Publications by authors named "Kryscilla Jian Zhang Yang"
Article Synopsis
- Retinol-binding protein 2 (RBP2) is important for absorbing dietary retinoids in the small intestine, and its absence in mice leads to increased body weight, impaired glucose metabolism, and higher liver triglycerides as they age.
- These issues are also seen in young mice on a high-fat diet, indicating a broader metabolic impact.
- RBP2 acts as a binding protein for monoacylglycerols (MAGs), engaging with the endocannabinoid 2-AG, which suggests that RBP2 plays a crucial role in regulating energy balance and signaling beyond its function in retinoid absorption.
Approximately 80-90% of all retinoids in the body are stored as retinyl esters (REs) in the liver. Adipose tissue also contributes significantly to RE storage. The present studies, employing genetic and nutritional interventions, explored factors that are responsible for regulating RE accumulation in the liver and adipose tissue and how these influence levels of retinoic acid (RA) and RA-responsive gene expression.
View Article and Find Full Text PDFPreliminary studies of liver regeneration induced by partial hepatectomy (PHE) identified a substantial depletion of hepatic retinoid stores, by greater than 70%, in regenerating livers of wild-type C57Bl/6J mice. To understand this, we compared responses of wild-type and lecithin:retinol acyltransferase (Lrat)-deficient mice, which totally lack hepatic retinoid stores, to PHE. The Lrat-deficient livers showed delayed regeneration in the first 24 h after PHE.
View Article and Find Full Text PDFArticle Synopsis
- Retinoids, derivatives of vitamin A, play crucial roles in regulating cell functions such as differentiation, growth, and death, and are key in research on embryonic development and diseases like cancer and skin disorders.
- Recent studies have shifted focus toward understanding how retinoids influence metabolic diseases, particularly obesity, diabetes, and dyslipidemia.
- This review highlights advancements in how retinoids affect fat cell formation, their signaling roles linking obesity to type II diabetes, their impact on insulin secretion and pancreatic function, and their involvement in liver fat accumulation.
Acyl CoA:diacylglycerol acyltransferase (DGAT) 1 catalyzes the final step of triglyceride (TG) synthesis. We show that acute administration of a DGAT1 inhibitor (DGAT1i) by oral gavage or genetic deletion of intestinal Dgat1 (intestine-Dgat1(-/-)) markedly reduced postprandial plasma TG and retinyl ester excursions by inhibiting chylomicron secretion in mice. Loss of DGAT1 activity did not affect the efficiency of retinol esterification, but it did reduce TG and retinoid accumulation in the small intestine.
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