Fuel Metabolism and Nutrition: Basic Principles Flashcards

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1
Q

Total energy produced by carbohydrates per gram

kcal/g

A

4 kcal/g

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2
Q

long-, medium- and short-chain transport

A

CMs transport the long-chain TG to the tissues. Med- and Short- chain fats are transported directly to the liver through the portal system without packaging into lipoprotein particles.

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3
Q

Two major precursors of polyunsaturated compounds such as prostaglandins and eicosanoids

Hint: essential fatty acids

A

linoleic acid

a-linolenic acid

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4
Q

comps tht get ox by . muscles during fasting

A

fatty acids released from adipose tsu and . KBs produced by the liver

* during exercise muscles use their own source of fuel (glycogen that was already stored) in addition to f.a. and kb

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5
Q

Total energy produced by 1g of fat (kcal/g)

A

9 kcal/g

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6
Q

Essential amino acids

A

valine, leucine, isoleucine

histidine, lysine

phenylalanine, tryptophan

methionine and threonine

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7
Q

Two major metabolic rxns carried out by the liver during the fasting state (with time frame)

A

Glycogenolysis- 2 to 3 hrs post meal

* the body runs out of glycogen within 30 hours

Gluconeogenesis- abt 4-6 hours of fasting

After 30 hr, gluconeogenesis is the major contributor to maintain blood sugar level

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8
Q

The main aa released from the muscles during the fasting state

A

alanine and glutamine

tissues such as gut and kidney metabolize the glu

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9
Q

Blood level of KB during starvation

A

inc.

Blood KB inc. because muscles don’t use KB ( used by brain as the source of energy) –> less req. gluconeogenesis –> less aa required –> muscle degradation stops

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10
Q

site of storage for glucose as glycogen- What’s unique about each?

A

Muscle- Oxidization and fuel

Liver-maintaining blood glucose

* excess glucose converts to TAG in the liver and gets packaged into VLDL.

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11
Q

Basic principle of fed state

A

fed state ~ right after meal

Ingested fuel will be used for immediate energy needs. Excess ingested fuel will be stored: TAG, Glycogen

Insulin promotes storage

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12
Q

resenthesize the digestive products of TAG

A

intestinal epithelial cells

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13
Q

digestive products of dietary fat

A

dietary fat( TAG- triacylglycerol)

digests into

fatty acids

and

2-monoacylglycerol

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14
Q

name two major ketone bodies prod. by the liver from acetyl-CoA during the fasting state

A

acetoacetate and B-hydroxybutarate.

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15
Q

Chylomicrons enter the blood via

A

lymph

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16
Q

Conseq. of Kwashiorkor

A
  1. dec. protein syn. (inc serum level of albumin)
  2. impacts regeneration of intestinal epithelial cells
  3. compensated by malabsorption
  4. hepatomegaly and distended abdomen ( lack of albumin in blood, inc. osm pressure diff. –> water accumulation .
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17
Q

tissues such as gut and kidney metabolize this aa- released from the muscles during the fasting state

A

glu

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18
Q

The fate of dietary fat and cholestrol

A

The same fate

dietary fat (TAG) digests into fatty acids and 2-MAG and resenthesized into TAG by intestianal epithelial cells, then packaged into chylomicrons and enter the blood stream via lymph.

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19
Q

The fatty acids of VLDL are stored in this tissue

A

adipose tissue

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20
Q

fatty acids of chylomicrons are stored in

A

adipose triglycerides

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21
Q

The role of adipose tissue during fasting

A

As glucagon inc. fat mobilizes and degrades into compnts.

F.A.s and glycerol re converted to glucose or ketone bodies by the liver

F.A.s are also used by the muscles to b ox 2 Co2 and H2O

22
Q

Basic principles of starvation

A

starvation~ prolonged fasting

changes in the usage of fuel storage that allows survival for prolonged period of time.

23
Q

Negative nitrogen balance

A

When the rate of excretion>ingestion

24
Q

Total energy produced by 1g of protein (kcal/g)

A

4 kcal/g

25
Q

Kowashiorkor

A

results from a diet adequate in calories, but low in protein

26
Q

Positive N balance

A

When ingestion > excretion ( Synthesis is dominant)

27
Q

Outline the fate of TAG as the main source of dietary fat

A

1- emulsification (bile salts)

2- digestion (pancreatic lipase) into f.a. and 2-monoglyceride

3- packed (micelles)

4- absorbtion (into intestinal epithelial cells)

5- resynthesis into TAG

6- packed into chylomicrons

7- enter lymph

8- enter blood circulation

28
Q

Basic principles of the fasting state

A

fasting state ~ in between meals and over-night

usage of stored fuel until the next meal Glucagon promotes release of energy from the storage

29
Q

Marasmus

A

results from a diet dificient/low in both cal. and protein

30
Q

during this state muscles dec. use of KB and ox. fa as primary source of energy

A

starvation- prolonged fasting (3-4days)

31
Q

sucrose and lactose digestion

A

by sucrase and lactase - enzymes that are part of the complexes of brush border enzymes (epithelial cells)

sucrose –> glucose + fructose

lactose –> glucose + galactose

32
Q

3 major steps for the production of ketone bodies by the liver

A

1- inc. glucagon, TAG break-down in adipose, f.a & glycerol are released into the blood

2- B-ox and f.a conversion to acetyl-CoA (liver)

3- acetyl-coA used by the liver to syn. ketone bodies: acetoacetate and B-hydroxybutarate

33
Q

The monosaccharides that are absorbed by the body (spc. BB enzyme complexes of epithelium)

A

main: glucose

to some extend: fructose and galactose

34
Q

name several major indicators of starvation state:

A

Inc. blood KB

Dec. in liver gluconeogenesis

Muscle protein is spared

Less urea is produced

35
Q

FAE’s (fatty acid esters) of glycerol

A

glycerides (mono, di and tri)- When the alcohol is glycerol.

36
Q

Total energy produced by 1 g of alcohol (Kcal/g)

A

7 kcal/g

37
Q

DEE

Daily energy expenditure

A

energy required for:

1- BMR- basic metabolic rate

and

2- Energy required for physical activity.

38
Q

how is muscle degradation is spared during prolonged fasting (3-4 days of starvation)

A

Brain shifts from using glu to KB. and muscles dec. using KB. As a result:

Blood KB inc. because muscles don’t use KB ( used by brain as the source of energy) –> less req. gluconeogenesis –> less aa required –> muscle degradation stops

39
Q

location for CM and VLDL formation

A

CMS are made only in intestinal epithelium cells, whereas VLDLs are also synth. in liver.

At the cellular level, CMs are made in the ER and later processed in the golgi- the process of glycosylation of apolipoproteins takes place in golgi.

40
Q

Fate of glucose upon digestion

A

1- majority of carbohydrates get digested to glucose

2- glucose gets oxidized into body fuel

3- Excess glucose gets strored as glycogen in the liver and muscle

4- In the liver, gets converted to TAG and transported into the circulation by VLDL.

41
Q

CM (Chylomicron) components

A

TGs, fat sol. Vits, and cholestrol coated with a layer of:

apolipoprotein (A and B), cholestrol ester, and phospholipids.

42
Q

hyperlipidemia

A

elevated blood lipid levels

normal is <150 mg/dL

43
Q

Energy production (general concept)

A

when fuels are oxidized to CO2 and H2O.

44
Q

sources of carbon for gluconeogenesis

A

lactate- produced by RBC’s and exercising muscles

glycerol- TG breakdown in adipose tsu

A.A.- mainly alanine from muscle breakdown

propionate (minor source) from oxidation of odd chain fatty acid

45
Q

a direct way to measure protein synthesis

A

through the measurment of serum albumin levels.

_ diets that are adequate in cal but low in protein leads to reduced serum albumin level

46
Q

The liver’s function during fasting

A

produce glucose- maintiain blood sugar level

ketone bodies prod.- to be released into the blood and serve as evergy source

47
Q
A

The conversion of acetoacetate to B-hyderoxybutarate

48
Q

The fate of aa’s spc. glu and ala, upon muscle degradation during fasting state

A

tsus metabolize the glu- gut and kidney

aa’s also travel to the liver where Cs are conv’d to

1- glucose

2- KB

3- N containing comps

49
Q
A
50
Q

the main product of f.a. oxidation that serves as a minor C contributor for gluconeogenesis (carried out by liver during the fasting state)

A

propionate

51
Q

name 4 enzymatic activities of brush border enzyme complexes

A

maltase

isomaltase

sucrase

lactase

52
Q

The enzymes that complete the digestion of starch (main dietary carb) to glucose

A

enzymes of the complexes with maltase and isomaltase activities located on the brush border of epithelial cells of small intestine.

Starch is the main form of carbohydrate storage in plants. The initial digestion is carried out by:

Salivary a-amylase (mouth)

Pancreatic a-amylase (intestine)