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Glucose, not fructose, led to increased satiety
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In exploratory analyses, researchers found that when the human brain is exposed to glucose but not fructose, there is a reduction in the activation of the hypothalamus, insula and striatum — regions of the brain that regulate appetite, motivation and reward processes. However, ingestion of glucose but not fructose led to an increase in satiety.
Kathleen A. Page, MD, of the section of endocrinology at Yale University School of Medicine, and colleagues conducted a masked, random-order, crossover study of 20 healthy adults who underwent two MRI sessions at the institution, combined with fructose or glucose drinks.
They found a greater reduction in hypothalamic cerebral blood flow (CBF) after glucose intake (–5.45 mL/g per minute) compared with fructose (2.84 mL/g per minute). Although glucose increased functional connectivity between the hypothalamus and the thalamus and striatum, fructose increased the connectivity between the hypothalamus and thalamus, but not the striatum, they wrote.
Fructose compared with glucose ingestion led to lower peak levels of serum glucose (P<.001), insulin (P<.001), and glucagon-like polypeptide 1 (P=.01), they added.
“To more definitively resolve the role of fructose in obesity, studies are needed that include obese persons and those at risk for developing obesity,” Jonathan Q. Purnell, MD, and Damien A. Fair, PA-C, PhD, of Oregon Health & Science University in Portland, wrote in an accompanying editorial.
Page and colleagues concluded that fructose consumption led to a unique pattern of regional CBF compared with glucose; with a more modest increase in systemic glucose, insulin and GLP-1 levels.
For more information:
Page KA. JAMA. 2013;309:63-70.
Purnell JQ. JAMA. 2013;309:85-86.
Disclosure: The researchers report no relevant financial disclosures.