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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
Function of Phosphatase
-removes phosphate group from substrate
26
Phosphofructokinase-2 (PFK-2)
- dephosphorylated PFK-2 is active | - active PFK-2 favors formation of fructose 2, 6-bisphosphate -> inc. PFK-1-> inc. glycolysis
27
Pyruvate Kinase
- 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
28
Lactate Dehydrogenase
- facilitates interconversion of pyruvate and lactate | - driven by [substrates]
29
Pyruvate Dehydrogenase
- 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
30
GTP
-substrate level phosphorylation in TCA cycle
31
Products of TCA Cycle
- 3 NADH | - 1 FADH
32
Citrate
- converts acetyl CoA and oxaloacetate to citrate | - TCA cycle
33
a-Ketogluterate DehydrogenasE
- converts a-ketogluterate to succinyl coA | - TCA cycle
34
Succinate Dehydrongenase
- converts succinate to fumarate | - TCA cycle
35
Malate Dehydrogenase
- converts malate to oxaloacetate | - TCA cycle
36
Electron Transport Chain
- 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
Glut 4
- allows glucose to enter cell and begin glycolysis - transporter - insulin sensitive (inc. glucose transport in response to insulin) - skeletal muscle, adipose tissue
38
Glut 2
- glucose transporter - liver - not insulin sensitive
39
Substrate Level Phosphorylation
-phorphorylation of ADP to ATP by high energy phosphate compounds formed during glycolysis
40
Glucose 6 Phosphatase
- present in liver and kidney - converts glucose 6 phosphateto glucose by removing a phosphate - gluconeogenesis
41
Fructose 1-6 BisPhosphatase
- converts fructose 1, 6 bisphosphate to fructose 6 phosphate - gluconeogenesis - deficiency: late hypoglycemia following fasting, severe lactic acidosis, inc. pyruvate, inc. ketones
42
PEP Carboxykinase
- converts pyruvate to oxaloacetate | - gluconeogenesis
43
Pyruvate Carboxylase
- converts pyruvate to oxaloacetate | - gluconeogenesis
44
Hemolytic Anemia Enzyme Deficiency
- G6PD deficiency | - pyruvate kinase deficiency
45
Glucagon
- 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
Insulin
- 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
Pyruvate Dehydrogenase Complex
- 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
Citrate
- citrate synthase converts acetyl coA and OAA to citrate - irreversible rxn - TCA cycle - where fatty acid synthesis takes off
49
a-Ketogluterate
- isocitrate dehydrogenase converts isocitrate to a-ketogluterate - produces CO2and NADH - TCA cycle - important entrance point for amino acids that contribute to gluconeogenesis
50
Succinyl CoA
- 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
GTP
-formed as succinyl coA is converted to succinate in the TCA cycle
52
Fumarate
- converted from succinate by succinate dehydrogenase - TCA cycle - FADH2 - entrance point for amino acids - byproduct of urea cycle
53
Malate
- converted from fumarate by fumarase - TCA cycle - also involved in gluconeogenesis
54
Oxaloacetate
- converted from malate by malate dehydrogenase - generates NADH - involved in gluconeogenesis
55
UDP-Glucose
-activated form of glucose used in glycogen synthesis
56
Glycogen Synthase
- 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
Branching Enzyme
- 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
Glycogen Phosphorylase
- 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
Debranching Enzyme
- 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
Glycogen Synthesis and Breakdown Regulation
- hormonal: insulin and glucagon - allosterically - regulation in fed state: glycogen synthase allosterically activated by G6P, glycogen phosphorylase is allosterically inhibited by G6P
61
Glucose-6-Phosphate Dehydrogense (G6PD)
- catalyzes first rxn in pentose phosphate pathway - rate limiting step - generates first NADPH
62
G6PD Deficiency
- 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
Pancreatic B Cell
- secrete insulin | - arranged in central core
64
Pancreatic A Cell
- secrete glucagon | - these cells sit next to insulin secreting cells
65
Key Intermediates for Metabolic Insulin Pathway
-PI3K and AKT
66
Key Intermediates for Mitogenic Insulin Pathway
-MAPK
67
Insulin Resistance
- 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
Incretin Effect
- oral glucose causes much more insulin secretion that when glucose is infused via IV - caused by GLP-1 and GIP
69
GLP-1
- 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
Catecholamines
- norepi and epi inc. blood glucose by inc cAMP | - elevated in stress
71
Corticosteroids
- cortisol is secreted in response to stress - results in inc. blood glucose - slow time course - chronic exposure associated with development diabetes
72
Growth Hormone
- produced by anterior pituitary gland - concentration inc. due to hypoglycemia and stress - tends to dec. insulin sensitivity
73
Somatostatin
- inhibits growth hormone - inhibitor of insulin and glucagon - inhibits gut motility, splanchnic blood flow and secretion of digestive enzymes
74
Oligosaccharides
- 3-9 sugars | - present in beans, onions, vegies
75
Starches
- long polymers of glucose - amylopectin: highly branches - amylose: unbranched - resistant starch: corn starch, slowly absorbed
76
Glycemic Index
- 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
Glycemic Load
-glycemic index x amount of food eaten
78
Fructose Metabolism
- 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
Fibers
-complex carb that is not digestible by humans
80
Types of Studies That Can Inform Nutritional Decisions
- animal studies - epidemiological studies - small randomized - large randomized: gold standard
81
Lactate
- byproduct of glycolysis | - very important carb source
82
Galactosemia
- 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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