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CHICAGO -- Consuming the artificial sweetener sucralose may predispose people to metabolic syndrome, researchers reported here.

At a cellular level, those who consumed sucralose experienced increased glucose uptake, inflammation, and adipogenesis -- all of which were most notable in people with obesity, according to Nabanita Kundu, PhD, of George Washington University (GWU) in Washington, D.C., and colleagues.

"We wanted to do a systematic study where we look at fat-derived stem cells and how these agents effect those looking at the gene expression and adipogenesis and inflammation, and also look at the human subjects' fat who have actually taken these agents over a period of time," explained senior study author Sabyasachi Sen, MD, also of GWU, during a presentation of the findings at The Endocrine Society's annual meeting.

Action Points Note that this study was published as an abstract and presented at a conference. These data and conclusions should be considered to be preliminary until published in a peer-reviewed journal.

The analysis included 18 participants of both normal and obese weight, most of whom had prediabetes. Following a 7-day food log, a fat biopsy was obtained from participants' subcutaneous fat to assess mRNA gene expression profile and other biochemical measures. Human adipose tissue-derived mesenchymal stromal cells (MSCs) exposed to varying levels of sucralose: 0 mM, 0.2 mM (equivalent to drinking 4 cans of diet soda per day), 0.45 mM, and 1.0 mM.

In the MSCs, sucralose was dose-dependently related to upregulation of genes related to adipogenesis, including CEBPa and FABP4 -- most prominent at the highest exposure.

In the fat samples from participants with obesity, there was a 2.5-fold increase in the upregulation of the glucose transporter GLUT4 (P=0.0005). The taste-receptor genes TAS1R3 and TAS2R3 were also altered, with a 1.5- and 1.8-fold upregulation, respectively (P=0.03 for both).

Adipogenic-related genes exposed to sucralose in people with obesity also saw several significant increases in regulation, ranging from 1.6- to 1.9-fold for the genes PLIN, PPARG, and CEBPA.

Other clinical measures were also affected in patients with obesity who consumed the artificial sweetener, marked by increased acute insulin response value in subjects with obesity (399.32 ± 207.22 vs 574.19 ± 505.76) and higher triglycerides in all consumers (126.9 ± 82.2 mg/dL vs 95.7 ± 23.4) compared to non-consumers.

In an interview with MedPage Today, Sen highlighted the take-home message of the findings is not to have consumers reach back for sugar. "Sweetened beverages have been shown to increase insulin resistance and promote diabetes ... it's not going to be the solution," he said.

Click here for video comments from study authors and discussants at ENDO 2018.

"The only part [in artificially sweetened beverages] that's not there is the calories -- it's not adding the calories, but it's doing everything else that glucose does. It shouldn't be the replacement from sweetened beverages because it's obviously causing inflammation, fat formation, and so on."

"But [are artificial sweeteners] causing some inflammation, some reactive oxygen species beyond what glucose does? I think there is some noise towards it, but I cannot say that for sure."

He said he's currently conducting a prospective study to assess other types of artificial sweeteners beyond sucralose, noting that most diet beverages on the shelves today contain combinations of various types of sweeteners, such as aspartame and saccharin, and everyday exposure is seldom exclusive to only sucralose.

Sen recommended healthcare providers steer their patients with obesity away from both sweetened and artificially-sweetened beverages.