Soojin Lee

Serum high-density lipoprotein cholesterol (HDL-C) levels and cholesterol excretion are closely associated with the risk of cardiovascular complications. The specific aim of the present study was to investigate the cholesterol lowering effect of mulberry fruit in rats fed a high cholesterol/cholic acid diet. Four-week supplementation with mulberry fruit extract significantly decreased serum and hepatic cholesterol (TC), serum low-density lipoprotein cholesterol (LDL-C), and fecal bile acid levels without changes in body weight and food intake (p < 0.05). Mulberry fruit extract significantly inhibited hepatic sterol-regulatory element binding protein (Srebp) 2 gene expression and upregulated hepatic mRNA levels of liver X receptor alpha (Lxr-α), ATP-binding cassette transporter 5 (Abcg5), and cholesterol 7 alpha-hydroxylase (Cyp7a1), which are involved in hepatic bile acid synthesis and cholesterol metabolism (p < 0.05). In addition, hepatic microRNA-33 expression was significantly inhibited by supplementation of mulberry fruit extract (p < 0.05). These results suggest the involvement of miR-33, its associated hepatic bile acid synthesis, HDL formation, and cholesterol metabolism in mulberry fruit-mediated beneficial effects on serum and hepatic lipid abnormalities.

Obesity is intimately related to a chronic inflammatory state, with augmentation of macrophage infiltration and pro-inflammatory cytokine secretion in white adipose tissue (WAT) and mitochondrial dysfunction in skeletal muscle. The specific aim of this study is to evaluate effects of tartary buckwheat extract (TB) on obesity-induced adipose tissue inflammation and muscle peroxisome proliferator-activated receptor-γ coactivator (PGC)-1α/sirtulin 1 (SIRT1) pathway in rats fed a high-fat diet. Sprague-Dawley rats were divided into four groups and fed either a normal diet (NOR), 45% high-fat diet (HF), HF + low dose of TB (TB-L; 5 g/kg diet), or HF + high dose of TB (TB-H; 10 g/kg diet) for 13 weeks. TB significantly reduced adipose tissue mass with decreased adipogenic gene expression of PPAR-γ and aP2. Serum nitric oxide levels and adipose tissue macrophage M1 polarization gene markers, such as iNOS, CD11c, and Arg1, and pro-inflammatory gene expression, including TNF-α, IL-6, and MCP-1, were remarkably downregulated in the TB-L and TB-H groups. Moreover, TB supplementation increased gene expression of PGC-1α and SIRT1, involved in muscle biogenesis and function. These results suggested that TB might attenuate obesity-induced inflammation and mitochondrial dysfunction by modulating adipose tissue inflammation and the muscle PGC-1α/SIRT1 pathway.