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Flashcards in Biochem 3 USMLE Deck (196):
1

NADPH is a procatabolicduct of this pathway

HMP shunt

2

NAD+ is generally used in _______ processes to carry reducing equivalents away as NADH

catabolic

3

NADPH is used in _____ processes (steroid and fatty acid synthesis) as a supply of reducing equivalents

anabolic

4

NADPH is used in these 3 ways:

1) anabolic processes
2) respiratory burst
3) P-450

5

where is hexokinase found

throughout the body

6

where is glucokinase found

liver

mneu: gLucokinase in Liver

7

describe the Km and Vmax of glucokinase in comparison to hexokinase

glucokinase has a lower affinity [higer Km] but higher capacity [ higher Vmax]

8

which one hexokinase or glucokinase is feedback inhibited by G6P

hexokinase

9

which one hexokinase or glucokinase phosphorylates excess glucose (e.g., after a meal) to sequester it in the liver as G6P

glucokinase

10

give the irreversible enzymes in glycolysis regulation

hexokinase/glucokinase
phosphofructokinase-1 (RLS)
pyrovate kinase
pyruvate dehydroginase

11

hexokinase/glucokinase converts D-glucose into what?
what is this inhibited by?

Glucose-6-P
Glucose-6-P(inh by product)

12

phosphofructokinase-1 (RLS) converts fructose 6-phosphate into what?
what is it inhibited by?
stimulated by?

Fructose-1,6-BP
inh by: ATP, citrate
stim by: AMP,Fructose-2,6-BP

13

pyrovate kinase converts phosphoenolpyruvate into what?
what is it inhibited by?
stimulated by?

pyruvate
stim: fructose-1,6-BP
inh: ATP, alanine

14

pyruvate dehydroginase converts pyuvate into what?
what is it inhibited by?

Acetyl CoA
inh: ATP, NADH
Acetyl-CoA

15

Glycolyc enzyme deficiencies such as hexokinase, glucose phosphate isomerase, aldolase, triosephosphate isomerase, phosphate glycerate kinase, enolase, and pyruvate kinase deficiencies are associated with what condition

hemolytic anemia

16

why do glycolytic enzyme deficiencies result in hemolytic anemia

RBCs metabolize glucose anaerobically (no mitochondria) and thus depend solely on glycolysis

17

The pyruvate dehydrogenase complex contains 3 enzymes that require 5 cofactors. What are these cofactors.

1) pyrophosphate (B1, thyamine; TTP)
2) FAD (B2, riboflavin)
3) NAD (B3, niacin)
4) CoA (B5, pantothenate)
5. Lipoic acid

18

Pyruvate dehydrogenase complex is similar to what other complex (same cofactors, similar substrate and action)

alpha ketoglutarate

19

give thee pyruvate dehydrogenate reaction.

pyruvate + NAD+ + CoA
-> acetyl CoA + CO2 + NADH

20

pyruvate dehydrogenase complex is activated by exercise because it increases these three things

NAD+/NADH ratio
ADP
Ca++

21

pyruvate dehydrogenase deficiency causes a backup of substrate which is?

pyruvate and alanine

22

pyruvate dehydrogenase deficiency results in this

lactic acidosis

23

pyruvate dehydrogenase deficiency is often seen in alcoholics due to a deficiency of this vitamen

B1

24

someone with a pyruvate dehydrogenase deficiency may present with this deficit

neurologic

25

what is the tx for pyruvate dehydrogenase deficiency

increase intake of ketogenic nutrients (e.g., high fat content or high lysine and leucine)

26

name the only purely ketogenic amino acids

lysine and leucine

27

how many ATP equivalents are needed to generate glucose from pyruvate

6

28

this AA serves as a carrier of amino groups form mm to liver

alanine

29

this can be used to replenish TCA cycle or in gluconeogenesis

oxaloacetate

30

This cycle transfers excess reducing equivalents from RBCs and mm to liver, allowing muscle to funcction anaerobically (net 2 ATP)

cori cycle

31

TCA cycle enzymes

Citrate
Isocitrate
alpha-Ketogluterate
Succinyl-CoA
Succinate
Fumarate
Malate
Oxaloacetate

mneu: Can I Keep Selling Sex For Money, Officer?

32

What does the TCA cycle produce per Acetyl-CoA?
how much do we multiply these numbers by if we are dealing with glucose?

3NADH,
1FADH2
2CO2
1GTP
12 ATP

2x w/ glucose

33

in the electron transport cha in 1 NADH gives how many ATP

3

34

in the electron transport cha in 1 FADH gives how many ATP

2

35

name 4 electron transport inhibitors that directly inhibit electron transport, causing a decrease of proton gradient and block ATP synthesis

rotenone, antimycin A, CN-, CO

36

This ATPase inhibitor directly inhibits mitochondrial ATPase, causing an increase of proton gradient, but no ATP is produceed because electron transport stops

oligomycin

37

Uncoupling agents like this increase the permeability of the membrane, causing a decrease of proton gradient and increase O2 consumption. ATP synthesis stops. Electron transport continues.

2,4 DNP

38

irreversible enzymes in gluconeogenesis

pyruvate carboxylase
PEP carboxykinase
Fructose-1,6-biphosphatase
Glucose-6-phosphate

mneu: Pathway Produces Fresh Glucose

39

pyruvate carboxylase is found here and converts this to this
It requires this
& is activated by this

mitochondria
pyruvate ->oxaloacetate
biotin, ATP
Acetyl-CoA

40

PEP carboxykinase is found here and converts this to this
It requires this

cytosol
oxaloacetate
->phosphoenolpyruvate
GTP

41

Fructose-1,6-biphosphatase is found here and converts this to this.

cytosol
fructose-1,6 bisphosphate
->fructose-6-P

42

where does gluconeogenesis occur

liver, kidney, intestinal epithelium

note: mm cannot participate in gluconeogenesis

43

deficiency of key gluconeogenic enzymes results in this

hypoglycemia

44

this dz is caused by a lack of glucose 6 phospatase in the liver

Von Gierke's

45

This pathway produces ribose-5-P for nucleotide synthesis
and produces NADPH from NADP+ for fatty acid and steroid biosynthesis and for maintaining reduced glutathione inside RBCs

Pentose Phosphate Pathway (HMP shunt)

46

All pentose Phosphate Pathway (HMP shunt) reactions occur here

cytoplasm

47

Is ATP used or produced in Pentose Phosphate Pathway (HMP shunt)

no

48

give sites of Pentose Phosphate Pathway (HMP shunt)

all sites of fatty acid or steroid synthesis (e.g., lactating mammary glands, liver, adrenal cortex

49

this is the rate-limiting enzyme in HMP shunt (which yields NADPH)

G6PD

50

NADPH is necessary to keep this reduced, which in turn detoxifies free radicals and peroxides

glutathione

51

decreased NADPH in RBCs lead to this due to poor RBC defense against oxidizing agents (fava beans, sulfonamides, primaquine) and antituberculosis drugs

hemolytic anemia

52

G6PD deficiency is more prevelent amun this racial group

blacks

53

this sign of G6PD deficiency describes when hemoglobin precipitates within RBCs

Heinz bodies

54

G6PD deficiency has this inheritance

x-linked recessive

55

This is a hereditary deficiency of aldolase B (recessive) Fructose-1-phosphate accumulates causing a decrease in available phosphate, which results in inhibition of glycogenolysis and gluconeogenesis.
Symptoms include hypoglycemia,jaundice, cirrhosis, vomiting

fructose intolerance

56

what is the tx for fructose intolerance

decrease intake of both fructose and sucrose (glucose + fructose)

57

this d/o involves a defect in fructokinases and is a benign, asymptomatic condition.
Symptoms: fructose appears in blood and urine.

essential fructosuria

58

essential fructosuria is a deficiency in this enzyme

fructokinase

59

fructose intolerance is a deficiency in this enzyme

aldolase B

60

This d/o is an absense of galactose-1-phosphate uridyltransferase. It is autosomal recessive. Damage is caused by accumulation of toxic substances (including galactitol) rather than absense of an essential compound.
Symptoms: cataracts, hepatosplenomegaly, mental retardation

galactosemia

61

tx of galactosemia

exclude galactose and lactose (galactose + glucose) from diet

62

this enzyme deficiency causes galactosemia and galactosuria, galactosuria, galactitol accumulation if galactose is present in ddiet.

galactokinase deficiency

63

this is an age dependent or hereditary intolerance to dairy often seen in blacks and asians. Symptoms include bloating, cramps and osmotic diarrhea.
Tx includes avoiding milk or adding lactase pills to diet

lactase deficiency

64

give the ketogenic essential amino acids

leucine, lysine

All essential amino acids: PriVaTe TIM HALL

65

give the glucogenic/ketogenic essential amino acids

Ile, Phe, Trp

All essential amino acids: PriVaTe TIM HALL

66

give the glucogenic essential amino acids

Met, Thr,Val, Arg, His

All essential amino acids: PriVaTe TIM HALL

67

which 2 AA are required during periods of growth

Arg
His

68

what are the acidic amino acids

Asp, Glu

mneu: Asp=aspartic ACID, Glu=glutamic ACID

69

At body pH (7.4) acidic amino acids (Asp, Glu)are _____ charged

negatively

70

what are the basic amino acids

arg, lys, his

71

At body pH (7.4) basic amino acids (Arg, lys)are _____ charged, but _____ has no net charge

positively

his

72

arg and lys have an extra _____ group

NH3

73

the MOST basic amino acid

arginine

74

thise 2 AA are found in high amounds in histones, which bind to negatively charged DNA

arg, lys

75

this cycle degrades amino acids into amino groups. It accounts for 90% of the nitrogen in the urine.

urea cycle

76

urea cycle occurs in this organ

liver

77

in what part of the cell does the urea cycle occur

carbamoyl phosphate incorporation occurs in the mitochondria; the remaining steps occur in the cytosol

78

urea cycle image p. 94

ornithine, Carbamoyl phosphate, Citrulline, Aspartate, Argininosuccinate, Fumarate, Arginine, urea

mneu: Ordinarily, Careless Crappers Are Also Frivolous About Urination

79

give the amino acid derivative of epinephrin

phenylalanine

80

give the amino acid derivative of thyroxine

phenylalanine

81

give the amino acid derivitive of NAD+/NADP+

tryptophan

82

give the amino acid derivative of melanin

phenylalanine

83

give the amino acid derivative of serotonin

tryptophan

84

give the amino acid derivative of melatonin

tryptophan

85

give the amino acid derivative of histamine

histadine

86

give the amino acid derivative of heme

Glycine

87

give the amino acid derivative of creatine

arginine

88

give the amino acid derivative of urea

arginine

89

give the amino acid derivative of nitric oxide

arginine

90

give the amino acid derivative of GABA

glutamate

91

give the amino acid derivative of dopamine

phenylalanine

92

give the amino acid derivative of norepinephnine

phenylalanine

93

In normal metabolism phenylalanine is converted into _____

tyrosine

94

in PKU there is decreased ________ or decreased tetrahydrobiopterin cofactor

phenylalanine hydroxylase

95

findings of phenylketonuria

mental retardation, growth retardation, fair skin, eczema, musty body odor.

mneu: d/o of AROMATIC amino acid metabolism -> musty body ODOR

96

tx of PKU

no phenylalanine in diet (e.g., aspartame, nutrasweet) and increase in tyrosine

97

when should you screen for PKU

at birth

98

name the 3 phenylketones

phenylacetate
phenyllactate
phenylpyruvate

99

what is the inheratiance of PKU & incidence

autosomal-recessive dz
1:10,000

100

this is a congenital deficiency of homogentisic acid oxidase in the degradative pathway of tyrosine.

alkaptonuria

101

in alkaptonuria, these cause the urine to turn black on standing

alkapton bodies

102

in alkaptonuria, in addition to dark urine this is also dark

connective tissue

103

pts w/ alkaptonuria may have debilitating

arthralgias

104

this d/o is a congenital deficiency of either of the follwoing:
1) tyrosinase (inability to synthesize melanin from tyrosine)
2) Defective tyrosine transporters (decrease amounts of tyrosine and thus melanin)
It can result from lack of migration of neural crest cells

albinism

105

lack of melanine results in an increase risk of this CA

skin CA

106

this dz results in excess homocysteine in the urine. Cysteine becomes essential. It can cause mental retardation, osteoporosis, tall stature, kyphosis, lens subluxation (downward and inward) and atherosclerosis (stroke and MI

homocystinuria

107

there are three forms of homocystinuria. Name the enzyme deficiency and give the dietary txs if there is one

1) cytathionine synthase deficiency (tx: decrease Met & increase Cys in diet)
2) decrease affinity of cystathionine synthase for pyridoxal phosphate (tx: increase vit. B6 in diet)
3) Methionine synthase deficiency

108

This is a common(1:7000) inherited defect of renal tubular amino acid transporter for Cystine, Ornithine, Lysine, and Arginine in kidneys. Excess cystine in urine can lead to the precipitation of cystine kidney stones

Cystinuria

mneu: COLA in the urine

109

this is a congenital deficiency of homogentisic acid oxidase in the degradative pathway of tyrosine.

alkaptonuria

110

in alkaptonuria, these cause the urine to turn black on standing

alkapton bodies

111

in alkaptonuria, in addition to dark urine this is also dark

connective tissue

112

pts w/ alkaptonuria may have debilitating

arthralgias

113

this d/o is a congenital deficiency of either of the follwoing:
1) tyrosinase (inability to synthesize melanin from tyrosine)
2) Defective tyrosine transporters (decrease amounts of tyrosine and thus melanin)
It can result from lack of migration of neural crest cells

albinism

114

tx for Cystinuria

acetazolamide to alkalinize the urine

115

this dz results from blocked degradation of BRANCHED AA (Ile, Val, Leu) due to decreease alpha ketoacid dehydrogenase. It causes increased alpha ketoacids in the blood, esp Leu. It causes severe CNS defects, mental retardation, and death.

maple syrup urine dz

mneu: urine smells like maple syrup. I Love Vermont maple syrup

116

tx for Cystinuria

acetazolamide to alkalinize the urine

117

this dz results from blocked degradation of BRANCHED AA (Ile, Val, Leu) due to decreease alpha ketoacid dehydrogenase. It causes increased alpha ketoacids in the blood, esp Leu. It causes severe CNS defects, mental retardation, and death.

maple syrup urine dz

mneu: urine smells like maple syrup. I Love Vermont maple syrup

118

what does SCID stand for?
What is the enzyme deficiency?What immune cells are involved?
Who does it effect

Severe combined (T and B) immuodeficiency dz.
Adenosine deaminase (ADA)deficiency
happens to kids

mneu: bubble boy

119

pathophysiology of SCID

excess ATP and dATP imbalances nucleotide pool via feedback inhibition of ribonucleotide reductase. This prevents DNA synthesis and thus decreases lymphocyte count.

120

This dz results from a purine salvage problem owing to absense of HGPRTase, which vonverts hypoxanthine, to inosine monophosphate (IMP) and guanine to guanosine monophosphate (GMP)

Lesch-Nyyhan syndrome

mneu: LNS- Lacks Nucleotide Salvage (purine)

121

inheratance of Lesch Nyhan syndrome

X-linked recessive.

122

LNS results in excess of this acid

uric acid

123

patient manifestation of Lesch-Nyhan syndrome

retardation, self-mutilation, aggression, hyperuricemia, gout, choreoathetosis

124

is the fasting state phosphorylated or non-phosphorylated

phosphorylated

mneu: in the fasting state phosphorylate

125

this hormone is required for adipose and skeletal mm uptake of glucose

insulin

mneu: INsulin moves glucose INto cells

126

where is insulin made (cells/organ)

Beta cells of pancreas

127

what receptors are found in the beta cells

GLUT 2

128

what receptors are found in mm and fat

GLUT 4

129

insulin inhibits the release of this hormone by alpha cells of pancreas

glucagon

130

is serum C-peptide present w/ exogenous insulin intake

no

131

what are the anabolic effects of insulin

1) glucose transport
2) glycogen synthesis and storage
3) triglyceride synthesis and storage
4)Na+ retention (kidneys)
5) protein sytnesis (mm

132

Name the tissues that don't need insulin for glucose uptake

Brain
RBCs
Intestine
Cornea
Kidney
Liver

mneu: BRICK L

133

Glucagon ______ (phosphorylates/Dephosphorylates), turns glycogen sytnase _____ and phosphorylase ____

phosphorylates
OFF
ON

134

Insulin______ (phosphorylates/Dephosphorylates), turns glycogen sytnase _____ and phosphorylase ____

dephosphorylates
ON
OFF

135

there are 12 types of these diseases all resulting in abnormal glycogen metabolism and accumulation of glycogen within cells

glycogen storage diseases

136

In this glycogen storage disease, there is a glucose 6-phosphatase deficiency

Von Gierke's dz (GSD type I)

137

Give some clinical findings of Von Gierke's dz (GSD type I)

severe fasting hypoglycemia, increased glycogen in the liver, hepatomegly, increased blood lactate

hint: the liver becomes a mm

138

In this glycogen storage disease, there is a lysosomal alpha 1,4-glucosidase deficiency

Pompe's dz (type II)

139

Give some findings of Pompe's dz

cardiomegly and systemic findings, leading to early death

mneu: Pompe's trashes the Pump
(heart, liver mm)

140

In this glycogen storage disease, there is a deficiency of debranching enzyme alpha 1,6 glucosidase

Cori's dz (type III)

141

give some clinical findings of Cori's dz

milder form of type I w/ normal blood lactate levels

142

In this glycogen storage disease, there is a deficiency of skeletal mm glycogen phosphorylase deficiency

McArdle's dz (type V)

mneu: McArdle's: Muscle

143

Give some findings of McArdle's dz

increased glycogen in mm but cannot greak it down, leading to painful cramps, myoglobinuria w/ strenuous exercise

144

this classification of dz is caused by a deficiency in one of the many lysosomal enzymes

lysosomal storage diseases

145

clinical findings are peripheral neuropahty of hands/feet, antiokeratomas, CV/renal dz. What is the dz? deficient lysosomal enzyme? Accumulated substrate? Inheritance?

Fabry's dz
alpha-galactosidase A
Ceramide trihexoside
XR

146

clinical findings are hepatosplenomegly, aseptic necrosis of femur, bone crises. What is the dz? deficient lysosomal enzyme? Accumulated substrate? Inheritance?

Gaucher's dz
B-glucocerbrosidase
Glucocerebroside
AR

147

clinical findings are progressive neurodegeneration, HSM, cherry red spot on macula What is the dz? deficient lysosomal enzyme? Accumulated substrate? Inheritance?

Niemann-Pick dz
Sphingomyelinase
Sphingomyelin
AR

mneu:NO MAN PICS (NIEMANN-PICK) his nose w/ his SPHINGER(SPHINGomylenase

148

clinical findings are progressive neurodegeneration, developmental delay, cherry-red spot, lysozymes w/ onion skin. What is the dz? deficient lysosomal enzyme? Accumulated substrate? Inheritance?

Tay-Sachs dz
Hexosaminidase A
GM2 ganglioside
AR

mneu: Tay-SaX (Tay-Sachs) lacks heXosaminidase

149

clinical findings are peripheral neuropathy, developmental delay, optic atrophy. What is the dz? deficient lysosomal enzyme? Accumulated substrate? Inheritance?

Krabbe's dz
B-galactosidase
Galactocerebroside
AR

150

clinical findings are central and peripheral demyelination w/ ataxia, dementia. What is the dz? deficient lysosomal enzyme? Accumulated substrate? Inheritance?

Metachromatic leukodystophy
Arylsulfatase A
Cerebroside sulfate
AR

151

clinical findings are developmental delay, gargoylism, airway obsxn, corneal clouding, HSM What is the dz? deficient lysosomal enzyme? Accumulated substrate? Inheritance?

Hurler's syndrome
alpha-L-iduronidase
Heparan sulfate & dermatan sufate
AR

152

clinical findings are mild Hurler's w/ aggressive behavior, no corneal clouding. What is the dz? deficient lysosomal enzyme? Accumulated substrate? Inheritance?

Hunter's syndrome
Iduronate sulfatase
heparan sulfate, dermatan sulfate
XR

mneu: HUNTERS aim for the X (X-linked recessive)

153

Where does fatty acid degradation occur

mitochondria
(where its products will be consumed)

154

in the liver, fatty acid and amino acids are broken down into ______ to be used by _____ & ______

ketone bodies (acetoacetate + hydroxybuterate
To be used in mm & brain).

155

when are ketone bodies found

prolonged starvation and diabetic ketoacidosis

156

how are ketone bodies excreted

urine

157

what are ketone bodies made from

HMG CoA

158

Ketone bodies are metabolized by the brain to 2 molecules of _______

acetyl-CoA

159

how do ketone bodies smell on the breath

like acetone (fruity odor)

160

What is the rate-limiting step in cholesterol synthesis

HMG-CoA reductase, which converts HMG-CoA to mevalonate.

161

What cholesterol drug inhibits HMG CoA reductase

Lovastatin

162

2/3 of plasma cholesterol is esterified by this

lecithin-cholesterol acyltransferase (LCAT)

163

this lipase is responsible for degradation of dietary TG in the small intestine

pancreatic lipase

164

this lipase is responsible for degradation TG circulating in chylomicrons and VLDLs

lipoprotein lipase

165

this lipase is responsible for degradation TG remaining in IDL

Hepatic TG lipase

166

this lipase is responsible for degradation of TG stored in adipocytes

hormone sensitive lipase

167

this major apolipoprotein Activates LCAT

AI

168

this major apolipoprotein Binds to LDL receptor

B-100

169

this major apolipoprotein is a Cofactor for lipoprotein lipase

CII

170

this major apolipoprotein mediates Extra (remnant) uptake

E

171

the cells in this part of the body convert FFA back to TG and package it in chylomicrons

intestines

172

give the 5 lipoproteins

chylomicrons, VLDL, IDL, LDL, HDL

173

this lipoprotein delivers dietary triglycerides to peripheral tissues and dietary cholesterol to the liver. It is secreted by intestinal epithelial cells. Excess causes pancreatitis, lipemia retinalis, and eruptive xanthomas

chylomicron

174

Apolipoprotein ____ mediates secetion of chylomicrons

B-48

175

Apolipoprotein ____ are used for formation of new HDL

A

176

Apolipoprotein ____ activates lipoprotein lipase

C-II

177

Apolipoprotein ____ mediates remnant uptake by liver

E

178

These lipoproteins deliver hepatic triglycerides to peripheral tissues.

VLDL

179

VLDL is secreted by this organ

liver

180

excess VLDL causes this dz

pancriatitis

181

this apolipoprotein mediates secretion of VLDL

B-100

182

this apolipoprotein mediates remnant uptake of VLDL by the liver

E

183

this lipoprotein is formed in the degradation of VLDL. It delivers triglycerides and cholesterol to the liver, where they are degraded to LDL

IDL

184

This lipoprotein delivers hepatic cholesterol to peripheral tissues It is formed by a lipoprotein lipase modification of VLDL in the peripheral tissue. It is taken up by target cells via receptor-mediated endocytosis. Excess causes atherosclerosis, xanthomas, and arcus cornae

LDL

185

this LDL apolipoprotein mediates binding to cell surface receptor for endocytosis

B-100

186

This lipoprotein mediates centripetal transport of cholesterol (reverse cholesterol transport, from perhiphery to liver). It acts as a repository for apoC and apo E (which are needed for chylomicron and VLDL metabolism). It is secreted from both liver and intestine

HDL

187

this HDL apolipoprotein helps form HDL sx

A

188

this HDL apolipoprotein in particular activates LCAT (which catalyzes esterification of cholesterol)

A-I

189

this HDL apolipoprotein mediates transfer of cholesterol esters to other lipoprotein particles.

CETP

190

LDL & HDL carry most cholesterol. ___ transports cholesterol from liver to tissue; ____ transports it from periphery to liver

LDL
HDL

191

This type of familial dyslipidemia results from a lipoprotein lipase deficiency or altered apolipoprotein CII. It results in increased chylomicrons which leads to elevated blood levels of TG & cholesterol

type I - hyperchylomicronemia

192

This type of familial dyslipidemia results from a decrease in LDL receptors. It results in an increase of LDL which leads to elevated cholesterol.

type IIa hypercholesterolemia

193

This type of familial dyslipidemia results from a hepatic overproduction of VLDL leading to an increase in LDL and VLDL leading to elevated TG & cholesterol

type IIb-combined hyperlipidemia

194

This type of familial dyslipidemia results from altered apolipoprotein E leading to an increase in IDL & VLDL resulting in elevated TG & cholesterol

type III-dysbetalipoproteinemia

195

This type of familial dyslipidemia results from hepatic overproduction of VLDL resulting in increased VLDL levels leading to elevated TGs in the blood

type IV-hypertriglyceridemia

196

This type of familial dyslipidemia results from increased production and decreased clearance of VLDL and chylomicrons leading to increased VLDL and chylomicrons resulting in elevated blood levels of TGs & cholesterol

type V-mixed hypertriglyceridemia