin restored the microbicidal activity of colostrum cells.

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“…Nutrition and some nutrients can influence the immune system and regulate directly by signaling pathways, as well as regulating hormones that, in turn, modulate the immune system. [30]. In this study, melatonin adsorbed to PEG microspheres exhibited anti-tumor activity against MCF-7 human breast cancer cells, especially when in coculture with colostrum MN cells, and this activity oscillated as a function of the time of day.…”

Section: Discussionmentioning

confidence: 60%

Nanodoses of melatonin induces apoptosis on human breast cancer cells co-cultured with colostrum cells

2019

Biointerface Res Appl Chem

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The aim of this study was to investigate the effect of melatonin nanodoses adsorbed to PEG microspheres during different phases of the day on oxidative stress and apoptosis in human colostrum mononuclear (MN) cells co-cultured with breast cancer tumor cells (MCF-7). The MCF-7 cells were obtained from the American Type Culture Collection, and the MN cells were obtained from volunteer donors. The cells were preincubated for 24 h with or without 100 ng.mL-1 melatonin (MLT), PEG microspheres (PEG) or 100 ng.mL-1 MLT adsorbed to PEG microspheres (PEG-MLT). Superoxide, superoxide dismutase (SOD), intracellular calcium and apoptosis in the MN cells, MCF-7 cells and co-cultures were determined. The MN cells and co-cultured cells during the nocturnal period and the MCF-7 cells during the diurnal period exhibited increased superoxide release in the presence of PEG-MLT. MN cells treated with MLT during both periods of the day exhibited the highest SOD concentrations, whereas the MCF-7 cells had high SOD levels when incubated with PEG-MLT during the nocturnal period. The nocturnal period co-culture, independent of treatment, showed the highest levels of the enzyme. The highest amount of intracellular Ca2+ release was observed in MN cells and MCF-7 cells co-cultured with PEG-MLT during the nocturnal period. Irrespective of the phase of the day, the highest apoptosis index was observed in co-cultures of cells incubated with MLT-PEG. These data suggest that nanodoses of melatonin-modified release plus physiological melatonin produced in higher concentrations during the night can increase the effective activity of this hormone against tumors.

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

Cited by 15 publications

References 55 publications

Leptin attenuates hypoxia‐induced apoptosis in human periodontal ligament cells via the reactive oxygen species–hypoxia‐inducible factor‐1α pathway

Leptin attenuates hypoxia‐induced apoptosis in human periodontal ligament cells via the reactive oxygen species–hypoxia‐inducible factor‐1α pathway

Resistin Modulates the Functional Activity of Colostral Macrophages from Mothers with Obesity and Diabetes

Nanodoses of melatonin induces apoptosis on human breast cancer cells co-cultured with colostrum cells

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