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NUTR 3210
Manfred Brauer

BETA-CAROTENE & Vit.A - Beta-carotene retinol if need vitA o Regulated by retinol-RBP - Retinol (made in liver) esterified to retinyl palmitate for transport in chylomicron or storage in liver o Palmityl CoA donates palmitate - Retinol must combine with RBP for transport in the blood - Retinyl esterase activity regulated by levels of retinol-RBP (in liver) o Retinyl palmitate retinol (via retinyl esterase) - Retinoic acid is Active form of Vit.A o Cells take up retinol and convert it into retinoic acid Vitamin D from Diet & Sun - DBP Transports 1) D3 2) 25-OH-VitD 3) 1,25-diOHvitD - D3 in animals, fortified foods & supplements - 25-OH vit D aka Calcidiol Homeostatic set point - 1,25-di OH vit D aka Calcitriol ACTIVE VitD - D2 is less bioactive then D3 - VitD3 25-OH Vit D (Enzyme 25-hydroxylase) - 25-OH vitD 1,25-diOH vit D (enzyme 1-hydroxylase) Calcitriol Signaling - With viamin A, retinol made in liver and circulated bound to RBP. Cells took up retinol (inactive form of vitamin A) and converted it into retinoic acid (active form vitA). - Vitamin D is converted into its active form calcitriol in the kidney and then is taken up by the cell in the active form, so no intracellular activation has taken place == Vit D is a hormone - If Calcium levels get to high, Calcitonin will work with Vitamin D to decrease Pathway 1: Type II Steroid Hormone Receptor (Gene Expression) - Calcitriol enters cell and is brought to the nucleus - It binds to VitD receptor and forms a transcription factor - Forms a new family of mRNA which get exported to the cytosol and brought to the RER for protein synthesis these calcium binding proteins are not active - Need post-translational mods to make them actively able tot bind calcium - VitK needed to act as a cofactor for the enzymes ot cause a gamma carboxylation of the proteins that make it able to bind Ca. - By making Ca binding proteins, able to carry out effects that raise blood Ca Pathyway 2: Plasma Membrane Receptor - Calcitriol binds to a cell surface vitamin D responsive receptor o Protein is referred to as Membrane Associated, Rapid Response Steroid (MARRS) receptor - A series of rapid signals results, including protein phosphorylation reactions that activate Ca transporters o Doesnt require vitK or gene expression so it is very fast - A lot of Ca can come into the cell because the huge gradient in extra vs intracellular calcium Nitrogen Balance NB = Intake (diet) Output/Losses (Urine, feces, sweat, skin) 1) Children & Pregnancy = Positive net Increase in stores of body protein 2) Adults = Zero no net gain or loss of body protein 3) Elderly = Negative net loss of body protein **Deficits in quality can be compensated for by an increase in quantity, and if quality is high then quantity can be marginal Adaptation to Starvation - Blood glucose always need to be maintained to support rbcs and the CNS Fed state Postabsorptive Fasting Starvation Exercise Anabolic Catabolic; Catabolic; Catabolic; Catabolic; Insulin Glucagon Glucagon & Glucagon & Epinephrine Glucocorticoids Thyroid (trigger for Hormones protein degradation) CHO is Once dietary Starts once Main source of Relies initially predominant substrates stop liver glycogen blood glucose on glycogen source entering the is depleted. is glycerol but once portal We turn to backbone of epinephrine circulation catabolism of triglycerides. takes effect have to start our muscle & Thyroid fats are degrading break down hormones metabolized glycogen in lean mass decrease & and can liver & muscle hard on body metab rate generate stores so want reduced. FA energy as long to switch to fat generated as carbs are catabolism from Tri around to can take up to breakdown support TCA two weeks for are converted cycle. No time body to use fat to ketones in to convert FA & breakdown the liver. to ketones. product of Overall need Once glycogen ketone bodies for energy is is gone (2- greatly 3hrs) fatigue reduced so limits exercise can be capacity supported by glycerol Iodine - Iodide because thats the form found in our bodies and most food sources - Deficiencies in developing countries (salt is iodized in developed) - T3 & T4 made in thyroid gland from PTM of thyroglobulin o Mostly T4 in circulation, but T3 (active form) is formed in liver o Levels of T3 monitored by Hypothalamus, ant.pit sends signals via TSH to thyroid to make more hormones when low
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