GLP-1 Release by Rare Sugar D-Allulose Ameliorates Sucrose-Induced Obesity and Glucose Intolerance in Ovariectomized Mice

Feb 27, 2026International journal of molecular sciences

Rare Sugar D-Allulose Boosts Gut Hormone to Reduce Sugar-Induced Obesity and Blood Sugar Problems in Mice Without Ovaries

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Abstract

Daily oral administration of D-allulose significantly suppressed visceral fat accumulation and improved insulin resistance in ovariectomized mice.

Estrogen deficiency after menopause is associated with increased visceral fat and insulin resistance, raising the risk of type 2 diabetes.
Ovariectomized (OVX) mice developed greater visceral obesity and glucose intolerance when fed a sucrose diet compared to sham-operated mice.
Two weeks of D-allulose treatment improved metabolic outcomes in sucrose-fed OVX mice, indicating a potential benefit for obesity and glucose intolerance.
The beneficial effects of D-allulose were significantly reduced in mice lacking GLP-1 receptors, suggesting a GLP-1-dependent mechanism.
D-allulose may offer a safer preventive strategy for metabolic dysfunction linked to menopause.

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Estrogen deficiency after menopause promotes visceral fat accumulation and insulin resistance, thereby increasing the risk of type 2 diabetes. Although hormone replacement therapy is partially effective, its use is limited by increased risks of cardiovascular disease and breast cancer, underscoring the need for safer preventive strategies. The rare sugar D-allulose has been reported to stimulate secretion of glucagon-like peptide-1 (GLP-1), a gut hormone, and improve obesity and glucose metabolism, suggesting its potential as a novel intervention for postmenopausal metabolic dysfunction. Here, we examined whether D-allulose improves obesity and glucose intolerance in a GLP-1-dependent manner under sucrose-fed conditions, using ovariectomized (OVX) female C57BL/6J mice as a model of menopause. OVX mice, but not sucrose-fed sham mice, developed exacerbated visceral obesity and glucose intolerance in response to dietary sucrose, despite similar total energy intake. Daily oral administration of D-allulose for two weeks significantly suppressed visceral fat accumulation, improved insulin resistance, and ameliorated glucose intolerance in sucrose-fed OVX mice. These beneficial effects were markedly attenuated in GLP-1 receptor knockout mice. Taken together, we found that sucrose intake after ovariectomy exacerbates visceral obesity and glucose intolerance, and that D-allulose effectively ameliorates these metabolic abnormalities. GLP-1-stimulating dietary components such as D-allulose may represent a safe and promising preventive strategy for metabolic dysfunction associated with menopause.

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GLP-1 Release by Rare Sugar D-Allulose Ameliorates Sucrose-Induced Obesity and Glucose Intolerance in Ovariectomized Mice

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