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biochemistry > Lipids > Flashcards

Lipids Flashcards

1
Q

Group of compounds related by certain physical properties: Insoluble in water, Soluble in nonpolar solvents

A

Lipids

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2
Q

Function of Lipids

A

Major source of energyProvide hydrophobic barrierServe as coenzymes, regulatorsHormonesMediators of inflammation

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3
Q

Amphipathic; have both hydrophilic and hydrophobic groups; enables formation of bilayers

A

Phospholipids

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4
Q

Long chains of carboxylic acids

A

Fatty acids

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5
Q

Degree of Saturation: Contain 0 double bond

A

Saturated Fatty Acids

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6
Q

Degree of Saturation: Contain 1 double bond

A

Monounsaturated Fatty Acids

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7
Q

Degree of Saturation: Contain >1 double bond

A

Polyunsaturated Fatty Acids

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8
Q

Are associated with increased risk of cardiovascular diseases

A

Trans- and saturated fatty acids

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9
Q

Are thought to be protective

A

Mono- and polyunsaturated fatty acids

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10
Q

Geometric Isomerism of Unsaturated Fatty Acids

A

Cis fatty acidsTrans fatty acids

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11
Q

On the opposite side of the double bond

A

Cis fatty acids

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12
Q

On the same sides of double bonds

A

Trans fatty acids

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13
Q

Fluidity decreases with

A

Increasing chain length Increasing saturation

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14
Q

Essential Fatty Acids

A

Linoleic AcidLinolenic AcidArachidonic Acid

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15
Q

Precursor of arachidonic acid 20:4 (5,8,11,14) which is essential in prostaglandin synthesis

A

Linoleic Acid

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16
Q

18:3 (9,12,15)Deficiency results in decreased vision and altered learning vision

A

Linolenic Acid

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17
Q

Becomes essential if Linoleic Acid is deficient

A

Arachidonic Acid

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18
Q

Numbering starts from the last carbon atom

A

Omega Fatty Acids

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19
Q

Are correlated with a decreased risk of cardiovascular disease; Lowers thromboxane production; Reduced tendency of platelets to aggregate

A

Omega-3 Fatty AcidOmega-6 Fatty Acid

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20
Q

Activation of Fatty Acids

A

Must first be activated before being used in metabolismEnzyme: fatty acyl-CoA synthetaseCo-factor: pantothenic acidEnergy used: 2 ATP equivalents

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21
Q

Formation of Palmitate (16:0)

A

Fatty Acid Synthesis

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22
Q

Fatty Acid Synthesis: Where does it occur?

A

In the cytosolMajor: liver and lactating mammary glandsMinor: adipose tissue

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23
Q

Fatty Acid Synthesis: Substrates

A

1 Acetyl CoA7 Malonyl CoA NADPHATP

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24
Q

Fatty Acid Synthesis: Product

A

Palmitate only

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25
Q

Fatty Acid Synthesis: Rate limiting step

A

Reaction: Acetyl CoA + ATP➡️Malonyl CoAEnzyme: Acetyl CoA carboxylase

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26
Q

Necessary co-factor for fatty acid synthesis

A

Biotin

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27
Q

Fatty Acid Synthesis: Step 1

A

Synthesis of cytoplasmic Acetyl CoA

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28
Q

Fatty Acid Synthesis: Step 2

A

Acetyl CoA carboxylated to Malonyl CoARate limiting stepEnzyme: Acetyl CoA carboxylaseCofactor: biotinActivators: insulin and citrate

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29
Q

Fatty Acid Synthesis: Step 3

A

Assembly of PalmitateEnzyme: Fatty acid synthase

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30
Q

Where does the cell primarily get the necessary NADPH?

A

Hexose monophosphate Pathway orPentose phosphate Pathway andNADPH-dependent malate dehydrogenase (malic enzyme)

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31
Q

Assembly is a sequence of steps

A

Condensation➡️Reduction➡️Dehydration➡️Reduction

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32
Q

Regulation of Lipogenesis

A

Activated by: Citrate, InsulinInhibited by: Fatty acyl-CoA, Glucagon, Epinephrine

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33
Q

Fate of Fatty Acids

A

Further elongation in smooth endoplasmic reticulum and mitochondria;Desaturation in the ER through mixed function oxidases (cytochrome b5)

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34
Q

Essential in the diet because they have double bonds that exceed the 9th carbon

A

Linoleic AcidLinolenic Acid

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35
Q

Esters of the trihydric alcohol Glycerol and fatty acids; Main storage forms of fatty acids; Coalesce within adipocytes to form oily droplets that are the major energy reserve of the body

A

Triacylglycerols (TAGs)

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36
Q

Synthesis of TAGs: Where does it occur?

A

LiverAdipose tissue

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37
Q

Synthesis of TAGs

A

Glycerol-3-phosphate + 3 fatty acyl CoA➡️triglyceride

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38
Q

Sources of glycerol-3-phosphate

A

DHAP from glycolysisPhosphorylation of free glycerol

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39
Q

DHAP from glycolysis

A

Enzyme: glycerol-3-phosphate dehydrogenaseIn liver and adipose tissue

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40
Q

Phosphorylation of free glycerol

A

Enzyme: glycerol kinaseIn liver only

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41
Q

What organs synthesize fatty acids?

A

LiverAdipose tissue

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42
Q

Hydrolyzes TAGs to yielding free fatty acids and glycerol; Can only release fatty acids from carbon 1 and carbon 3 of the TAG in stored fat

A

Hormone-sensitive Lipase

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43
Q

Bound to Albumin in blood for beta-oxidation

A

Free fatty acids

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44
Q

Carbon backbone for gluconeogenesis

A

Glycerol

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45
Q

Increase glucagonIncrease cAMP➡️phosphorylation

A

Active Hormone-sensitive lipase

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46
Q

Increase InsulinDecrease cAMP➡️dephosphorylation

A

Inactive Hormone-sensitive lipase

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47
Q

Removal of Acetyl CoA fragments from ends of Fatty acids; Acetyl CoA can enter the citric acid cycle; generates NADH and FADH2 that can enter the ETC

A

Beta-oxidation of Fatty Acids

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48
Q

Beta-oxidation of Fatty Acids: Where does it occur?

A

In the mitochondria of almost all cells but fatty acid activation occurs in the cytosol;Exceptions are: neurons, RBC, testis, kidney medulla

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49
Q

Beta-oxidation of Fatty Acids: Substrate

A

PalmitateNAD+ + FADATP

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50
Q

Beta-oxidation of Fatty Acids: Products

A

8 Acetyl CoA7 FADH27 NADH

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51
Q

Beta-oxidation of Fatty Acids: Rate limiting step

A

Reaction: fatty acyl CoA + Carnitine➡️fatty acyl carnitine + CoAEnzyme: carnithine acyltransferase

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52
Q

Beta-oxidation of Fatty Acids reverses the process of fatty acid synthesis by

A

Oxidizing and releasing units of acetyl-CoA

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53
Q

Oxidation of a fatty acid with an odd number of carbon atoms will yield

A

Acetyl CoAPropionyl-CoA

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54
Q

Propionyl-CoA is converted to a TCA intermediate

A

Succinyl-CoA

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55
Q

Propionyl-CoA carboxylase requires

A

Biotin

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56
Q

Methylmalonyl-CoA mutase requires

A

Vit. B12

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57
Q

Oxidize very long chains of fatty acids (C20, C22)

A

Peroxisomes

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58
Q

Oxidation of unsaturated FAs require an additional enzyme

A

3,2 enoyl-CoA isomerase

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59
Q

Energy Yield of Beta-oxidation

A

129 ATP

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60
Q

Regulation of Beta-oxidation

A

Activated by: GlucagonInhibited by: Malonyl-CoA, Insulin

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61
Q

Alcohol leads to fat accumulation in the liver, called steatosis, which ultimately leads to cirrhosis; Alcohol dehydrogenase eats up NAD+ to reduce beta-oxidation in the liver

A

Fatty liver

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62
Q

Can occur in newborn and manifest as hypoglycemia from impaired FA oxidation and muscle weakness from lipid accumulation

A

Carnitine Deficiency

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63
Q

Affects only the liver resulting in reduced FA oxidation and ketogenesis with hypoglycemia

A

CPT I Deficiency

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64
Q

Affects skeletal muscle and when severe the liver

A

CPT II Deficiency

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65
Q

Decreased FA oxidation; During fasting, hypoglycemia can become profound due to lack of ATP to support gluconeogenesis; can manifest as Sudden Infant Death Syndrome

A

Medium-chain Fatty Acyl-CoA Dehydrogenase Deficiency (MCAD)

66
Q

Caused by eating unripe fruit of the akee tree , which contains hypoglycin, a toxin that inactivates medium and short-chain Acyl CoA dehydrogenase and leads to hypoglycemia

A

Jamaican Vomiting Sickness

67
Q

Rare neurologic disorder due to a defect that causes accumulation of Phytanic Acid which is found in plant foodstuff and blocks Beta-oxidation; Causes neurologic symptoms due to improper myelinization

A

Refsum’s Disease

68
Q

Cerebrohepatorenal syndrome, which occurs in individuals with rare inherited absence of peroxisomes in all tissues; Characterized by liver dysfunction with jaundice, marked mental retardation, weakness, hypotonia, and craniofacial dysmorphism

A

Zellweger’s Syndrome

69
Q

Defect in peroxisomal activation of VLCFA leads to accumulation of VLCFA in blood and tissues; Initial abnormalities are apathy and behavioral change; Visual loss, spasticity and ataxia follow

A

X-linked Adrenoleukodystrophy

70
Q

Converts acetyl CoA to ketone bodies

A

Ketogenesis

71
Q

Ketogenesis: Where does it occur?

A

In liver mitochondria

72
Q

Ketogenesis: Substrate

A

Acetyl CoA

73
Q

Ketogenesis: Products

A

Ketone Bodies

74
Q

Ketogenesis: Rate limiting step

A

Reaction: Acetoacetyl CoA + Acetyl CoA➡️HMG-CoAEnzyme: HMG CoA synthase

75
Q

6-Hydroxybutyrate➡️Acetoacetate➡️Acetyl-CoA

A

Ketogenolysis

76
Q

Can serve as fuel for extrahepatic tissues especially during fasting

A

Ketone Bodies

77
Q

In prolonged starvation and diabetic ketoacidosis, oxaloacetate is depleted for gluconeogenesis; In alcoholism, excess NADH shunts oxaloacetate to malate; Rate of Ketone Body Formation > Rate of Ketone Body Use

A

Ketoacidosis

78
Q

A steroid alcohol; Very hydrophobic compound; has a single hydroxyl group

A

Cholesterol

79
Q

Adrenal hormone not derived from cholesterol

A

Epinephrine

80
Q

De novo synthesis of Cholesterol

A

Cholesterol Synthesis

81
Q

Cholesterol Synthesis: Where does it occur?

A

Virtually all cells, in the cytosol and smooth endoplasmic reticulumMajority: in the liver and intestines

82
Q

Cholesterol Synthesis: Substrate

A

Acetyl CoANADPHATP

83
Q

Cholesterol Synthesis: Product

A

Lanosterol➡️Cholesterol

84
Q

Cholesterol Synthesis: Rate limiting step

A

Reaction: HMG CoA➡️mevalonateEnzyme: HMG CoA reductase

85
Q

Drugs used for the treatment of hypercholesterolemia, to reduce the risk for cardiovascular diseases

A

Statins

86
Q

Cholesterol Synthesis: Step 1

A

Biosynthesis of mevalonateRate limiting step

87
Q

Cholesterol Synthesis: Step 2

A

Formation of isoprenoid units(Isopentenyl diphosphate)

88
Q

Cholesterol Synthesis: Step 3

A

Six isoprenoid units form isoprene

89
Q

Cholesterol Synthesis: Step 4

A

Formation of Lanosterol

90
Q

Cholesterol Synthesis: Step 5

A

Formation of Cholesterol

91
Q

An intermediate in the pathway

A

Farnesyl pyrophosphate

92
Q

How does the Acetyl CoA reach the cytosol for cholesterol biosynthesis?

A

Citrate shuttle

93
Q

High cholesterol limits the expression of HMG-CoA reductase gene by transcription factor (SREBP)

A

Production inhibition

94
Q

Insulin dephosphorylates and activates; Glucagon phosphorylates and inactivates

A

Enzyme phosphorylation

95
Q

Elimination through conversion to bile salts then secretion into the bile

A

Cholesterol degradation

96
Q

Synthesized in the liver from cholesterol

A

Bile Acids

97
Q

Rate limiting enzyme of Bile Acids

A

Cholesterol-7-alpha-hydroxylase

98
Q

Regulation of Bile Acids

A

Activated by: CholesterolInhibited by: Bile Acids

99
Q

Bile acid conjugated with either glycine or taurine; Primary means of excreting cholesterol; Emulsify lipids in the intestines

A

Bile salts

100
Q

Excreted bile is reabsorbed in?

A

Terminal ileum95% reabsorbed5% excreted in feces = amount that liver must make

101
Q

Steroid Hormone Synthesis: What is it for?

A

Precursor of ALL steroid hormonesGlucocorticoids (Cortisol)Mineralocorticoids (Aldosterone)Sex Hormones (Testosterone and Estradiol)

102
Q

Steroid Hormone Synthesis: Location

A

In the smooth endoplasmic reticulum of the adrenal cortex, ovaries, testes, placenta

103
Q

Steroid Hormone Synthesis: Substrate

A

CholesterolPregnenolone - “mother hormone” from which all other hormones are derived

104
Q

Steroid Hormone Synthesis: Rate limiting step

A

Reaction: Cholesterol➡️PregnenoloneEnzyme: DesmolaseBlocker: Aminogluthetimide

105
Q

Lipid digestion begins in the

A

Stomach

106
Q

Reach the capillaries of skeletal muscle and adipose tissue; Triglycerides broken to FA and glycerol via lipoprotein lipase

A

Chylomicrons

107
Q

Directly enter adjacent muscle cells or adipocytes, or may be transported in blood bound to albumin

A

Free fatty acids

108
Q

Converted to DHAP then enters glycolysis or gluconeogenesis

A

Glycerol

109
Q

Manifests as steatorrhea (greasy stools); results in deficiency in fat-soluble vitamins and essential fatty acids

A

Lipid Malabsorption

110
Q

Causes of Lipid Malabsorption

A

Liver DiseasePancreatic DiseaseCholelithiasisShortened bowelIntestinal mucosa defects

111
Q

Spherical macromolecule complexes composed of neutral lipid core surrounded by shell of amphipathic apoptoteins, phospholipid and nonesterified cholesterol

A

Plasma Lipoproteins

112
Q

Functions of Lipid Transport

A

1) Keep their component lipids soluble as they transport them in plasma2) Provides an efficient mechanism for transporting their lipid contents to and from the tissues

113
Q

Represent the protein moiety of lipoproteins; Some are integral while others are free to transfer to other lipoproteins

A

Apolipoproteins or APO Proteins

114
Q

Transport dietary triglyceride and cholesterol from intestine to tissues

A

Chylomicrons

115
Q

Apoproteins: Chylomicrons assembly + secretion; Secreted by epithelial cells

A

Apo B-48

116
Q

Apoproteins: Chylomicron, VLDL; Cofactor for lipoprotein lipase; Shuttled by HDLs

A

Apo C-II

117
Q

Apoproteins: Chylomicron, VLDL; Mediates uptake of chylomicron remnant

A

Apo E

118
Q

Transport triglyceride from liver to tissues

A

VLDL

119
Q

Picks up Cholesterol from HDL to become LDL; Picked up by the liver

A

IDL

120
Q

Delivers cholesterol into cells

A

LDL

121
Q

Picks up cholesterol accumulating in blood vessels; Delivers cholesterol to liver and steroidogenic tissues via scavenger receptor; Shuttles apo C-II and apo E in blood

A

HDL

122
Q

Apoproteins: HDL; Activates LCAT

A

Apo A-I

123
Q

Apoproteins: LDL, VLDL; Binds to LDL and VLDL receptors

A

Apo B-100

124
Q

Deposition of Cholesterol and Cholesterol esters in the artery walls especially from oxidized LDL; Oxidized LDLs can cause endothelial damage

A

Atherosclerosis

125
Q

Lipoprotein lipase deficiency; High VLDL and Chylomicron; Low LDL and HDL; Xanthomas and pancreatitis

A

Type I Familial Lipoprotein Lipase

126
Q

LDL receptors deficiency; High LDL; Xanthomas and Xanthelasmas with increased risk of atherosclerosis and coronary heart disease

A

Type II Familial Hypercholesterolemia

127
Q

Apo E deficiency; High remnants of VLDL and chylomicron with increased risk of atherosclerosis and coronary heart disease

A

Type III Familial Dysbetalipoproteinemia

128
Q

Increased VLDL production; Triad of: Coronary Artery Disease, DM type 2, Obesity

A

Type IV Familial Hypertriglyceridemia

129
Q

Apo B-48 and 100 deficiency; No chylomicron, No VLDL/LDL; Intestinal malabsorption with accumulation of lipids in intestine and liver

A

Abetalipoproteinemia

130
Q

Apo A1 deficiency; No HDL; Triglycerides and atherosclerosis

A

Familial a-lipoprotein Deficiency: Tangier’s DiseaseFisheye Disease

131
Q

High HDL; Associated with benefits to health and longevity

A

Familial Hyperalphalipoproteinemia

132
Q

High LpA; Early atherosclerosis and Thrombosis

A

Familial Lipoprotein A Excess

133
Q

Predominant lipids of cell membranes; Degraded by phospholipases

A

Phospholipids

134
Q

Most abundant phospholipids; Represent a large proportion of the body’s store of choline, important in nervous transmission, as acetylcholine and as a store of labile methyl groups

A

Phosphatidylcholine

135
Q

Also found in cell membranes; plays a role in programmed cell death

A

Phosphatidylethanolamine (Cephalin) and Phosphatidylserine (for apoptosis)

136
Q

Major lipid component of lung surfactant; Inadequate levels lead to Respiratory Distress Syndrome in the newborn

A

Dipalmitoylphosphatidylcholine (DPPC) or Dipalmitoyllecithin

137
Q

Reservoir for arachidonic acid in the membranes; Source of 2nd messengers

A

Phosphatidylinositol

138
Q

2 molecules of phosphatidic acid esterified through their phosphate groups to an additional molecule of glycerol; Found only in mitochondria and is essential for mitochondrial function; Antigenic

A

Cardiolipin

139
Q

Part of the glycocalyx located on the outer layer of the cell membrane and functions in cell recognition and cell adhesion; Found in high concentrations in nervous tissues

A

Glycolipids

140
Q

Sphingosine + Fatty Acid

A

Ceramide

141
Q

Ceramide + Glucose or Galactose

A

Cerebroside

142
Q

Ceramide + N-acetylneuramic acid

A

Ganglioside

143
Q

Ceramide + Oligosaccharide

A

Globoside

144
Q

Ceramide + Sulfated Galactose

A

Sulfatides

145
Q

Only significant sphingophospholipid in humans where it is an important constituent of the myelin sheath of nerves

A

Sphingomyelin

146
Q

Deficiency in phospholipids and sphingolipids from white matter resulting in increase CSF phospholipids

A

Demyelinating Diseases

147
Q

Lipid storage diseases often manifested in childhood lipid synthesis is Normal; Lipid degradation in lysosomes is Abnormal

A

Sphingolipidoses

148
Q

Hexosaminidase A Deficiency; Cherry red macula, MR and Hypotonia

A

Tay-Sach’s Disease

149
Q

Alpha-galactosidase Deficiency; X-linked recessive, Rash, Renal failure

A

Fabry’s Disease

150
Q

Ceramidase Deficiency; Triad of Skin rash, Hoarseness, Bone malformation

A

Farber’s Disease

151
Q

Arylsulfatase A Deficiency; Psychologic disturbance in adults due to demyelination

A

Metachromic Leukodystrophy

152
Q

Beta-Galactosidase Deficiency; Mental Retardation

A

Krabbe’s Disease

153
Q

Beta-Glucosidase Deficiency; Hepatosplenomegaly + erosion of long bones

A

Gaucher’s Disease

154
Q

Sphingomyelinase Deficiency; Hepatosplenomegaly

A

Neimann-Pick Disease

155
Q

Potent compounds that elicit a wide range of physiologic and pathologic responses

A

Eicosanoids

156
Q

3 main kinds of Eicosanoids

A

ProstaglandinThromboxaneLeukotrienes

157
Q

Eicosanoids: Dietary precursor

A

Linoleic Acid

158
Q

Eicosanoids: Immediate precursor

A

Arachidonic Acid

159
Q

Synthesized in platelets; Cause vasoconstriction and platelet aggregation

A

Thromboxane (TXA2)

160
Q

Produced by blood vessel walls; Inhibitors of platelet aggregation

A

Prostacyclin (PGI2)

161
Q

Mixture of leukotrienes C4, D4, and E4; Potent bronchoconstrictors

A

Slow-Reacting Substances of Anaphylaxis (SRS-A)

biochemistry (7 decks)

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