10.2 Glycogenesis and glycogen-lysis Flashcards
Glycogenesis vs Glycogenolysis
Glycogenesis
-formation of glycogen occurs in liver and skeletal muscle
glycogenolysis
- breadown of glucogen
- in muscle cells: glucose-6- phosphate is trapped
- inhepatocytes: contain glucose-6-phosphatase allowing glucose to elave cella nd enter blood streme
how does glucose become glycogen
blood glucose — hexokinase + atp –> glucose 6 phosphate + ADP —- mutase–>
glucose 1 phsopahte —-pyrophosphorylase —> uridine diphosphate glucose
— glycogen synthase –> glycogen
how does glycogen -> glucose
glycogen — glycogen phosphorylate + Pi –> glucose 1 phospahte — mutase –> glucose 6 phosphate — glucose 6 phosphatase —> blood glucose
what is gluconeogenesis
forming sugar from non carbohydrate molecules
- mostly in liver
- pnv pyruvate — pyruvate carboylase –> oxaloacetate — pep carboxykinase — (lots of steps)—> fructose 1.6 bisphosphate — fructose 1,6 bisphosphatase — *more steps u dont need to know — glucose 6 phosphatase —> glucose
*costs 6 ATP
how are lipids metabolized
- Fats are the body’s most concentrated source of energy
- only triglycerides are routinely oxidized for enrgy
- > glycerol backbone: conv into glyceraldehyde phosphate
- > fatty acids undergo beta oxidation -> 2 acetyl CoA
how are proteins metabolized
- broken down into aa and recycled or modified to fomr diff N contaiing compounds
- excess AA used for anabolic purposes and oxidized for enrgy/cov to fat
- key mol in conversation = Glutamic acid, steps are:
1. transamination
2. oxidative seamination
3. Keto acid modification
describe transamination of protein metabolism
AAs can transfer their amine group to α-ketoglutaric acid forming glutamate
*amino acids converted to other metabolic products,
conv amino acid + alpha ketoglutarate —amino transferase + cofactor (B6, PLP)—> glutamate + alpha keto acid
describe the oxidative deamination step of protein metabolism
- in liver, aminegroup of glutamic acid is removed as ammonia (NH3) regenerating α-ketoglutarate
- NH3is combined with CO2, yielding urea and water
*regenerating the keto acid (alpha keto glutarate)
describe keto acid moficiation of protein metabolism
- goal of AA degredation is to produce molecules that can be
- > oxidized in krebs cycle
- > converted to ketones or glucose
- Keto acids can produce metabolites pyruvate, acetyl CoA, α-ketoglutarate and oxaloacetate
absorptive vs postabsorptive states
- if you eat 3 reg meals a day you are in
- > absorptive state for 4 hours during and after each meal
- > post absorptive state: time when GI tract is empty and energy is supplied by body reserves
*postabsorptive mechanisms can sustain the body for several weeks of fasting
absorptive states of carbohydrates
- in liver: fructose and galacotse -> glucose
- liver and skeletal muscle store glucose as glycogen
- Most fat synthesized in the liver is packaged with proteins as very low density lipoproteins (VLDLs) and released for storage
absorptive states of fats
- fat enters the lymph in form of chylomicrons -> hydrolyzed to FA and glycerol ebfore can pass throuhg capillary walls
- lipoprotein lipase catalyzes fat hydrolysis and is active in capillaries of mucle and fat
- adipase cells, skeletal muscle cells and liver cells use TG as primary energy source
absorptive states of AA
- soem aa delivered to liver & demainated to keto acids or conv to fat for storage
- also sued for protein syn
what are the effects of insulin on metabolism
- directs essentailly ALL events of absorptive state
- Glucose-induced insulin release is enhanced by the GI tract hormones:
- > Glucose-dependent insulinotropic peptide (GIP)
- > Glucagon-like peptide-1 (GLP1)
- how
- inc in blood glucose stim beta cells of pancreatic islets
- inc blood insulin -> targets itssue cells
- inc glucose into cells, generating ATP, glycogen and glycerol
- used in cellular resp to make atp
what is the goal of postabsorptive state
*mostly catabolic rxn
- goal is to maintain glood glucose levels at 70-110 mg glucose, mainly for brain
- most events are to main glucose available for brain so save it for the brain
what are the major metabolic events of the postabsorptive state
- Major metabolic thrust
- catabolism and replacement of flues in blood
- preaking down stuff, proteins -> aa, glycosen -> glucose etc
- Major energy fules
- gluocose to brain
- a lot of other cells use fatty acids or ketons
- Liver metabolism
- conv amino acids -> keto acids -> glucose
sources of blood glucose for the psot absorptive stae
- Glycogenolysis in liver: first reserve used
- Glycogenolysis in skeletal muscle
- before glucose form lvier is exhausted, glycogen stores in skeletal muscle start to break down
- Lipolysis in adipose tissue and liver
- glycerol used for gluconeogensis
- Catabolism of cellular protein
- major source during prolonged fasting; limited amount of protein can be broken down before damage
*amount of fat in body determines how long a person can survive without food
what is glucose sparing
- in prolonged fasting body uses more nonc arb sources and saves glucose for main
- reuslts in production of ketone bodies
- after 4-5 days w/o food brain also uses ketone bodies bc all glucose reserve sused
what are the principle pathways of the postabsorptive state
- Muscle
- breaks down glycogen to use as energy source in tissues
- some pyruvate acid sent to liver for breakdown
- protein can also be broken down into amino acids and sent to liver
- Fat
- release fat stores by breaking fown triglycerides
- into blodo stream and goes to liver and conv to glucose or keto acids
- or used for enrgy
- release fat stores by breaking fown triglycerides
- Liver
- generates glucose from glycerol, pyruvic acid, lactic acids, keto acids
- glucose made used as enrgy for brain (only works for 4-5 days)
hormonal control in post absorptive state
* glucagon
- released by pancreatic islets when low blood glucose
- stimulates fat breakdown from adipost to inc FA in plasma (glucose sparing mechanism and alternative energy soruce)
- stim lvier cells to do glycogenolysis and gluconeogenesis
