- digestion/absorption - some for immediate needs -rest stores until postabsorptive state (~4 hours after meal)

- chemical (food) to kinetic (exercise) - between chemical (AA to glucose) -heat lost in conversions

- energy (4kcal/g) - required by brain, nerves, RBCs

- 15% stored energy - structural component of proteins - precursors neurotransmitters - urea from amine groups

export_endocrine 1 Flashcards by Chelsea Liebowitz

Macromolecules

1) proteins (AAs)
2) carbs (glucose)

3) fats (lipids)

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where does energy from food go?

heat loss
1) food assimilation (5-10%)

2) biochemical inefficiency (50%)
3) conversion to high energy bonds (basal metabolic) (20-40%)
4) external work (5-25%)

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anabolic state

digestion/absorption
some for immediate needs

-rest stores until postabsorptive state (~4 hours after meal)

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energy conversion

chemical (food) to kinetic (exercise)
between chemical (AA to glucose)

-heat lost in conversions

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fxns of carbs

energy (4kcal/g)

- required by brain, nerves, RBCs

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what happens to carbs (glucose?)

stored as fat/glycogen
1/4-1/3 in liver glycogen
1/3-1/2 muscle glycogen
large portion to FA synthesis (later in day)

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glucose storage trail…

GI–>liver–>
1) glycogen

2) a-glycerol phosphate
3) FAs

2-3–> triglycerides–>VLDL–>adipose tissue

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glucose goes to 4 places…

1) use as energy (brain)
2) liver

3) adipose (–>a-glycerol phosphate or FAs–>triglycerides)
4) muscle (glycogen)

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what metabolizes glucose?

glucokinase

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products of glucose

1) glycogen
2) a-glycerol phosphate

3) FAs
4) non-essential AAs
5) nucleic acids
6) energy

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what absorbs nutrients and brings them to the liver?

portal vein

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how does glucose enter adipose tissue?

via insulin responsive glucose transporter (GLUT4)

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insulin after meal

increases with glucose

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fructose pathway

liver –> a-gp –> triglycerol –> VLDL

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fxns of fat

1) energy (~85% of stored)
2) structure of cell membrane

3) temp regulation
4) signaling molecules

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essential FAs and fxns

linolenic and linoleic
-formation of healthy cells

development of brain and NS
hormone like substances (BP, immune, etc)

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storage of lipids..

GI–> chylomicrons –> adipose tissue –> monoglyceride/FAs –> trigyceride

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what breaks down lipids?

bile salts

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where do chylomicrons go?

lymphatic system

-hydrolyzed by lipases in adipose and skeletal muscle

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how do lipids get to the liver?

from FAs from lipolysis in adipose tissue

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what does the liver do with FAs?

packaged into VLDLs then reexported

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low insulin and lipids in liver…

ketone bodies from incomplete FA oxidation

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what happens to FA in adipose tissue?

FA reesterified into triglycerides

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fxns of AAs

15% stored energy
structural component of proteins
precursors neurotransmitters
urea from amine groups

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nonessential AAs

derived de novo from carbs

important essential AAs for nutrient signaling

- valine - luecine -isoluecine all branching

destinations of AAs (and path):

1 ) liver --> a-ketoacids --> CO2+H20+energy or FAs 2) liver --> NH3 --> urea 3) muscle -->proteins

anabolism

keeping AA for TCA cycle to build on

digestions of proteins:

breakdown by pancreatic proteases into AAs or dipeptides | -transported by specific AA transporters

what can be done with AA in the liver?

- oxidation for gluconeogenesis - deamination to keto acids (enter TCA and moved to FAs) -detox to urea

what do muscles use for gluconeogenesis?

AAs

problems during postabsorptive state

1) no new glucose | 2) plasma glucose must be stable (60-80 when waking up)

compensation methods in postabsorptive state

1) produce glucose from stores (gluconeogenesis and glycogenolysis) 2) sparing glucose by use of fat for energy

gluconeogenesis

- done in liver, kidney, and intestines - TAG metabolism releases glycerol --> glucose - muscle catabolized to AAs - ala and glu primary AAs that enter pathway directly

hormones that control gluconeogenesis

1) glucagon (inc glucose production) 2) epinephrine (inc ") 3) cortisol (in ") 4) insulin (dec ")

can fats be made into glucose?

NO | -only used as energy as keytone bodies

glycogenolysis

glycogen released from liver as glucose | -or glycogen from muscle through Cori cycle

how does glycogen from muscle turn into glucose (Cori cycle)?

glycogen --> G-6-P --> glycolysis in blood--> pyruvate and lactate --> liver --> gluconeogenesis --> glucose

why store energy as lipids?

1) more energy dense 2) doesn't need to store with water 3) spares glucose for neurons

can neurons use FAs?

lyposysis

glucose sparing but doesn't contribute to glucose

how does liver prep for a fast?

FAs --> oxidized --> Acetyl CoA --> ketones

anabolic steriods

insulin, sex steriods, GH, thyroxine

catabolic steroids

glucagon, epinephrine, glucocoricoids, GH, thyroxine

what controls fast/fed state?

insulin

main effects of insulin?

inc glucose oxidation and fat, glycogen, protein synthesis

inc levels of glucagon affect

inc glycogenolysis, gluconeogenesis, ketogenesis

cortisol

turns on PEPCK, necessary for liver to do gluconeogenesis

where is insulin and glucagon released from?

pancreas B-cell- insulin a-cell- glucagon

insulin/glucagon in high/low glucose environment?

high- inc insulin, dec glucagon | lox- dec insulin, inc glucagon

when insulin levels are high where does glucose go?

- inc uptake to adipocytes and muscle - liver stops producing de novo -liver uptakes

hormones released from GI to pancreas?

- GLP-1 (enhance insulin sec) (from bile) | - GIP

3 types of signals from GI to pancreas

1) hormones 2) neural 3) nutrients

what is GLUT4 translocation?

inc insulin, moves GLUT4 to cell surface, inc intake of glucose into cells

absorptive state overview

- inc insulin - cell uptake of glucose - glycogen storage in liver and muscles - trigly storage in adipose - uptake of AA and protein synth

post absorptive state overview

- glucagon inc - stim glycogenolysis in liver (G6P) - muscle, <3, liver, kidneys use FA and major fuel source - stim lipolysis and ketogenesis

how much energy for muscles comes from FA metabolism?

85%

effects of glucagon in liver

- inc glycogenolysis - inc gluconeogenesis -inc ketogenesis

epinephrine

- released from adrenal medulla - stimulates cAMP -inc glucose levels

cortisol

- secreted by adrenal gland - acts like glucagon -needed for gluconeogenesis

type 1 diabetes

- destruction of B-cells | - lack of insulin production

type 2 diabetes

-insulin resistance

pancreatectomy

- no insulin or glucagon - rely on cortisol and epi to inc blood glucose -if treated with insulin can counteract bc no glucagon

type 1 diabetes effects on glucagon

- inc glucagon - inc gluconeogenesis and glycogenolysis - inc FA and glycerol due to unchecked lipolysis - inc ketones due to incomplete oxidation of FAs

diabetic ketoacidosis

extreme elevated ketone levels

export_endocrine 1 Flashcards

(65 cards)