Consumption of Diet Soda Sweetened with Sucralose and Acesulfame‐Potassium Alters Inflammatory Transcriptome Pathways in Females with Overweight and Obesity

Sylvetsky, Allison C.; Sen, Sabyasachi; Merkel, Patrick; Dore, Fiona J.; Stern, David B.; Henry, Curtis J.; Cai, Hongyi; Walter, Peter J.; Crandall, Keith A.; Rother, Kristina I.; Hubal, Monica J.

doi:10.1002/mnfr.201901166

Cited by 20 publications

(17 citation statements)

References 50 publications

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“…Our results highlight the need for further in vivo studies, measuring production and accumulation of reactive oxygen species, in a dose-dependent fashion as well as increased fat accumulation, leading to increased insulin resistance and CVD. In fact, our in vivo study [22] indicates that sucralose promotes acute inflammatory response and our in vitro results suggest that rapid and immediate ROS accumulation may be the mechanism. Our results explain adverse associations between NNS consumption and cardiometabolic health reported in epidemiological studies at a cellular level.…”

Section: Discussionmentioning

confidence: 54%

Sucralose promotes accumulation of reactive oxygen species (ROS) and adipogenesis in mesenchymal stromal cells

et al. 2020

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Consumption of non-nutritive sweeteners (NNS) has been consistently associated with obesity and cardiometabolic disease in epidemiologic studies. Herein, we investigated effects of sucralose, a widely used NNS, at a cellular level. We wanted to investigate effect of sucralose on reactive oxygen species accumulation and adipogenesis in a human adipocyte tissue-derived mesenchymal stromal cells (MSCs) in a controlled fashion. Methods: In vitro experiments were conducted on commercially available MSCs obtained from human adipose tissue. hMSCs were exposed with sucralose at 0.2 mM (a concentration which could plausibly be observed in the circulatory system of high NNS consumers) up to 1.0 mM (supra-physiologic concentration) in the presence of both normal and high glucose media to detect a dose response based on the outcome measures. Reactive oxygen species (ROS) were detected using Mitosox Red staining and further analyzed by ImageJ and gene expression analysis. Effect of sucralose on adipogenic differentiation was observed in different concentrations of sucralose followed by gene expression analysis and Oil Red O staining. Results: Increased ROS accumulation was observed within 72 h of exposure. Increased adipogenesis was also noted when exposed to higher dose of sucralose. Conclusion: Sucralose promotes ROS accumulation and adipogenesis in human adipose tissue derived mesenchymal stromal cells.

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Section: Discussionmentioning

confidence: 54%

Sucralose promotes accumulation of reactive oxygen species (ROS) and adipogenesis in mesenchymal stromal cells

et al. 2020

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“…The most pronounced sex-specific differences were those observed for immune-related genes. In humans, while obesity is commonly associated with low-grade chronic inflammation, Ace-K has been shown to dysregulate inflammatory homeostasis in adipose tissue [17], effects of which in our study were more pronounced in females as compared to males. Cxcr3, for example, contributes to T-cell recruitment into adipose tissue in obese mice [53].…”

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confidence: 40%

“…Treatment of mouse and human precursor cells by Ace-K has been shown to induce adipogenesis, indicating that these compounds influence adipocyte differentiation [16]. In obese human subjects, consumption of diet drinks containing Ace-K leads to a dysregulation in inflammatory pathways within the adipose tissue [17].…”

Section: Introductionmentioning

confidence: 99%

Intake of the Artificial Sweetener Acesulfame-Potassium Alone and in Combination with a High-Fat Diet Leads to Differential and Sex-Specific Effects on Metabolic Function in Mice

Pe¹,

Vickers²,

Cm³

2021

Preprint

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Sugar-sweetened beverages are associated with metabolic dysfunction, particularly in those with increased risk factors. Artificial sweeteners (AS) are often promoted as a healthier alternative, yet findings remain conflicting as to their effects on metabolic function. Further, there is a lack of data exploring the interaction between AS and high-fat diets (HFD). We therefore examined the effects of HFD and the AS Acesulfame-potassium (Ace-K) on glucose intolerance and adipose tissue physiology in male and female C57BL/6 mice. 40 mice were randomised to receive either a) a control diet (CDCon; standard control diet/water), b) control diet and Ace-k (CDAS; CD/7.5mM AS in drinking water), c) HFD (HFCon; HFD (45%kcal from fat)/water), or d) HF and AS (HFAS; HFD/7.5mM AS in drinking water) for 6 weeks. A HFD increased body weight in male and female mice independently of AS supplementation. AS induced sex-specific effects protecting against HFD-induced hyperglycaemia and adipocyte hypertrophy in male mice and reducing inflammatory gene expression in the adipose tissue. Conversely in females, AS induced hyperinsulinemia in HFD mice and increased expression of immune-related genes. These findings suggest that supplementation of HFD with AS exacerbates metabolic dysfunction in female mice. This work supports the importance of studying sexually dimorphic responses to an altered nutritional environment and highlights the need for further investigation into the intake of AS, particularly in those already at risk of metabolic disease such as the obese or overweight.

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“…The scientific literature is replete with narrative reviews claiming to address mechanisms “…responsible for the development of metabolic syndrome associated with NNS [non-nutrivie sweetener] consumption” [ 5 ] and that “…contribute to the negative metabolic effects of non-nutritive sweeteners…” [ 6 ], “…demonstrating the role of the microbiota in glucose intolerance in response to noncaloric artificial sweeteners…” [ 7 ]. Indeed, it seems that researchers assume that (new) mechanistic evidence of adverse effects will be found even before experiments are run, pre-registering research protocols with titles, such as “Low-calorie Sweeteners Induce Metabolic Dysregulation Via Alterations in Adipose Signaling” (ClinicalTrials.gov Identifier NCT03125356; an uncontrolled trial that, in fact, found no metabolic dysregulation or changes in any higher-level physiological markers or outcomes [ 8 ]).…”

Section: Perspectivementioning

confidence: 99%

Is There an Academic Bias against Low-Energy Sweeteners?

Mela¹

2022

Nutrients

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This perspective considers evidence of a common academic bias against low-energy sweeteners (LES). The core proposition is that this bias is manifested in research and reporting focused on generating and placing a negative spin on LESs, largely through selective citation, interpretation and reporting. The evidence centres on three inter-related points, which together may generate a misleading impression of the balance of evidence: (1) basic and mechanistic research on LES perpetuates “explanations” for unsubstantiated adverse effects of LES; (2) the literature on LES—particularly narrative reviews and commentaries—continually reprises hypotheses of adverse effects without acknowledging where these hypotheses have been rigorously tested and rejected; and (3) negative interpretations of the effects of LES largely rely upon selectively emphasising lower-quality research whilst ignoring or dismissing higher-quality evidence. The expert community should consider these issues in assuring scientific integrity and balance in the academic discourse on LES, and how this is translated into messages for public health and consumers.

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Consumption of Diet Soda Sweetened with Sucralose and Acesulfame‐Potassium Alters Inflammatory Transcriptome Pathways in Females with Overweight and Obesity

Cited by 20 publications

References 50 publications

Sucralose promotes accumulation of reactive oxygen species (ROS) and adipogenesis in mesenchymal stromal cells

Sucralose promotes accumulation of reactive oxygen species (ROS) and adipogenesis in mesenchymal stromal cells

Intake of the Artificial Sweetener Acesulfame-Potassium Alone and in Combination with a High-Fat Diet Leads to Differential and Sex-Specific Effects on Metabolic Function in Mice

Is There an Academic Bias against Low-Energy Sweeteners?

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