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CHICAGO – 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).
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.
Participants had three scans, spaced at least 2 days apart and occurring after a 12-hour overnight fast. A scan with arterial spin labeling acquisition was taken before and 10 minutes after participants drank a 300-mL beverage consisting of just water, or either a 75-g glucose solution or 2 mmol/L sucralose.
Twenty-five of the participants had blood drawn at 0, 40, and 60 minutes after drinking the study beverage, to track levels of serum insulin, ghrelin, GLP-1, and peptide YY – all hormones that help regulate appetite and satiety.
Hormone levels for individuals who had the non–glucose beverages were similar, regardless of BMI. However, there were significant differences in cerebral blood flow between obese and nonobese participants. Mr. Ge, an undergraduate student, and his collaborators looked at the contributions of the individual brain structures to the significantly higher activation seen after sucralose consumption by the high-BMI participants. Individuals with obesity had significantly more activity in the amygdala than did the lean participants (P = .0088) after drinking the sucralose beverage; also, in lean individuals, hypothalamic activity decreased after sucralose consumption, while activity increased slightly in the high-BMI participants (P = .017).
Eating behavior after drinking the various beverages also differed depending on beverage type and BMI status. After the overnight fast and study beverage consumption, participants were offered unlimited access to a buffet-style meal. The beverage type had no significant effect on calorie consumption at the buffet for the lean study participants. However, obese individuals consumed significantly more calories than did lean individuals after ingesting sucralose (1,191 kcal vs. 731 kcal; P = .01). Caloric intake was not significantly different between the high- and low-BMI groups after consumption of water or glucose.
None of the study authors reported conflicts of interest.
SOURCE: Ge B et al. ENDO 2018, Abstract SUN-070.
CHICAGO – 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).
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.
Participants had three scans, spaced at least 2 days apart and occurring after a 12-hour overnight fast. A scan with arterial spin labeling acquisition was taken before and 10 minutes after participants drank a 300-mL beverage consisting of just water, or either a 75-g glucose solution or 2 mmol/L sucralose.
Twenty-five of the participants had blood drawn at 0, 40, and 60 minutes after drinking the study beverage, to track levels of serum insulin, ghrelin, GLP-1, and peptide YY – all hormones that help regulate appetite and satiety.
Hormone levels for individuals who had the non–glucose beverages were similar, regardless of BMI. However, there were significant differences in cerebral blood flow between obese and nonobese participants. Mr. Ge, an undergraduate student, and his collaborators looked at the contributions of the individual brain structures to the significantly higher activation seen after sucralose consumption by the high-BMI participants. Individuals with obesity had significantly more activity in the amygdala than did the lean participants (P = .0088) after drinking the sucralose beverage; also, in lean individuals, hypothalamic activity decreased after sucralose consumption, while activity increased slightly in the high-BMI participants (P = .017).
Eating behavior after drinking the various beverages also differed depending on beverage type and BMI status. After the overnight fast and study beverage consumption, participants were offered unlimited access to a buffet-style meal. The beverage type had no significant effect on calorie consumption at the buffet for the lean study participants. However, obese individuals consumed significantly more calories than did lean individuals after ingesting sucralose (1,191 kcal vs. 731 kcal; P = .01). Caloric intake was not significantly different between the high- and low-BMI groups after consumption of water or glucose.
None of the study authors reported conflicts of interest.
SOURCE: Ge B et al. ENDO 2018, Abstract SUN-070.
CHICAGO – 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).
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.
Participants had three scans, spaced at least 2 days apart and occurring after a 12-hour overnight fast. A scan with arterial spin labeling acquisition was taken before and 10 minutes after participants drank a 300-mL beverage consisting of just water, or either a 75-g glucose solution or 2 mmol/L sucralose.
Twenty-five of the participants had blood drawn at 0, 40, and 60 minutes after drinking the study beverage, to track levels of serum insulin, ghrelin, GLP-1, and peptide YY – all hormones that help regulate appetite and satiety.
Hormone levels for individuals who had the non–glucose beverages were similar, regardless of BMI. However, there were significant differences in cerebral blood flow between obese and nonobese participants. Mr. Ge, an undergraduate student, and his collaborators looked at the contributions of the individual brain structures to the significantly higher activation seen after sucralose consumption by the high-BMI participants. Individuals with obesity had significantly more activity in the amygdala than did the lean participants (P = .0088) after drinking the sucralose beverage; also, in lean individuals, hypothalamic activity decreased after sucralose consumption, while activity increased slightly in the high-BMI participants (P = .017).
Eating behavior after drinking the various beverages also differed depending on beverage type and BMI status. After the overnight fast and study beverage consumption, participants were offered unlimited access to a buffet-style meal. The beverage type had no significant effect on calorie consumption at the buffet for the lean study participants. However, obese individuals consumed significantly more calories than did lean individuals after ingesting sucralose (1,191 kcal vs. 731 kcal; P = .01). Caloric intake was not significantly different between the high- and low-BMI groups after consumption of water or glucose.
None of the study authors reported conflicts of interest.
SOURCE: Ge B et al. ENDO 2018, Abstract SUN-070.
REPORTING FROM ENDO 2018
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.