Nagoya University · Medicine
Professor Hiroaki Oda's research lab focuses on the intersection of circadian rhythms, lipid metabolism, and metabolic health, particularly in the context of eating behavior and dietary patterns. The lab investigates how meal timing—especially breakfast skipping and delayed feeding—affects the hepatic circadian clock and subsequent dysregulation of lipid metabolism, contributing to conditions like fatty liver and obesity. A central theme is chrononutrition, exploring how regular eating habits can entrain biological clocks and improve metabolic parameters such as cholesterol and triglyceride levels. The lab also examines the role of metabolic and hormonal pathways, including insulin and renin-angiotensin system components, in metabolic and cardiovascular diseases.
Figures are computed from collected data and may differ slightly.
The circadian clock is closely related to human health, such as metabolic syndrome and cardiovascular disease. Our previous study revealed that irregular feeding induced abnormal lipid metabolism with disruption of the hepatic circadian clock. We hypothesized that breakfast skipping induces lipid abnormalities, such as adiposity, by altering the hepatic circadian oscillation of clock and lipid metabolism-related genes. Here, we established a delayed first active-phase meal (DFAM) protocol as a b
fibrate, hypercholesterolemia, hypertriglyceridemia, 3-hydroxy-3-methylglutaryl coenzyme A reductase extent the putative risk factors listed above interact with lipid abnormalities in patients with uraemia. inhibitor Finally, no data are available to address the important issue of whether risk factor modification will improve the ESRD patient survival.
Well-regulated eating habits are said to be important for health. A major breakthrough was the discovery of the negative regulatory feedback for transcription via the binding of Clock/Bmal1 to E-box, which forms the basis of biological clocks. Well-regulated eating habits normalize the liver clock gene, the rhythm of CYP7A1 gene, and blood cholesterol levels through insulin secretion. Moreover, well-regulated eating habits actively contribute to better lipid metabolism such as obesity, even if a
Metabolic syndrome has become a global health challenge and was recently reported to be positively correlated with increased sucrose consumption. Mechanistic analyses of excess sucrose-induced progression of metabolic syndrome have been focused mainly on abnormal hepatic lipogenesis, and the exact contribution of excess sucrose to metabolic disorders remains controversial. Considering that carbohydrate and lipid metabolisms exhibit clear circadian rhythms, here we investigated the possible contr
Recently, involvement of remnant-like particle cholesterol (RLP-C) in atherosclerosis was reported, but this parameter has not been adequately investigated in hemodialysis (HD) patients. The present study investigated the relationship between the RLP-C level and total cholesterol (TC), triglycerides (TG), low density lipoprotein cholesterol (LDL-C), high density lipoprotein cholesterol (HDL-C), lipid peroxides (malone dialdehyde, MDA), apolipoprotein (Apo) A-I, and ApoB. In addition, the fractio
The etiology of metabolic syndrome involves several complicated factors. One of the main factors contributing to metabolic syndrome has been proposed to be excessive intake of sucrose, which disturbs hepatic lipid metabolism, resulting in fatty liver. However, the mechanism by which sucrose induces fatty liver remains to be elucidated. Considering feeding behavior important for metabolism, we investigated whether time-restricted feeding of high sucrose diet (HSD), only in the active phase (the d
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