School of Medicine and Health Sciences Poster Presentations
Artificial Sweetener such as Sucralose May Promote Inflammation in Human Subcutaneous Fat-derived Mesenchymal Stromal Cells (MSCs)
Document Type
Poster
Keywords
Sweetners; Adipogenesis; MSCs
Publication Date
Spring 2017
Abstract
Artificial sweeteners are extensively used as alternatives for caloric sugars, particularly among individuals with obesity and diabetes, who have an increased cardiovascular disease (CVD) risk. Sucralose is a common artificial sweetener used as a low calorie sweetener (LCS) in multiple food products. MSCs are multipotent mesenchymal tissue derived cells, which differentiates into fat, bone, muscle and cartilage depending on the body’s repair needs, cell environment or culture media conditions. Based on human epidemiological studies that shows an association with LCS use and obesity, we decided to investigate whether varying concentrations of sucralose in an obesogenic environment alter differentiation of MSCs more towards adipogenesis and promote inflammation in MSCs. We cultured commercially obtained MSCs (Lonza, Inc) in Adipogenic Media (Lonza, Inc) with sucralose (0, 0.2, 0.45, 1.0 mM) for 12 days. After 12 days MSCs were stained with Oil Red O stain for imaging and lipolysis quantification using a plate reader (520nm). Rest of the cultured MSCs were collected for RT-PCR. Results: Lipolysis and staining experiments indicate that intracellular fat droplet accumulation increased in parallel with increasing sucralose concentrations. Using RT-PCR, we noted higher expression of adipogenic genes such as CEBPa (1.32x fold), and FABP4 (1.04x) at 0.2mM of sucralose concentration (a high but physiological concentration). In comparison, 1mM sucralose (reflecting supra-physiologic concentrations) showed markedly increased expression of CEBPa (3.45x), and FABP4 (4.06x). MSCs cultured in sucralose (1mM) upregulated the antioxidant glutathione peroxidase-3 (2 .00x) possibly in response to increased superoxide accumulation and cellular inflammation. Increased expression of sweet taste receptor subunit T1R2 (2.45x) was also noted. In summary, upregulation of adipogenic genes such as CEBPa and FABP-4 in hMSCs, cultured in near physiological concentrations of sucralose, indicate possible causality between increased fat deposition and sweetener use. Further studies at physiological concentrations of sucralose using multipotent cells like MSCs in-vivo along with human studies are needed to establish whether sucralose use leads to increased fat deposition particularly in a high CVD risk population of obesity, prediabetes and diabetes.
Creative Commons License
This work is licensed under a Creative Commons Attribution-Noncommercial-No Derivative Works 4.0 License.
Open Access
1
Artificial Sweetener such as Sucralose May Promote Inflammation in Human Subcutaneous Fat-derived Mesenchymal Stromal Cells (MSCs)
Artificial sweeteners are extensively used as alternatives for caloric sugars, particularly among individuals with obesity and diabetes, who have an increased cardiovascular disease (CVD) risk. Sucralose is a common artificial sweetener used as a low calorie sweetener (LCS) in multiple food products. MSCs are multipotent mesenchymal tissue derived cells, which differentiates into fat, bone, muscle and cartilage depending on the body’s repair needs, cell environment or culture media conditions. Based on human epidemiological studies that shows an association with LCS use and obesity, we decided to investigate whether varying concentrations of sucralose in an obesogenic environment alter differentiation of MSCs more towards adipogenesis and promote inflammation in MSCs. We cultured commercially obtained MSCs (Lonza, Inc) in Adipogenic Media (Lonza, Inc) with sucralose (0, 0.2, 0.45, 1.0 mM) for 12 days. After 12 days MSCs were stained with Oil Red O stain for imaging and lipolysis quantification using a plate reader (520nm). Rest of the cultured MSCs were collected for RT-PCR. Results: Lipolysis and staining experiments indicate that intracellular fat droplet accumulation increased in parallel with increasing sucralose concentrations. Using RT-PCR, we noted higher expression of adipogenic genes such as CEBPa (1.32x fold), and FABP4 (1.04x) at 0.2mM of sucralose concentration (a high but physiological concentration). In comparison, 1mM sucralose (reflecting supra-physiologic concentrations) showed markedly increased expression of CEBPa (3.45x), and FABP4 (4.06x). MSCs cultured in sucralose (1mM) upregulated the antioxidant glutathione peroxidase-3 (2 .00x) possibly in response to increased superoxide accumulation and cellular inflammation. Increased expression of sweet taste receptor subunit T1R2 (2.45x) was also noted. In summary, upregulation of adipogenic genes such as CEBPa and FABP-4 in hMSCs, cultured in near physiological concentrations of sucralose, indicate possible causality between increased fat deposition and sweetener use. Further studies at physiological concentrations of sucralose using multipotent cells like MSCs in-vivo along with human studies are needed to establish whether sucralose use leads to increased fat deposition particularly in a high CVD risk population of obesity, prediabetes and diabetes.
Comments
Poster to be presented at GW Annual Research Days 2017.