Molecular, Genetic, and Biochemical Nutrition Commons^™

Role Of Vitamin A Status And Its Catabolism In The Regulation Of Glucose And Lipid Homeostasis In Rats Under Physiological And Disease Conditions, Yang Li

Doctoral Dissertations

The increased number of individuals with metabolic diseases has become a public health concern. Vitamin A (VA, retinol) is required to maintain the general health of an individual. How VA contributes to the regulation of glucose and lipid homeostasis in normal and metabolic disease states is unclear. VA’s physiological activities are mainly mediated by its metabolite, retinoic acid (RA), which activates several transcriptional factors in the nuclear receptor super family and in turn, regulates the expression of numerous genes for macronutrient metabolism. For the RA production, retinol is first oxidized into retinal and then from retinal to RA. We hypothesize …

Feeding State, Vitamin A Status And Atypical Protein Kinase C Modulate The Insulin-Regulated Gene Expression In Rat Hepatocytes, Wei Chen

Doctoral Dissertations

Hormonal and nutritional stimuli coordinately regulate the glucose and lipid metabolism in the liver. Dysregulated hormonal balance and nutrient metabolism not only disrupt the energy homeostasis, but also predispose individuals to the development of obesity and its related metabolic diseases. Research presented in this dissertation investigated the effects of a nutritional factor, vitamin A (VA), and a potential component of insulin signaling cascade, atypical protein kinase C (aPKC), on the glucose and lipid metabolic genes transcription in primary hepatocytes from Zucker lean (ZL) and fatty (ZF) rats.

To examine VA effects, we put ZL and ZF rats with different VA …

Regulation Of Apolipoprotein C-Iii Gene Expression By Nuclear Receptors Hepatocyte Nuclear Factor 4 Alpha And Chicken Ovalbumin Upstream Promoter Transcription Factor Ii, But Not Retinoids In Hepatic Cells, Meredith Lee Howell

Masters Theses

Retinoic acid (RA) treatment induces hyperlipidemia in humans and animals. RA regulates the expression levels of various genes through the induction, repression, or coactivation of nuclear receptors, mediating its effects. RA-induced hyperlipidemia has been attributed to the induction of apolipoprotein CIII (gene, Apoc3), which inhibits lipoprotein lipase activity (LPL). We have shown that vitamin A (VA) status and retinoid treatment regulates hepatic lipogenic gene expression, suggesting that the induction of lipogenic genes may also contribute to hyperlipidemia. To test the hypothesis that retinoids may not affect Apoc3 expression, we analyzed the expression levels of Apoc3 mRNA in response to …