macro exam 2 🍒

whats the most concentrated source of energy & how many kcals per gram

dietary fat - 9kcal/gram

role of lipids in body fat

stored energy, protects internal organs, insulates against heat loss

role of lipids as molecular components

cell membrane, steroid hormone precursor, and precursor for bile acids

whats the simplest lipid

fatty acids

how do fatty acids travel throughout the body

lipoproteins or albumin. due to their hydrophobic nature, they cannot travel in the blood.

whats the general structure of a fatty acid

straight hydrocarbon chain with a methyl end (hydrophobic) and a carboxylic end (hydrophillic)

how many C does a SCFA contain

6 or less

how many C does a MCFA contain

8-14

how many C does a LCFA contain

14 or moreho

how many C does a very long chain FA contain

22 or more

how many double bonds does a SFA contain

none, its saturated with hydrogens

how many double bonds does a MUFA contain

one

how many double bonds does a PUFA cotain

more than one

how does a diet higher in SFA associate with CVD risk

increased risk

how does a diet higher in MUFA associate with CVD risk

reduced risk

how does a diet higher in PUFA associate with CVD risk

reduces risk

which two SFAs increase LDL cholesterol

myristic and palmitic

which SFA has a little affect on LDL cholesterol

stearic

what are some reasons that CVD and SFA literature is inconsistent?

• they dont contrast high/low intake well

• they lack multiple diet assessments

  • assessing diet is tricky

which fat sources are higher in SFA

tropical oils and animal fats

which fat source is uniquely high in MUFA

olive oil

which fat sources are higher in PUFA

vegetable oils

whats the number 1 source of calories

cooking oils

whats the number 1 source of SFA

red meat and dairy

whats the meaning of cis

• same side

• the primary configuration in naturally occurring foods

whats the meaning of trans

• opposite side

• the result of partial hydrogenation of veggie oils

• increased shelf life

fatty acid nomenclature: delta system

• starts counting carbons from the carboxyl end

  • includes chain length, number of bonds, and position of double bonds

fatty acid nomenclature: omega system

• counts from the methyl end (CH3)

• includes the number of bonds and the position of the first double bond

what are the two essential fatty acids

linoleic acid and linolenic acid

linoleic acid properties

• plant & vegetable oils

• omego-6-fatty acids

  • 18:2 n-6

linolenic acid properties

• flax products

• omega-3-fatty acid

  • 18:3 n-3

what is the primary storage form of fat

triglycerides

which fats are liquid at room temp

short chain or unsaturatedwhi

which fats are solid at room temperature

longer chain or saturatedh

how can TGs in the adipose be used for energy

FAs can be cleaved and oxidized via the TCA cycle

glycerol can be used in gluconeogenesis

cholestrol characteristics

• important in plasma membranes

• precursor for steroids (bile acid, sex hormone, cortisol, vitamin d)

  • found in animal products, shellfish, and shrimp

phytosterols characteristics

• plant sterols, similar to cholestrol in animals

• can lower cholesterol (excretion)

phospholipid characteristics

• component of cell membranes

• intracellular signaling

• found in soy, egg yolk, fish

sphingolipids

• found in the plasma membrane, abundant in the CNS

  • includes ceramide, sphingomyelin, cerebrosides, and gangliosides

ceramide characteristics

• simplest sphingolipid

• in excess and in certain tissues

  • role in metabolic dz

sphingomyelin

important for nervous system function (mylein sheath)

cerebrosides

formed when a sugar attatches to ceramide

facillitates nerve impulses

gangliosides

multiple sugar units attatched to a ceramide

function as receptors and important in cell communication

where does TG digestion begin

the mouth with lingual lipase yielding FAs and diglycerides

how are TGs digested in the stomach

gastric lipase digests short & medium chain FAs yielding FAs and diglycerides

TG digestion in the SI

CCK facillitates:

• gallbladder releases bile to emulsify lipids

• pancreas releases pancreatic lipase and bicarbonate

  • pancreatic lipase does most of the digestion yielding monglycerides and FAs

what enzyme facillitates the most of lipid digestion

pancreatic lipase

cholesteroll digestion in the SI

free cholesterol doesnt require action

dietary chholesterol is esterified to a FA (FA removed by cholesterol eterase)

phospholipid digestion in the SI

hydrolyzed by phospholipase A producing a lysophospholipid and a FFA

how are lipids absorbed?

• digestion products: monoglycerides, FAs, free cholesterol, and lysophospholipids

• these products combine with bile and micelles (circular structures that transport lipids)

  • micelles allow lipids to travel

TG & cholesterol absorbtion

• lipid absorbtion is mostly facillitated diffision and some passive diffusion

• FATP: fatty acid transport protein and NPC1L1 transports cholesterol and phytosterol

  • within the enterocyte, cholesteol and longer chain FA travel to the ER for reformation

what enzyme is primarily responsible for lipid digestion?

pancreatic lipase

what are the three classes of lipoproteins

exogenous lipid transport (dietary), endogenous lipid transport (stored fat), and reverse cholesterol transport

exogenous lipid transport (dietary)

CM with apoB48

endogenous lipid transport (stored fat)

VLDL lineage with apoB100

lineage: VLDL slowly become IDL and then LDL as lipids are removed

reverse cholesterol transport

HDL with apo-A1

excess cholesterol transported back to the live for excretion

when ready to export from the gut, what happens to longer chain fatty acids

they are packaged into CM within the ER. they exit the enterocyte and enter the lymphatic system where they fuse with the membrane and are released (exocytosis) to enter the blood stream through the left subclavian vein. 

where to the CM deliver the TGs

tissues for energy (heart, muscle, adipose)

what happens to adipose when FAs enter

they are converted back to TG and stored (high fat meals), ready to be used when energy demand exceeds energy intake.

what happens to muscle when FAs enter

they are used for energy (greedy)

what happens to the liver when FAs enter

glycerol will enter and go to glycolysis

T/F: if fat is stored in your adipose tissue, you will gain weight long term

false

what happens (generally) when we fast (about 3 hours)

we start mobilizing stored adipose tissue for fuel

when we fast and see a rise in glucagon and a drop in insulin, what else occurs

the hormone sensitive lipase is stimulated to yield FAs (and glycerol) which will attach to albumin and circulate in the blood. they will then go to the liver to be secreted as VLDL

where does VLDL assembly (using TG) occur

the ER of the liver

when the VLDL travels through the blood, it looses TGs. what is the progression VLDL undergoes

VLDL → IDL → LDL

what happens to leftover LDL after it circulates as VLDL in the blood

they are rich in cholesterol and they are removed by LCL receptors

what is LDL clearance

taking LDL out of the blood via LDL receptor

when fasting (high glucagon) what is increased and what is decreased?

• CM

• VLDL secretion

• adipose lipolysis

• fatty acid secretion

  • glycerol used in gluconeogenesis

decreased: 

• CM

increased:

• VLDL secretion

• adipose lipolysis

• fatty acid secretion

• glycerol used in gluconeogenesis

when postprandial (high insulin) what is increased and what is decreased?

increased: 

• CM

decreased:

• VLDL secretion

• adipose lipolysis

• fatty acid secretion

what happens during prolonged fasting

we run out of stored glycogen and need to rely on our body fat. the skeletal muscle uses FAs, the liver produces ketones, and glucose is saved for the tissues that absolutely need it.

HDL cholesterol is secreted by:

the liver and some by the gut

HDL carries out

reverse cholesterol transport

cholesterol is removed

which of the following lipoproteins contains cholesterol?

• HDL

• IDL

• VLDL

• CM

• LDL

which lipoprotein is the most enriched with cholesterol

LDL

whats the purpose of beta oxidation

to extract energy from fatty acids

when and where does beta oxidation occur

in the mitochondria within the muscle and liver during prolonged fasting/starvation or overnight

what two things need to happen before beta oxidation 

fatty acid activation and transportation into the mitochondrial matrix

whats the process of fatty acid activation

coA is added to the FA. this requires ATP and will create a fatty acyl coA

what is the process of fatty acid transports to the mitochondrial matric

the carnatine shuttlewha

whats the process of the carnitine shuttle

CAT 1: passes the FA from coA to carnitine

CAT 2: passes the FA from carnitine back to coA

what happens in each cycle of beta oxidation

a fatty acid loses 2 carbons

acetyl coA is produced and can enter the TCA

NADH and FADH2 is produced and can enter the ETC

what is the first step in beta oxidation of saturated FAs

inserting a double bond

what happens to the first step in beta oxidation for unsaturated FAs

it is skipped

we get 1.5 fewer ATPs

what does an odd numbered carbobn chain FA produce

several acetyl coA and one propionyl Coa (which can be converted to glucose)

what is the basis of ketogenesis

ketones forming when we rely on adipose tissue for energy in long periods of fasting or dietary CHO is restricted

when does ketogenesis ramp up

when acetyl coa is abundant

TCA cannot keep running (OAA) is limiting

where does ketogenesis occur

the mitochondria of the liver

what are the three ketones

acetoacetate (most abundant)

beta hydroxybuterate

acetone

what uses ketones

heart and skeletal muscle

brain (long period)wha

what cannot use ketones

the liver (lacks an enzyme)

how are ketones used for energy

beta hydroxybutyrate and acetoacetate can become acetyl coa and enert the TCA

acetone cannot be used for energy

what is ketosis

a mild increase in ketone bodies (low carb/energy diets)ket

what is ketoacidosis

a serious complication of T1 or advanced T2DM

extreme hyperglycemia, unrestrained breakdown of adipose

blood pH drops inducing low BP, dehydration, coma, and death

what happens when we fast, eat low CHO, or exersise at low intensity for long periods

insulin is low

glucagon is high

how does insulin and glucagon promote/inhibit beta oxidation and ketogenesis

glucagon promotes and insulin inhibits

what happens to excess FAs

stored in adipose

what happens to excess CHO

glycolysis and glycogen replenishment, reamining converts to FA

what happens with excess PRO

can be converted to FA

where does FAS occur

lipogenic tissues (liver, adipose)