Fuel Metabolism and Nutrition: Basic Principles Flashcards
Total energy produced by carbohydrates per gram
kcal/g
4 kcal/g
long-, medium- and short-chain transport
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.
Two major precursors of polyunsaturated compounds such as prostaglandins and eicosanoids
Hint: essential fatty acids
linoleic acid
a-linolenic acid
comps tht get ox by . muscles during fasting
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
Total energy produced by 1g of fat (kcal/g)
9 kcal/g
Essential amino acids
valine, leucine, isoleucine
histidine, lysine
phenylalanine, tryptophan
methionine and threonine
Two major metabolic rxns carried out by the liver during the fasting state (with time frame)
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
The main aa released from the muscles during the fasting state
alanine and glutamine
tissues such as gut and kidney metabolize the glu
Blood level of KB during starvation
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
site of storage for glucose as glycogen- What’s unique about each?
Muscle- Oxidization and fuel
Liver-maintaining blood glucose
* excess glucose converts to TAG in the liver and gets packaged into VLDL.
Basic principle of fed state
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
resenthesize the digestive products of TAG
intestinal epithelial cells
digestive products of dietary fat
dietary fat( TAG- triacylglycerol)
digests into
fatty acids
and
2-monoacylglycerol
name two major ketone bodies prod. by the liver from acetyl-CoA during the fasting state
acetoacetate and B-hydroxybutarate.
Chylomicrons enter the blood via
lymph
Conseq. of Kwashiorkor
- dec. protein syn. (inc serum level of albumin)
- impacts regeneration of intestinal epithelial cells
- compensated by malabsorption
- hepatomegaly and distended abdomen ( lack of albumin in blood, inc. osm pressure diff. –> water accumulation .
tissues such as gut and kidney metabolize this aa- released from the muscles during the fasting state
glu
The fate of dietary fat and cholestrol
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.
The fatty acids of VLDL are stored in this tissue
adipose tissue
fatty acids of chylomicrons are stored in
adipose triglycerides
The role of adipose tissue during fasting
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
Basic principles of starvation
starvation~ prolonged fasting
changes in the usage of fuel storage that allows survival for prolonged period of time.
Negative nitrogen balance
When the rate of excretion>ingestion
Total energy produced by 1g of protein (kcal/g)
4 kcal/g
Kowashiorkor
results from a diet adequate in calories, but low in protein
Positive N balance
When ingestion > excretion ( Synthesis is dominant)
Outline the fate of TAG as the main source of dietary fat
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
Basic principles of the fasting state
fasting state ~ in between meals and over-night
usage of stored fuel until the next meal Glucagon promotes release of energy from the storage
Marasmus
results from a diet dificient/low in both cal. and protein
during this state muscles dec. use of KB and ox. fa as primary source of energy
starvation- prolonged fasting (3-4days)
sucrose and lactose digestion
by sucrase and lactase - enzymes that are part of the complexes of brush border enzymes (epithelial cells)
sucrose –> glucose + fructose
lactose –> glucose + galactose
3 major steps for the production of ketone bodies by the liver
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
The monosaccharides that are absorbed by the body (spc. BB enzyme complexes of epithelium)
main: glucose
to some extend: fructose and galactose
name several major indicators of starvation state:
Inc. blood KB
Dec. in liver gluconeogenesis
Muscle protein is spared
Less urea is produced
FAE’s (fatty acid esters) of glycerol
glycerides (mono, di and tri)- When the alcohol is glycerol.
Total energy produced by 1 g of alcohol (Kcal/g)
7 kcal/g
DEE
Daily energy expenditure
energy required for:
1- BMR- basic metabolic rate
and
2- Energy required for physical activity.
how is muscle degradation is spared during prolonged fasting (3-4 days of starvation)
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
location for CM and VLDL formation
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.
Fate of glucose upon digestion
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.
CM (Chylomicron) components
TGs, fat sol. Vits, and cholestrol coated with a layer of:
apolipoprotein (A and B), cholestrol ester, and phospholipids.
hyperlipidemia
elevated blood lipid levels
normal is <150 mg/dL
Energy production (general concept)
when fuels are oxidized to CO2 and H2O.
sources of carbon for gluconeogenesis
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
a direct way to measure protein synthesis
through the measurment of serum albumin levels.
_ diets that are adequate in cal but low in protein leads to reduced serum albumin level
The liver’s function during fasting
produce glucose- maintiain blood sugar level
ketone bodies prod.- to be released into the blood and serve as evergy source
The conversion of acetoacetate to B-hyderoxybutarate
The fate of aa’s spc. glu and ala, upon muscle degradation during fasting state
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
the main product of f.a. oxidation that serves as a minor C contributor for gluconeogenesis (carried out by liver during the fasting state)
propionate
name 4 enzymatic activities of brush border enzyme complexes
maltase
isomaltase
sucrase
lactase
The enzymes that complete the digestion of starch (main dietary carb) to glucose
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)
