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WEEK 9:
the starved state:
| Question | Answer |
|---|---|
| fasting state | occurs 2-4 hours after a meal and is catabolic (breaks down) |
| staved state occurs when | after 3 or more days |
| gluconeogenesis | protein converted to glucose |
| main priorities during starvation (2) | maintain adequate blood glucose for tissues mobilise fatty acids and synthesise/ release ketone bodies |
| energy source in brain | glucose normally but ketones in starvation as FAs cant cross BBB as bound to albumin |
| energy source in muscle | glucose, FA, and ketone bodies |
| how is glycogen converted into glucose | using G6P |
| energy source in heart | FAs, ketone bodies, lactate (no glycogen reserves) |
| energy source in adipose tissue | needs glycerol 3 phosphate to create triacylglycerols so will need glucose for glycolytic intermediate dihydroxyacetone phosphate (reduction G3P) |
| liver fuel use | provides fuel to brain muscle and peripheral organs by metabolising carbohydrates to form glycogen turning fatty acids into ketone bodies and using amino acid carbon skeletons (a-ketoacids) as its own energy source |
| liver main role in starving state | produce glucose by glycogenolysis and gluconeogenesis and produce ketone bodies from non glucose dependent tissues |
| in the liver to make fuel, what process occurs first | glycogen degradation followed by gluconeogenesis |
| process occurring in glycogenolysis | increases glucagon to insulin ration = PKA mediated phosphorylation of glycogen phosphorylase kinase -> increased phosphorylation of glycogen phosphorylase -> glycogen broken down -> glucose |
| skeletons from gluconeogenesis derived from | glucogenic amino acids, lactate form muscle and glycerol from adipose tissue |
| breaking down of amino acids in gluconeogenesis results in | increased nitrogen which is converted to urea (output decreases as starvation continues) |
| how does fatty acid metabolism to increase gluconeogenesis | major energy source in liver originating in TAGs from adipose tissue -> malonyl CoA drop permitting CPT1 to activate B-oxidation-> NADH produced inhibits TCA cycle -> acetyl CoA produced activates pyruvate carboxylase + inhibits pyruvate dehydrogenase |
| when does ketone body synthesis (acetoacetate and 3-hydroxybutyrate) favoured | when acetyl CoA exceeds TCA cycle capacity |
| carbohydrate metabolism | glucose transport depressed as GLUT4 insulin sensitive and insulin decreases so reduction in insulin means less glucose entering cell so less glycolysis and less TAG synthesis |
| fat metabolism | adipose TAGs mobilised during lipolysis which releases FAs and glycerol -> glycerol used by liver for gluconeogenesis and mediated by HSL |
| HSL enhanced by | elevated catecholamines eg adrealine |
| increased release of fatty acids | hydrolysis of TAGs releases FAs and are bound to albumin they act as fuel for many tissues where glycerol can also be used as a gluconeogenic precursor in the liver |
| decreased uptake of fatty acids in adipose tissue due to | adipose LPL activity is low |
| during fasting, muscles use what as an energy source | fatty acids and ketone bodies instead of glucose (for contraction as glycogen depleted, FAs mobilised from TAG in adipose tissue and becomes dominant energy source) |
| during carb metabolism, glucose transport is | DEPRESSED as GLUT-4 is insulin sensitive (insulin is low in starved state) leading to reduced glycolysis |
| during lipid metabolism what occurs during first 2 weeks | muscles use FAs from adipose tissue and ketone bodies from liver |
| during lipid metabolism what occurs after 3 weeks | muscle reduces use of ketone bodies (save for the brain as brain cannot use FAs) |
| what happens during the early fast of protein metabolism which is initiated by fall in insulin | rapid breakdown of muscle protein (increased liver gluconeogenesis) where pattern of AA released by skeletal muscle during starvation is not reflective of the composition of muscle protein (alanine and glutamine account for over 50% of AA released) |
| what happens in the brain in prolonged fasting (beyond 2-3 weeks) | plasma ketone levels rise significantly, largely replacing glucose (some glucose still needed to made neurotransmitters) so since glucose isnt needed protein catabolism for gluconeogenesis isnt needed (protein breakdown reduced) |
| importance of kidneys in starvation | is the site of gluconeogenesis (releases enzymes of gluconeogenesis) so in fasting 50% gluconeogenesis occurs here and uses self generated glucose to compensate for acidosis by ketone bodies by excretion |
| diabetes mellitus | relatively common heterogenous metabolic disease characterised by hyperglycemia and relative/ absolute deficiency in insulin |
| type 1 diabetes | insulin deficiency caused by autoimmune attack on beta cells leading to hyperglycaemia and ketoacidosis and hypertriacylglycerolemia |
| type 2 diabetes | caused by combination of insulin resistance and dysfunctional b-cells leading to hyperglycemia and dyslipidemia (in liver FAs converted to TAG and secreted as VLDL) |
| fasting (catabolic state) starts when | 4 hours after meal |
Created by:
kablooey
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