Salecan improves diet-induced obesity and hepatic steatosis by regulating citrate cycle intermediates.

Salecan, a naturally occurring β-glucan, represents an approved novel food ingredient in China. Although its numerous health benefits are acknowledged, the underlying mechanisms addressing obesity and hepatic steatosis remain uncertain. This investigation integrated a mouse model of diet-induced obesity with clinical observations in obese children to investigate the effects and underlying mechanisms of Salecan. In the animal model, obese mice were administered Salecan by gavage for 8 weeks. Salecan significantly promoted weight loss, reduced blood glucose levels, and improved insulin resistance in obese mice. It also reduced food intake without altering systemic energy metabolism, as evidenced by unchanged overall energy expenditure and maintained substrate utilization patterns. Notably, Salecan suppressed adipocyte hypertrophy within white adipose tissue and mitigated hepatic lipid accumulation. Metabolomic analysis revealed that Salecan markedly altered the serum metabolic profile of obese mice, particularly by elevating the levels of citrate cycle cycle intermediates, including α-ketoglutarate (AKG), fumarate, and malate. In the clinical component, serum AKG levels were significantly lower in obese children relative to healthy controls. They exhibited inverse correlations with body mass index, abdominal circumference, and triglyceride levels. The findings validate that Salecan mediates anti-obesity effects by regulating the citrate cycle in murine models, thereby strengthening its potential as a nutritional intervention for obesity and hepatic steatosis.