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111: Anatomy/Phys 2 > 10.2 Glycogenesis and glycogen-lysis > Flashcards

10.2 Glycogenesis and glycogen-lysis Flashcards

1
Q

Glycogenesis vs Glycogenolysis

A

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
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2
Q

how does glucose become glycogen

A

blood glucose — hexokinase + atp –> glucose 6 phosphate + ADP —- mutase–>

glucose 1 phsopahte —-pyrophosphorylase —> uridine diphosphate glucose

— glycogen synthase –> glycogen

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3
Q

how does glycogen -> glucose

A

glycogen — glycogen phosphorylate + Pi –> glucose 1 phospahte — mutase –> glucose 6 phosphate — glucose 6 phosphatase —> blood glucose

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4
Q

what is gluconeogenesis

A

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

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5
Q

how are lipids metabolized

A
  • 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
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6
Q

how are proteins metabolized

A
  • 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
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7
Q

describe transamination of protein metabolism

A

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

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8
Q

describe the oxidative deamination step of protein metabolism

A
  • 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)

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9
Q

describe keto acid moficiation of protein metabolism

A
  • 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
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10
Q

absorptive vs postabsorptive states

A
  • 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

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11
Q

absorptive states of carbohydrates

A
  • 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
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12
Q

absorptive states of fats

A
  • 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
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13
Q

absorptive states of AA

A
  • soem aa delivered to liver & demainated to keto acids or conv to fat for storage
  • also sued for protein syn
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14
Q

what are the effects of insulin on metabolism

A
  • 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
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15
Q

what is the goal of postabsorptive state

A

*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
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16
Q

what are the major metabolic events of the postabsorptive state

A
  • 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
17
Q

sources of blood glucose for the psot absorptive stae

A
  1. Glycogenolysis in liver: first reserve used
  2. Glycogenolysis in skeletal muscle
    • before glucose form lvier is exhausted, glycogen stores in skeletal muscle start to break down
  3. Lipolysis in adipose tissue and liver
    • glycerol used for gluconeogensis
  4. 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

18
Q

what is glucose sparing

A
  • 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
19
Q

what are the principle pathways of the postabsorptive state

A
  • 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
  • Liver
    • generates glucose from glycerol, pyruvic acid, lactic acids, keto acids
    • glucose made used as enrgy for brain (only works for 4-5 days)
20
Q

hormonal control in post absorptive state

A

* 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

111: Anatomy/Phys 2 (31 decks)

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