Search Results (3)

Background/Objectives: This study aimed to identify the regulatory system of lipoprotein lipase (LPL), glycosylphosphatidylinositol-anchored high-density lipoprotein (HDL)-binding protein 1 (GPIHBP1), and hepatic triglyceride lipase (HTGL) in the peripheral bloodstream. Methods: In total, 207 individuals (100 males and 107 females) who were diagnosed with normal glucose tolerance or prediabetes during their comprehensive health checkup were investigated. Results: Circulating LPL levels were positively correlated with the GPIHBP1 and HDL-cholesterol (HDL-C) levels, and negatively correlated with body mass index (BMI), waist circumference (WC), Homeostasis Model Assessment of Insulin Resistance (HOMA-IR) scores, triglyceride–glucose index, and triglyceride, fasting insulin, ferritin, and C-reactive protein (CRP) levels. The GPIHBP1 level was positively correlated with LPL and HTGL levels, and negatively correlated with estimated glomerular filtration rate (eGFR). The HTGL level was positively correlated with BMI, WC, HOMA-IR score, and GPIHBP1, low-density lipoprotein cholesterol (LDL-C), fasting insulin, and ferritin levels. Meanwhile, it was negatively correlated with HDL-C levels. The multiple regression analysis revealed that the circulating LPL level was independently affected by BMI, red blood cell (RBC) count, GPIHBP1, fasting plasma glucose (FPG), fasting insulin, HDL-C, CRP, and ferritin levels. The GPIHBP1 level was independently affected by age, eGFR, FPG, LPL, and HTGL levels and RBC count. The HTGL level was independently affected by WC, GPIHBP1 and LDL-C levels. Conclusions: LPL and HTGL levels reflect insulin resistance. In particular, individuals with a greater insulin resistance present with a lower LPL level and a higher HTGL level. An increased GPIHBP1 level might compensate for decreased LPL levels due to insulin resistance. Full article

p-coumaric acid (p-CA), a common plant phenolic acid with multiple bioactivities, has a lipid-lowering effect. As a dietary polyphenol, its low toxicity, with the advantages of prophylactic and long-term administration, makes it a potential drug for prophylaxis and the treatment of nonalcoholic fatty liver disease (NAFLD). However, the mechanism by which it regulates lipid metabolism is still unclear. In this study, we studied the effect of p-CA on the down-regulation of accumulated lipids in vivo and in vitro. p-CA increased a number of lipase expressions, including hormone-sensitive lipase (HSL), monoacylglycerol lipase (MGL) and hepatic triglyceride lipase (HTGL), as well as the expression of genes related to fatty acid oxidation, including long-chain fatty acyl-CoA synthetase 1 (ACSL1), carnitine palmitoyltransferase-1 (CPT1), by activating peroxisome proliferator-activated receptor α, and γ (PPARα and γ). Furthermore, p-CA promoted adenosine 5′-monophosphate (AMP)-activated protein kinase (AMPK) phosphorylation and enhanced the expression of the mammalian suppressor of Sec4 (MSS4), a critical protein that can inhibit lipid droplet growth. Thus, p-CA can decrease lipid accumulation and inhibit lipid droplet fusion, which are correlated with the enhancement of liver lipases and genes related to fatty acid oxidation as an activator of PPARs. Therefore, p-CA is capable of regulating lipid metabolism and is a potential therapeutic drug or health care product for hyperlipidemia and fatty liver. Full article

In a recent study, we showed that konjac glucomannan (KGM) inhibits rice gruel-induced postprandial increases in plasma glucose and insulin levels. To extend this research, we investigated the effects of KGM addition to rice gruel on pre- and postprandial concentrations of circulating lipoprotein lipase (LPL), glycosylphosphatidylinositol-anchored high-density lipoprotein-binding protein 1 (GPIHBP1), hepatic triglyceride lipase (HTGL), free fatty acids (FFA), and triglycerides (TG). A total of 13 Japanese men, without diabetes, dyslipidemia, or gastrointestinal diseases, interchangeably ingested rice gruel containing no KGM (0%G), rice gruel supplemented with 0.4% KGM (0.4%G), and rice gruel supplemented with 0.8% KGM (0.8%G), every Sunday for 3 weeks. Blood samples were obtained at baseline and at 30, 60, and 120 min after ingestion to measure the abovementioned lipid parameters. Lipid parameters showed small, but significant, changes. Significant reductions were found in circulating FFA levels among all participants. Circulating TG levels significantly declined at 30 min and then remained nearly constant in the 0.8%G group but exhibited no significant difference in the 0%G and 0.4%G groups. Although circulating levels of LPL and GPIHBP1 significantly decreased in the 0%G and 0.4%G groups, they increased at 120 min in the 0.8%G group. Participants in the 0%G and 0.4%G groups showed significant decreases in circulating HTGL levels, which was not observed in the 0.8%G group. Our results demonstrate the novel pleiotropic effects of KGM. Supplementation of rice gruel with KGM powder led to TG reduction accompanied by LPL and GPIHBP1 elevation and HTGL stabilization, thereby attenuating TG metabolism. Full article