lecture 21- 22 Flashcards

1
Q

saturated fats

A

straight

solid at room temp

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2
Q

unsaturated fats

A

kink

liquid at room temp

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3
Q

omega __ and omega ___ can not be made in the body and has to be ___ by the diet

A

6
3
supplemented

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4
Q

omegas help with

A

lipids involved in barrier function of the skin

structure and function of cell membrane

precursors to eicosinoid (hormones- inflammation reaction)

endocannabinoid messenger molecules

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5
Q

___ are 6x more efficient than glycogen at storing energy

A

triacylglycerols

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6
Q

two things that make triacylglycerols good at storage are

A

complete oxidation of one gram of tri produces 2 times more ATP than complete oxidation of one gram of glycogen

one gram of stored glycogen binds two grams of H20, while stored Tri bind none

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7
Q

___ hydrolyze tri to release fatty acids

A

lipases

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8
Q

length of survival during starvation depends primarily on the amount of stored ___

A

triacylglycerols

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9
Q

___ are a major source of every for the heart and (part of the ) kidney

A

fatty acids

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10
Q

cholesterol is an important component of membranes and a precursor to ___

A

bile salts
vitamin D
steroid hormones

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11
Q

Fatty acids are conjugated to CoA after they enter the cell. Beta oxidation occurs in the

A

matrix of the mitochondria

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12
Q

oxidation reactions occur at the beta carbon, so this process is referred to as ___

A

Beta oxidation

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13
Q

Products of beta oxidation of fatty acids

A

acetyl CoA
FADH2
NADH
H+

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14
Q

Acetyl CoA can be oxidized to CO2 in the ___. converted to ketone bodies or used for other pathways

A

TCA cycle

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15
Q

NADH and FADH2 can be used by oxidative phosphorylation to make ____

A

ATP

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16
Q

More than ___ times as much ATP can be made from the total oxidation of 1 gram of palmitic acid(16 carbons (palmitoyl ACP)) in comparison to 1 gram of glucose

A

2

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17
Q

fatty acid synthesis occurs in the

A

cytoplasm

liver and in adipose tissues

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18
Q

most intermediates of fatty acid synthesis are carried by ___

A

ACP

acyl carrier protein

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19
Q

reduction of fatty acid synthesis involves

A

NADPH

product of PPP

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20
Q

fatty acids are built ___

A

2 carbons at a time

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21
Q

fatty acids uses the 3 carbon ___ and CO2 is released in each cycle

A

malonyl ACP

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22
Q

fatty acid synthesis continues until chain reached ___ carbons

A

16 carbons (palmitoyl ACP)

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23
Q

synthesis of ___ is the commitment step of fatty acid synthesis

A

Malonyl CoA

Acetyl CoA + ATP + HCO3- (acetyl CoA carboxylase) = Malyonyl Coa

24
Q

what are some inhibitors to the commitment step of fatty acid synthesis

A

Acetyl CoA (acetyl CoA carboxylase) = Malyonyl Coa

palmotoyl acid (16 chain end product)
AMP
Glucagon
Epinephrine

(all these things trigger the cell to say Iow blood glucose, need to break down storage or make glucose for energy)

25
Q

what are some activators to the commitment step of fatty acid synthesis

A

Acetyl CoA (acetyl CoA carboxylase) = Malyonyl Coa

citrate
insulin

(insulin means high glucose in blood, glucose can be used to make other stuff)

26
Q

___ is important for fatty acid transport into Mitochondrial matrix for beta oxidation

A

carnitine

27
Q

beta oxidation is ___ by malonyl CoA

A

inhibited

carnitine (carnitine acyltransferase 1)= Acyl carnitine

this process blocked by malonyl CoA
-stops the transport of fatty acids into mitochondrial matrix and therefore B oxidation

28
Q

Triacylglycerol and cholesterol are nearly ___ in water. they are carried in the blood as lipoprotein complexes

A

insoluable

29
Q

the surface of lipoprotein complexes resemble the surface of membranes, containing phospholipids, proteins and cholesterol. The hydrophobic components ___ and ___ are buried in the interior of the complex

A

Triacylglycerol

cholesteryl esters

30
Q

dietary Triacylglycerol and cholesterol are carried in complexes called ___ that are produecd in the small intestine

A

chylomicrons

31
Q

endogenous Triacylglycerol and cholesterol made by the liver are released into the blood in a complex called the ___

A

very low density lipoprotein

VLDL

32
Q

abnormalities in blood lipids and lipoproteins can help in the diagnosis of

A

hypothyroidism
cushings
pancreatitis

33
Q

liver produces VLDL which has high ___ and low ___. as

A

Triacylglycerol

cholesterol

34
Q

the VLDL moves through the body the Triacylglycerol are broken down (hydrolyzes) by ___ which is present in the capillaries of ___

A

lipoprotein lipase

muscle, adipose and other tissues

35
Q

IDL with lipoprotein lipase =

A

LDL and fatty acids

36
Q

fatty acids are used for energy by ___ , for synthesis of other molecules such as ___ or for storage in the form of ____

A

muscles, heart

phospholipids

triacylglycerols (in adipose)

37
Q

LDL is taken into the cell by ___ to deliver cholesterol required for membrane and biosynthetic processes

A

endocytosis

38
Q

LDL is taken up by the ___ to regulate LDL levels in the blood

A

liver

39
Q

fattu acids in the blood are bound to ___ to protect cells from the detergent properties of free fatty acids

A

serum albumin

40
Q

type of dog that gets hyperlipidemia

A

miniature schnauzers

41
Q

after a meal- blood glucose and insulin are high, triacylglycerols synthesis will be ___ in adipocytes because glucose from blood is converted to glycerol 3 phosphate, which is required for triacylglycerols synthesis. triacylglycerol breakdown will be ___ because high insulin and low glucagon ___ hormone sensitive lipase

A

high

low

inhibit

42
Q

DURING FASTING
BG and insulin are low, Tri synthesis in adipocycles will ___, because they have little glucose to covert to glycerol 3 phosphate. Tri deg will ___ because hormone sensitive lipase is stimulated by high glucagon and low insulin. This leads to the release of fatty acids to the blood that can be oxidized by the tissues to make ____

A

decrease

increase

ATP

43
Q

during faster the liver will convert fatty acids from adipose tissue into ____

A

ketone bodies

44
Q

ketone bodies are exported form the liver and can be taken up by other tissues and converted to ____

A

Acetyl CoA

45
Q

what tissues can use ketones for energy

A

cardiac muscle

renal cortex

46
Q

during starvation, in the liver, oxaloacetate drops as it is used for gluconeogenesis, this will ___ the TCA cycle in liver cells. which leads to the accumulation of acetyl CoA from B oxidation of fatty acids and increases ketone body synthesis by the liver

A

decrease

47
Q

during starvation, the tissues of the body, including the brain, will adapt yo use ___ as their major source of energy, this helps preserve protein in muscles and other tissues until triacylglycerols reserves are depleted

A

ketone bodies

48
Q

how do liver cells get their energy

A

B oxidation

making fatty acids***

49
Q

what are the advantages of converting fatty acids to ketone bodies?

A

much more soluble. less soap like, easier to convert

50
Q

what is the downside of the liver converting fatty acids to ketone bodies?

A

ketoacidosis

decrease in pH of the body

51
Q

low blood glucose can be caused by

A

fasting
pregnancy
lactation

52
Q

low insulin or low insulin response can be caused by

A

Diabetes

53
Q

explain diabetic ketoacidosis

A

glucose can not be taking into cells,

Liver tries to make more glucose by breaking down fatty acids. This releases ketones as a bi product

excess ketones lead to PH drop

leads to coma and death

54
Q

Bovine ketosis due to pregnancy/lactation have a higher risk of fatty liver. Treatments are ___

A
55
Q

in Sheep ketosis can happen late in pregnancy if ewe is carrying more than 1 fetus.

Symptoms:
Treament:

A

fatty liver and high mortality

56
Q

equine hyperlipidemia

caused by stress, obesity, lactation and pregnancy.

high serum lipids occur which results in accumulation of triacylglycerols in liver, kidneys and other organs

treatment

A

feeding tube

57
Q

feline hepatic lipidosis

occurs when cat refused to eat for several days. triacylglycerols build up in liver and disrupt normal function

treatment

A

feeding tube