Key result
Chestnut-derived ellagitannins reduce body weight ~36% vs western diet alone in male mice.
Why the study?
Western diet consumption accelerates metabolic syndrome and type 2 diabetes mellitus, and it was unknown whether chestnut-derived ellagitannins (FT50) modulate associated early metabolic alterations.
Does chestnut extract (FT50) supplementation prevent metabolic dysfunction and preserve beta cell function in male mice fed a western diet?
Does chestnut extract (FT50) supplementation prevent metabolic dysfunction and preserve beta cell function in male mice fed a western diet?
Chestnut-derived ellagitannins (FT50) may attenuate early metabolic alterations and preserve beta cell function in mice exposed to a western diet.
BackgroundWestern diet (WD) consumption accelerates the development of metabolic syndrome (MetS) and type 2 diabetes mellitus (T2DM). This study investigated whether chestnut-derived ellagitannins (FT50) modulate early metabolic alterations associated with WD feeding in C57BL/6J male mice.MethodsMale C57BL/6J mice were fed either a western diet (WD) or a WD supplemented with chestnut extract (FT50) for 12 weeks. Body weight, adiposity, glucose tolerance, and indices of insulin action were monitored throughout the study. Glucose and insulin homeostasis were assessed by measuring fasting glucose levels, insulin levels, and the HOMA-IR index. Pancreatic function was evaluated by ex vivo Ca2+ imaging in pancreas tissue slices to assess beta cell activation dynamics and islet network coordination.ResultsWD feeding induced significant body weight gain, adiposity, hyperglycemia, glucose intolerance, changes consistent with impaired insulin action, and partially compensatory hyperinsulinemia. Supplementation with FT50 prevented weight gain and fat accumulation, reduced organ hypertrophy, and was associated with improved glucose and insulin-related parameters without affecting the caloric intake. FT50-fed mice showed improved glucose tolerance from week 4 onward, accompanied by a lower HOMA-IR values and reduced hyperinsulinemia, consistent with improved indirect markers of insulin action relative to WD-fed mice. Ex vivo Ca2+ imaging in pancreas tissue slices revealed that in FT50-fed mice, beta cells have higher activation thresholds, longer activation delays, and lower Ca2+ activity during the plateau phase, while their network coordination is preserved.ConclusionsIn sum, these effects indicate reduced beta cell excitability and are consistent with an attenuation of early metabolic alterations under WD conditions. Overall, these findings suggest that FT50 supplementation modulates early WD-induced metabolic changes in male mice. However, the study is limited to early-stage alterations, does not address later stages of metabolic disease, and does not establish direct effects on insulin sensitivity. Within these constraints, chestnut extract represents a potentially promising bioactive dietary intervention for modulating early metabolic responses to WD.
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Klemen et al. (2026) studied Western diet-induced metabolic dysfunction (n=21). Chestnut-derived ellagitannins (FT50) vs. Western diet (WD) was evaluated on Body weight at 12 weeks (g) (p=0.0002). Chestnut-derived ellagitannins (FT50) supplementation significantly reduced body weight to 24.5 g compared to 38.3 g with western diet alone in male mice.
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