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DEMS Unit 2 > Biochem Basics + Carbohydrates > Flashcards

Biochem Basics + Carbohydrates Flashcards

1
Q

Components of Energy Expenditure

A
  • basal metabolic rate (75% in sedentary person)
  • thermic effect of food (8%)
  • physical activity energy expenditure (30-40%)
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2
Q

Hierarchy of Fuels

A
  • alcohol: 7kcal/g, no storage pool
  • protein: 4 kcal/gram, no true storage pool
  • glucose: 4kcal/gram, storage as glycogen in liver and muscle (muscle glycogen cannot be released as glucose)
  • fat: 9kcal/g, large storage pool
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3
Q

Most Accurate Way of Measuring Total Energy Expendature

A
  • doubly labeled water
  • if a person’s weight is stable, then EI=TEE
  • TEE= 25-35kcal/kg/day
  • for 70kg person, EI should be about 2100 kcal/day
  • this means a measure of TEE accurately predicts energy intake if weight is stable
  • note: carbs= 4 kcal/g
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4
Q

Body Energy Stores

A

-fat: greatest amount (120,000 kcal)
-carbs: 2,000 kcal (mostly in form of glycogen in muscle and liver)
-

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5
Q

Most Accurate Way to Measure Body Composition

A

-DEXA scan

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6
Q

Counter Regulatory Hormones

A
  • glucagon
  • cortisol
  • catecholamines
  • growth hormone
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7
Q

Glycolysis

A
  • carbohydrate pathway
  • when: excess glucose in blood (after meal)
  • where: cytoplasm/cytosol
  • what: results in breakdown of 6 carbon glucose to 2 pyruvate and 2 ATP
  • who: glucose-> pyruvate, if O2 not present or no mitochondria, pyrvate -> lactate
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8
Q

Tricarboxylic Acid Cycle (TCA Cycle)

A
  • carbohydrate pathway
  • what: conversion of pyruvate to NADH, FADH2, and GTP
  • where: in cell
  • when: when oxygen and mitochondira are present
  • who: pyruvate-> CO2, GTP (ATP), NADH, and FADH2
  • in mitochondria matrix
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9
Q

Electron Transport

A
  • carbohydrate pathway
  • where: mitochondrial membrane
  • who: NADH and FADH2 -> ATP from ADP, O2 is consumed and H2O is produced in oxidative phosphorylation
  • in mitochrondria
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10
Q

Gluconeogenesis

A
  • carbohydrate pathway
  • when: in state of negative energy balance
  • what: break down of carbon skeletons -> glucose, new glucose production
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11
Q

Glycogen

A
  • carbohydrate pathway
  • what: storage of excess glucose, immediately available in low energy states, highly brached polymer of glucose
  • where: most glycogen is stored in the liver and skeletal muscle
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12
Q

Pentose Phosphate Pathway (Hexose Monophosphate Shunt)

A
  • carbohydrate pathway
  • what: activated when glucose is present in excess or need for pathway products
  • who: generates NADPH for biosynthesis of fatty acids and steroids and ribose for synthesis of nucleotides
  • where: mammary gland, adrenal cortex, liver, adipose tissues, in cytosol
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13
Q

NADPH

A
  • created in pentose phosphate pathway (HMS)

- provides energy for synthesis of fatty acids and steroid hormones

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14
Q

Ribose

A
  • formed in pentose phosphate pathway (HMS)

- used as building block in synthesis of RNA and DNA

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15
Q

Triacylglycerol Synthesis (De Novo Lipogenesis)

A
  • fat pathway
  • who: glucose + acetyl coA -> fatty acids
  • what: glucose conversion to fat
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16
Q

Beta Oxidation

A
  • fat pathway
  • fatty acids are taken up by tissues such as liver and muscle where they are catabolized two carbons at a time in a process called beta oxidation
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17
Q

Ketogenesis

A
  • fat pathway
  • production of ketone bodies from fat
  • produced when insulin is very low ans counter-regulatory hormones are very high
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18
Q

Triglycerol Degredation

A
  • fat pathway
  • when: in negative energy balance
  • what: stored fat from adipose tissue can provide energy to oxidizing tissues such as muscle and liver as an alternative to glucose
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19
Q

Urea Cycle

A
  • protein pathway
  • pathway involved in disposal of nitrogen derived from the metabolism of amino acids
  • urea enters blood as blood urea nitrogen (BUN)
  • exreted by kidneys
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20
Q

Hexokinase

A
  • enzyme that phosphorylates glucose to glucose-6-phosphate
  • key step in glycolysis: activation of glucose, first ATP investment
  • present in most tissues except liver and pancreatic beta cells
  • at low [glucose], hexokinase sequesters glucose in the tissue
  • inhibited by glucose-6-p
  • irreversible rxn
  • not very selective
  • present in all cells
  • low Km for sugars
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21
Q

Glucokinase

A
  • enzyme that phosphorylates glucose to glucose-6-phosphate
  • key step in glycolysis: activation of glucose, first ATP investment
  • present in liver, beta cells of pancreas
  • at high [glucose] excess glucose is stored in liver
  • higher Vmax and Km than hexokinase
  • inhibited by fructose-6-p
  • irreversible rxn
  • selective for glucose
  • high Km for glucose
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22
Q

Km

A

-[substrate] at which rxn is half maximal

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23
Q

Phosphofructokinase-1

A
  • enzyme that phosphorylates fructose-6-phosphate to fructose 1, 6-bisphosphate
  • part of glycolysis
  • rate limiting step
  • activated by AMP, fructose-2, 6-bisphosphate
  • inhibited by ATP, citrate
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24
Q

Function of Kinase

A

-uses ATP to phosphorylate a substrate

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25
Q

Function of Phosphatase

A

-removes phosphate group from substrate

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26
Q

Phosphofructokinase-2 (PFK-2)

A
  • dephosphorylated PFK-2 is active

- active PFK-2 favors formation of fructose 2, 6-bisphosphate -> inc. PFK-1-> inc. glycolysis

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27
Q

Pyruvate Kinase

A
  • enzyme that converts phosphoenolpyruvate (PEP) to pyruvate
  • key step of glycolysis
  • activated by fructose-1, 6-bisphosphate
  • inhibited by ATP, alanine, phosphorylated (inhibited) by PKA
  • irreversible rxn
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28
Q

Lactate Dehydrogenase

A
  • facilitates interconversion of pyruvate and lactate

- driven by [substrates]

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29
Q

Pyruvate Dehydrogenase

A
  • key step in TCA cycle
  • mitochondrial enzyme complex linking glycolysis and TCA cycle
  • active in fed state (inc. insulin)
  • rxn: NAD+ + CoA + pyruvate -> acetyl CoA + CO2 + NADH
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30
Q

GTP

A

-substrate level phosphorylation in TCA cycle

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31
Q

Products of TCA Cycle

A
  • 3 NADH

- 1 FADH

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32
Q

Citrate

A
  • converts acetyl CoA and oxaloacetate to citrate

- TCA cycle

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33
Q

a-Ketogluterate DehydrogenasE

A
  • converts a-ketogluterate to succinyl coA

- TCA cycle

34
Q

Succinate Dehydrongenase

A
  • converts succinate to fumarate

- TCA cycle

35
Q

Malate Dehydrogenase

A
  • converts malate to oxaloacetate

- TCA cycle

36
Q

Electron Transport Chain

A
  • NADH (and FADH) electrons from glycolysis enter mitochondria
  • passage of e- results in formation of proton gradient that couples with oxidative phorphorylation to drive production of ATP
37
Q

Glut 4

A
  • allows glucose to enter cell and begin glycolysis
  • transporter
  • insulin sensitive (inc. glucose transport in response to insulin)
  • skeletal muscle, adipose tissue
38
Q

Glut 2

A
  • glucose transporter
  • liver
  • not insulin sensitive
39
Q

Substrate Level Phosphorylation

A

-phorphorylation of ADP to ATP by high energy phosphate compounds formed during glycolysis

40
Q

Glucose 6 Phosphatase

A
  • present in liver and kidney
  • converts glucose 6 phosphateto glucose by removing a phosphate
  • gluconeogenesis
41
Q

Fructose 1-6 BisPhosphatase

A
  • converts fructose 1, 6 bisphosphate to fructose 6 phosphate
  • gluconeogenesis
  • deficiency: late hypoglycemia following fasting, severe lactic acidosis, inc. pyruvate, inc. ketones
42
Q

PEP Carboxykinase

A
  • converts pyruvate to oxaloacetate

- gluconeogenesis

43
Q

Pyruvate Carboxylase

A
  • converts pyruvate to oxaloacetate

- gluconeogenesis

44
Q

Hemolytic Anemia Enzyme Deficiency

A
  • G6PD deficiency

- pyruvate kinase deficiency

45
Q

Glucagon

A
  • causes phosphorylation
  • synthesized in pancreatic a cells
  • action: interacts with G protein that inc. intracellular levels of cAMP
  • causes inc. in gluconeogenesis and glycogenolysis
  • inc. liver glucose production
  • reciprocally regulated by insulin and vice cersa
  • also promotes lipolysis and ketogenesis
  • regulation: secreted in response to hypoglycemia and inhibited by hyperglycemia
  • degraded in liver, half life of 5 min
46
Q

Insulin

A
  • causes dephosphorylation
  • intermediates in metabolic pathway: PI3K, AKT
  • intermediates in mitogenic pathway: MAP kinase
  • derived from pro-insulin by cleavage of connecting peptide (C peptide)
  • exposure of islet cells to inc. glucose results in surge of insulin followed by decline and then rise as long as glucose remains high
  • initiators: glucose, amino acids, sulfonylurea drugs (glyburide)
  • inhibitors: diazoxide, somatostatin, a adrenergic agents, glucose toxicity
  • inc. glucose -> inc. ATP-> intracellular signal-> inc Ca-> exocytosis of insulin
  • inc. insulin/dec. catecholamines inhibit lipolysis
  • very low insulin -> ketogenesis
47
Q

Pyruvate Dehydrogenase Complex

A
  • in mitochondrial matrix
  • converts pyruvate to acetyl coA in aerobic, fed conditions
  • inhibited by acetyl coA, ATP, fatty acids, and NADH
  • inactive in phosphorylated state
  • active in dephosphorylated state
  • activated by AMP, CoA, and NAD+
  • thiamine (vit B1) deficiency: inability to oxidize pyruvate-> wernicke encephalopathy
  • TCA cycle
48
Q

Citrate

A
  • citrate synthase converts acetyl coA and OAA to citrate
  • irreversible rxn
  • TCA cycle
  • where fatty acid synthesis takes off
49
Q

a-Ketogluterate

A
  • isocitrate dehydrogenase converts isocitrate to a-ketogluterate
  • produces CO2and NADH
  • TCA cycle
  • important entrance point for amino acids that contribute to gluconeogenesis
50
Q

Succinyl CoA

A
  • a-ketogluterate dehydrogenase converts a-ketogluterate to succinyl coA
  • CO2 and NADH are made
  • TCA cycle
  • important entrance point for amino acids and fatty acid products
51
Q

GTP

A

-formed as succinyl coA is converted to succinate in the TCA cycle

52
Q

Fumarate

A
  • converted from succinate by succinate dehydrogenase
  • TCA cycle
  • FADH2
  • entrance point for amino acids
  • byproduct of urea cycle
53
Q

Malate

A
  • converted from fumarate by fumarase
  • TCA cycle
  • also involved in gluconeogenesis
54
Q

Oxaloacetate

A
  • converted from malate by malate dehydrogenase
  • generates NADH
  • involved in gluconeogenesis
55
Q

UDP-Glucose

A

-activated form of glucose used in glycogen synthesis

56
Q

Glycogen Synthase

A
  • catalyzes the transfer of glucose from UDP glucose to grown glycogen chain
  • forms an a-1,4 glycosidic linkage
  • key regulated enzyme in glycogen synthesis
  • glycogenin is enzyme that forms initiating site for glycogen synthesis
  • activated by G6P in fed state
57
Q

Branching Enzyme

A
  • forms a-1,6 linkages in glycogen synthesis
  • branching inc. solubility of glycogen
  • branching inc. rate of glycogen synthesis and degredation
  • deficiency: abnormal non-branched glycogen acculumates in the liver and skeletal muscle
  • hypoglycemia not a prominent sx
58
Q

Glycogen Phosphorylase

A
  • catalyzes cleavage of glycogen to G-1-P
  • key regulated enzyme in glycolysis
  • inhibited by G6P in fed state
  • activated in exercise by inc. Ca binding to calmodulin-> activation of phosphorylase kinase -> phosphorylates glycogen phosphorylase (activation)-> glycogen degredation
  • activated by AMP in muscle during exercise
  • deficiency: hepatomegally, short stature, mild muscle weakness
  • tx: raw cornstarch
59
Q

Debranching Enzyme

A
  • converts the branched glycogen structure into a linear one, which allows for further cleavage by glycogen posphorylase
  • accumulation of abnormal glycogen in liver and muscle
60
Q

Glycogen Synthesis and Breakdown Regulation

A
  • hormonal: insulin and glucagon
  • allosterically
  • regulation in fed state: glycogen synthase allosterically activated by G6P, glycogen phosphorylase is allosterically inhibited by G6P
61
Q

Glucose-6-Phosphate Dehydrogense (G6PD)

A
  • catalyzes first rxn in pentose phosphate pathway
  • rate limiting step
  • generates first NADPH
62
Q

G6PD Deficiency

A
  • severe fasting hypoglycemia occurring within 3-4 hours after a meal
  • certain compounds such as sulfa antibiotics, antimalarial drugs, and fava beans react with GSH and deplete it
  • leads to RBC rigidity -> destruction and hemolytic anemia
  • most severe glycogen storage disease
  • enlarged liver
  • the deficient enzyme is responsible for producing free glucose to leave the liver
  • tx: constant supply of oral glucose
63
Q

Pancreatic B Cell

A
  • secrete insulin

- arranged in central core

64
Q

Pancreatic A Cell

A
  • secrete glucagon

- these cells sit next to insulin secreting cells

65
Q

Key Intermediates for Metabolic Insulin Pathway

A

-PI3K and AKT

66
Q

Key Intermediates for Mitogenic Insulin Pathway

67
Q

Insulin Resistance

A
  • action of insulin is reduced in peripheral tissues
  • initially beta cells secrete more insulin
  • becomes type 2 diabetes
  • generally NOT caused by issues with insulin receptor
  • caused by abnormal phosphorylation of serine/threonine
68
Q

Incretin Effect

A
  • oral glucose causes much more insulin secretion that when glucose is infused via IV
  • caused by GLP-1 and GIP
69
Q

GLP-1

A
  • production: product of glucagon gene expressed in pancreatic alpha cells and L cells of intestinal mucosa
  • secretion: stimulated by presence of nutrients in gut
  • actions: potent insulin releasing substance, inhibits glucagon secretion, inhibits GI motility, inhibits appetite
  • degredation: short half life, broken down by DPP-4
70
Q

Catecholamines

A
  • norepi and epi inc. blood glucose by inc cAMP

- elevated in stress

71
Q

Corticosteroids

A
  • cortisol is secreted in response to stress
  • results in inc. blood glucose
  • slow time course
  • chronic exposure associated with development diabetes
72
Q

Growth Hormone

A
  • produced by anterior pituitary gland
  • concentration inc. due to hypoglycemia and stress
  • tends to dec. insulin sensitivity
73
Q

Somatostatin

A
  • inhibits growth hormone
  • inhibitor of insulin and glucagon
  • inhibits gut motility, splanchnic blood flow and secretion of digestive enzymes
74
Q

Oligosaccharides

A
  • 3-9 sugars

- present in beans, onions, vegies

75
Q

Starches

A
  • long polymers of glucose
  • amylopectin: highly branches
  • amylose: unbranched
  • resistant starch: corn starch, slowly absorbed
76
Q

Glycemic Index

A
  • ranks carbs based on their rate of glycemic response (conversion to glucose within the human body).
  • uses a scale of 0 to 100, with higher values given to foods that cause the most rapid rise in blood sugar
  • low GI 70
77
Q

Glycemic Load

A

-glycemic index x amount of food eaten

78
Q

Fructose Metabolism

A
  • bypasses PFK in glycolysis pathway and result is that it is rapidly driven down glycolysis and less regulated than glucose
  • intolerance: hypoglycemia, sx follow introduction of fructose, N/V,
79
Q

Fibers

A

-complex carb that is not digestible by humans

80
Q

Types of Studies That Can Inform Nutritional Decisions

A
  • animal studies
  • epidemiological studies
  • small randomized
  • large randomized: gold standard
81
Q

Lactate

A
  • byproduct of glycolysis

- very important carb source

82
Q

Galactosemia

A
  • deficiency in enzyme that produces UDP galactose: galactose-1-phosphate uridyltransferase (GALT)
  • jaundice, cataracts, N/V
  • tx: restrict lactose

DEMS Unit 2 (4 decks)

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