Conference Coverage

Sucralose sparks appetite in obese, not lean, individuals

 

Key clinical point: Sucralose ingestion upped activity in brain appetite centers only for those with obesity.

Major finding: Cerebral blood flow for regions of interest was 2.10 mL/100g per min versus –0.79 mL/100g per min after sucralose consumption by obese individuals (P = .002).

Study details: Randomized placebo-controlled trial in 15 lean participants and 15 with obesity.

Disclosures: The authors reported no external sources of funding and no conflicts of interest.

Source: Ge B et al. ENDO 2018, Abstract SUN-070.


 

REPORTING FROM ENDO 2018

Consumption of a sucralose-laden beverage stimulated appetite centers of the brain in individuals with obesity but not in lean participants of a recent study, even though hunger and satiety hormone levels didn’t change. Those with obesity also consumed more calories after ingesting the artificial sweetener, though lean participants did not.

The study compared acute effects of consuming a set amount of glucose, sucralose, or water as the control, finding that sucralose consumption resulted in a significant increase in blood flow to certain areas of the brains of study participants with obesity but not in lean individuals (2.10 mL/100g per min vs. –.079 mL/100g per min; P = .002).

Brandon Ge of the University of Southern California, Los Angeles Kari Oakes/MDedge News

Brandon Ge

Brandon Ge and his collaborators at the University of Southern California, Los Angeles, assessed changes in serum levels of hunger- and appetite-associated hormones. They also used functional magnetic resonance imaging (fMRI) to see how the various substances affected areas of the brain that are associated with appetite and satiety as well as reward circuit pathways. Finally, individuals in the study were allowed unrestricted access to food 90 minutes after consuming the study substance, and food intake was tracked and compared among participants.

Whether responses to caloric and noncaloric sweeteners are different between individuals with and without obesity has not been well established, though recent in vitro and in vivo studies have suggested an association.

“A proposed mechanism is that noncaloric sweeteners uncouple sweetness from calorie intake, which may impact neurophysiological regulators of feeding behavior,” wrote Mr. Ge and his collaborators in an abstract presented at the annual meeting of the Endocrine Society. Still, the work attempts to fill a knowledge gap: “Little evidence, however, has determined the relationship between obesity status and neurophysiological and feeding responses to caloric and non-caloric sweetener consumption,” they wrote.

Of the 30 participants aged 19-24 years, 16 were female; half were lean, with a body mass index of 19-25 kg/m2; the remainder met obesity criteria, with BMIs greater than 30 kg/m2.

For the brain-imaging portion of the study, arterial spin labeling fMRI was used to examine blood flow in a number of predetermined regions of interest. These included the hypothalamus, amygdala, dorsal striatum, insula, and anterior cingulate cortex.

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