Artificial Sweeteners Do Not Induce Adipogenesis In the Absence of Proadipogenic Inducers in 3T3-L1 Cells.
Location
Poster #25
Department
Biology
Abstract
We set out to investigate the effects of some of the most common sweeteners used in the United States (Saccharine, Acesulfame-K, Sucralose, Trivia™, and Erythritol) on adipogenesis using 3T3-L1 preadipocyte fibroblasts differentiated into fully mature adipocytes. Preadipocyte fibroblasts were cultured and differentiated in media containing proadipogenic inducers plus artificial sweeteners, as well as media containing only the sweeteners to observe the effect of the sweeteners alone. Morphological changes in the 3T3-L1 cell line were monitored during differentiation with and without sweeteners using microscopy and image analysis of the accumulation of intracellular lipids. There was a significant accumulation of intracellular lipids during differentiation in all cells cultured with artificial sweeteners, in the presence of proadipogenic inducers, thus suggesting a direct effect on adipogenesis. However, there was no significant lipid droplet formation when cells where cultured in the presence of the sweeteners without any proadipogenic inducers. Previous in vitro studies investigating the effects of artificial sweeteners on adipogenesis studies have found that some artificial sweeteners, such as Saccharine regulate adipocyte differentiation and metabolism through a sweet taste receptor-independent mechanism, suggesting that absorbed artificial sweeteners may regulate aspects of adipose tissue biology. However, those studies did not address the effect of the sweeteners alone. Therefore, the question whether sweeteners alone are capable of inducing adipogenesis in vitro still remains, and more studies are being conducted in our group to look for other changes not detectable by microscopy and image analysis (for example potential audiogenic gene expression). While adipogenesis is considered an important factor in the pathophysiology of obesity and obesity-related complications, including Type 2 Diabetes (T2D), the relationship between artificial sweeteners and adipogenesis may be more complicated. More recently, a study of the relationships between artificial sweeteners and risk of T2D in a large-scale prospective cohort showed that higher consumers of artificial sweeteners had higher risks of developing T2D. Since artificial sweeteners are present in thousands of products and consumed by millions of individuals, it is important to understand the true effect of these substances on adipogenesis, given its role in the pathophysiology of obesity and obesity-related complications.
Faculty Sponsor
Gabriel Guzman
Artificial Sweeteners Do Not Induce Adipogenesis In the Absence of Proadipogenic Inducers in 3T3-L1 Cells.
Poster #25
We set out to investigate the effects of some of the most common sweeteners used in the United States (Saccharine, Acesulfame-K, Sucralose, Trivia™, and Erythritol) on adipogenesis using 3T3-L1 preadipocyte fibroblasts differentiated into fully mature adipocytes. Preadipocyte fibroblasts were cultured and differentiated in media containing proadipogenic inducers plus artificial sweeteners, as well as media containing only the sweeteners to observe the effect of the sweeteners alone. Morphological changes in the 3T3-L1 cell line were monitored during differentiation with and without sweeteners using microscopy and image analysis of the accumulation of intracellular lipids. There was a significant accumulation of intracellular lipids during differentiation in all cells cultured with artificial sweeteners, in the presence of proadipogenic inducers, thus suggesting a direct effect on adipogenesis. However, there was no significant lipid droplet formation when cells where cultured in the presence of the sweeteners without any proadipogenic inducers. Previous in vitro studies investigating the effects of artificial sweeteners on adipogenesis studies have found that some artificial sweeteners, such as Saccharine regulate adipocyte differentiation and metabolism through a sweet taste receptor-independent mechanism, suggesting that absorbed artificial sweeteners may regulate aspects of adipose tissue biology. However, those studies did not address the effect of the sweeteners alone. Therefore, the question whether sweeteners alone are capable of inducing adipogenesis in vitro still remains, and more studies are being conducted in our group to look for other changes not detectable by microscopy and image analysis (for example potential audiogenic gene expression). While adipogenesis is considered an important factor in the pathophysiology of obesity and obesity-related complications, including Type 2 Diabetes (T2D), the relationship between artificial sweeteners and adipogenesis may be more complicated. More recently, a study of the relationships between artificial sweeteners and risk of T2D in a large-scale prospective cohort showed that higher consumers of artificial sweeteners had higher risks of developing T2D. Since artificial sweeteners are present in thousands of products and consumed by millions of individuals, it is important to understand the true effect of these substances on adipogenesis, given its role in the pathophysiology of obesity and obesity-related complications.