Metabolism and hormones Flashcards

1
Q

describe glycolysis. where does it occur? does it require o2?

A

glycolysis - break down of 6 carbon sugar into two 3 carbon sugars
- occurs in cytoplasm w/o need for o2
- regulatory enzymes made by free ribosomes

requires 2 P from ATP to get started

end with 2 NADH, 2 pyruvic acids, 2 ATP

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2
Q

what is the intermediate step of the citric acid cycle?

A

pyruvic acid get transformed into acetyl coa
- 1st formation of CO2
releases NADH

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3
Q

describe the citric acid cycle. what is produced in the end? does it occur?

A

occurs in matrix of mitochondria
oxaloacetic acid (6C) + acetyl CoA (2 C) = citric acid
- 2 CO2 released
- H lost to NAD and FAD
- energy + GDP = GTP

by the end of citric acid cycle, all carbons from glucose have been released as CO2
- source of CO2 in blood and expiration

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4
Q

where does electron transport occur and how does that increase efficiency?

A

occurs along plasma membrane of cristi of the mitochondria
- increases efficiency bc only one component is moving

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5
Q

why do we need redox reaction for the hydrogens on NAD? how does affinity affect energy?

A

need redox bc E in hydrogens are too high - too much heat would be released
- controlled rxns allow decrease of energy
- extra energy used to move H ions from inner matrix to outer

increasing chemical affinity means that there is less E to hold onto the electron
- at end of chemical affinity chain, e- recombined with H and moved back into matrix

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6
Q

how does ATP synthase work?

A

the H gradient made by the electron transport chain allows H to move down its gradient into the intracellular matrix thru the ATP synthase
- rotor that spins - energy causes ADP + P = ATP

creates 34 app

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7
Q

describe glycogenesis and glycogenolysis

A

glycogenesis - glucose made into glycogen
- anabolic

glycogenolysis - glycogen to glucose
- catabolism
- only certain cells (liver) can do this

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8
Q

describe gluconeogenesis. where does this not occur? what is beta oxidation?

A

body uses energy storage other than glucose

beta oxidation - FA catabolism
- long chain FA broken into 2 C groups - acetyl CoA
- occurs especially in heart
- enters where GP3 would be

does not occur in the brain, tease, erythrocyte, kidney medulla

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9
Q

describe where fats and amino acids can enter the carbohydrate catabolism pathway

A

fats
- glycerol can enter during glycolysis
- fatty acids - B oxidation for acetyl CoA

aa’s - can enter at pyruvic acid or acetyl CoA step

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10
Q

describe the absorptive state

A

blood levels of AA, lipids, and glucose are elevated
increased glucose causes increase in insulin

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11
Q

describe the post absorptive state

A

AA, glucose and lipids moved into cells for usage or storage
- decreased levels i the blood

hormone - glucagon
- maintain homeostatic glucose in the blood.

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12
Q

describe malnutrition and malnourishment

A

malnutrition - ingestion of too few/many calories

malnourishment - improper balance of carbs, proteins or lipids
- enough calories but not enough vitamins or minerals

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13
Q

describe growth hormone. what is its effects on blood AA, FA, glucose> what is it produced by?

A

produced by andenohypophesis (anterior pituitary)
- regulated by hypothalamus

  • decrease in blood AA - increased protein synthesis
  • increase in blood FA - used for energy instead of glucose
  • increase in blood glucose: can cause DM2 due to increased insulin
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14
Q

describe the thyroid system. what is it related by?

A

adenohypophesis releases thyroid stimulating hormone
- regulated by hypothalamus

thyroglobulin - inactive form
- stood in center portion
- lysosomes break down inactive parts of thyroglobulin

T3/T4 + iodide move into plasma membrane

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15
Q

what is the function of T3/4 and iodide? how does it affect blood levels of FA and glucose?

A

important for metabolism and brain development/activity
- functions similar to steroid hormones
- modulates gene expression

increases blood levels of FA
lowers blood levels of glucose - taken out of blood

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16
Q

what are the diseases associated with T3/4 and iodide?

A

Goiter - caused by insufficient iodide, thyroid overproduced insufficient functional thyroid

Grave’s disease - too much thyroid
- bulging eyeball
- feel hot, hard to gain weight, diarrhea

low iodide/thyroid hormone
- cold, slower metabolism, constipation
- mental lethargy

16
Q

what are the diseases associated with T3/4 and iodide?

A

Goiter - caused by insufficient iodide, thyroid overproduced insufficient functional thyroid

Grave’s disease - too much thyroid
- bulging eyeball
- feel hot, hard to gain weight, diarrhea

low iodide/thyroid hormone
- cold, slower metabolism, constipation
- mental lethargy

17
Q

where are cortisol and epinephrine produced?

A

cortisol - zona fasciculata of adrenal cortex
epinephrine - adrenal medulla

18
Q

what is cushing’s disease?

A

tumor in adrenal gland - too much cortisol
- thinning of upper limbs
- proteins broken down for gluconeogenesis
- flushing of face - plethora
- striations and bulge at base of neck
- weight gain, long for wounds to heal

19
Q

what is cortisol released by? how does is affect blood levels of FA, AA, glucose?

A

stimulated by stress factors - regulation by adenohypophysis and hypothalamus

increases all 3
- protein breakdown
- increases gluconeoenesis
- decreases cellular glucose uptake (except in brain) - glucose saver
- lipolysis

20
Q

what is epinephrine release stimulated by> how does it affect blood levels of FA, AA, glucose?

A

stimulated by exercise and stress

no affect on AA
increased blood levels of FA
- lipolysis
increased blood levels of glucose
- glucose saver
- glycogenolysis
- gluconeogenesis

21
Q

what is insulin release stimulated by>? what releases it? what effects does it have on blood levels of FA, AA, glucose

A

released by pancreas, stimulated by increase in blood glucose levels, AA
- stimulated by vagus nerve

decrease in all 3 in blood
- increased protein synthesis - less blood AA
- increased lipogenesis
- increased uptake by cells, glycogenesis

22
Q

what is glucagon release stimulated by? what releases it? what effects does it have on blood levels of FA, Aa, glucose

A

released by pancreas in response to decrease in blood sugar, AA, sympathetic NS stimulation

no affect on AA
- increase in blood levels of FA - increased lipolysis
- increase blood levels of glucose - increased glycogenolysis