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NS Preliminary Exam > CARBies > Flashcards

CARBies Flashcards

1
Q

Functions of carbs

A
  • energy

- prevents protein catabolism

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2
Q

Which body parts use carbs for energy?

A
  • red blood cells
  • muscle, especially during exercise, and only carbs for high-intensity anaerobic exercise
  • brain: 60% of glucose utilization at rest
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3
Q

Classification of carbs

A
  • simple sugars: monosaccharides and disaccharides

- complex carbs: oligosaccharides (3-9 monos) and polysaccharides (10-1000s)

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4
Q

examples of monosaccharides

A
  • glucose (ingested as di or poly)
  • galactose
  • fructose: found mainly in fruits and veggies
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5
Q

examples of disaccharides

A
  • maltose (glucose x2)
  • lactose (glucose and galactose)
  • sucrose (glucose and fructose): table sugar and honey
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6
Q

examples of polysaccharides

A
  • starch: storage form of glucose in plants
  • glycogen: “ in animals
  • fiber: structural component of plants
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7
Q

good sources of complex carbs

A

grains, legumes, root veggies

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8
Q

whole grain-what is it?

A

includes endosperm (inside) but also outer layers of germ and bran

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9
Q

high fructose corn syrup

A
  • made of corn

- 55% fructose, 45% glucose

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10
Q

what’s wrong with fructose?

A
  • once consumed, fructose is converted to glucose/glycogen or fatty acids (TGs) and STORED IN THE LIVER
  • can lead to non-alcoholic fatty liver disease
  • increases triglycerides
  • increases LDL cholesterol
  • increases visceral fat
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11
Q

health benefits of fiber

A
  • slows breakdown of starch into glucose (think eating an apple vs apple juice)
  • lowers LDL
  • prevents formation of small blood clots that lead to heart attacks or strokes
  • lowers risk of some cancers (colorectal)
  • feeds healthy gut bacteria
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12
Q

where are dietary carbs found? where are they not found?

A

found: fruits, starches, veggies, added sugars, legumes, milk
not found: animal source foods and fats
-most abundant macronutrient in plant foods

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13
Q

hypoglycemia

A

low blood sugar

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14
Q

describe the digestion of starch, from mouth to absorption. include fiber

A
  • mouth: salivary amylase in the mouth starts to digest starch into maltose and small polysaccharides. teeth tear fiber apart into smaller pieces and saliva moistens it.
  • stomach: HCl denatures all proteins in order to digest protein. this includes salivary amylase. no starch digestion occurs here. fiber slows gastric emptying.

-small intestine: pancreas releases pancreatic amylase into the small intestine. this continues to turn starch into disaccharides and small polysaccharides. these are still not absorbable. Brush border disaccharidase enzymes on villi turn these into monosaccharides
—maltase turns maltose into glucose x2
—lactase turns lactose into glucose and galactose
—sucrase turns sucrose into glucose and fructose
Intestinal epithelial cells called enterocytes absorb these monosaccharides.
Fiber is still not ingested, and it slows absorption of other nutrients (this is why it slows sugar spikes).

-Large intestine/colon: Gut bacteria finally digest fiber into SCFAs and gas. Fiber regulates bowel activity, and it binds to bile and cholesterol and some minerals, carrying out of the body (this is why it lowers LDL cholesterol).

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15
Q

enterocytes

A

absorptive cells in the intestinal wall (intestinal cells) that absorb monosaccharides–only monosaccharides absorbed by enterocytes.

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16
Q

what happens to monosaccharides once they are absorbed into the bloodstream?

A

they are sent to the liver via the portal vein. in the liver, fructose and galactose are converted to glucose/glycogen. The exception to this is excessive fructose consumption, when it is turned into TGs.

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17
Q

3 possible fates of glucose once they are sent to the liver

A
  1. used immediately for fuel
  2. stored as glycogen (90% in skeletal muscle)
  3. converted to fatty acids and stored in adipose tissue in the body or liver
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18
Q

Lipogenesis

A

“fat-making.” When glucose is made into fatty acids or triglycerides. this happens when you eat too much fructose or sugar, because the liver and skeletal muscle only have so much glycogen storage capacity. once this fills up, lipogenesis occurs. fatty acids are combined with glycerol to make TGs and are stored in adipose tissue/the liver.

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19
Q

euglycemia

A

normal blood glucose levels

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20
Q

hypoglycemia

A

low blood glucose levels

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21
Q

hyperglycemia

A

high blood glucose levels

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22
Q

glycemic index

A

the increase in blood glucose 2 hours after consuming 50 g of carb-containing food

  • measures how quickly carbs are converted to blood glucose
  • low is less than 55
  • high is greater than 70
  • medium is 55-69
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23
Q

4 hormones involved in blood glucose regulation

A
  • insulin (pancreas)
  • glucagon (pancreas)
  • epinephrine (adrenal)
  • cortisol (adrenal)
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24
Q

insulin

A
  • hormone secreted by beta cells in pancreas
  • stimulated by hyperglycemia (high blood glucose)
  • functions to transport glucose into cells and decrease blood glucose: storage in adipose and muscle tissue
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25
Q

glucagon

A
  • hormone secreted by alpha-cells of pancreas
  • opposite of insulin
  • stimulated by hypoglycemia (low blood glucose) and exercise stress
  • stimulates breakdown of glycogen in the liver (glycogenolysis), stimulates gluconeogenesis in the liver, and increases blood glucose levels
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26
Q

epinephrine

A
  • hormone secreted by adrenal gland
  • stimulated by exercise stress and low blood glucose
  • promotes glycogen breakdown and glucose release from liver, increases blood glucose
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27
Q

cortisol

A
  • hormone secreted by adrenal gland
  • stimulated by exercise stress and low blood glucose
  • promotes breakdown of protein and therefore gluconeogenesis and increases blood glucose (not ideal)
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28
Q

glycogenesis

A

“glycogen-making.” the synthesis of glycogen from glucose (stimulated by insulin)

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29
Q

explain how insulin stores glucose in the muscle cells

A

insulin enters the bloodstream from the pancreas. insulin binds to the insulin receptor on the outside of the muscle cell. this binding signals a transduction cascade of glut-4 protein inside muscle cell. this sends glut-4 protein to the surface of the cell and then glucose is able to enter the muscle cell via glut-4. Muscle cells take in 90% of glucose.

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30
Q

glycogenolysis

A

“glycogen-breakdown.” the breakdown of glycogen to glucose (stimulated by glucagon)

31
Q

gluconeogenesis

A

“making new glucose.” the synthesis of glucose from NON-CARB SOURCES in the liver and kidneys. (substrates: pyruvate, lactate, amino acids, and glycerol from TGs…NOT fatty acids)
-stimulated by glucagon and cortisol (for proteins)

32
Q

what are the 4 glucogenic substrates for gluconeogenesis? what is NOT a substrate for this?

A

substrates: pyruvate, lactate, amino acids, and glycerol from TGs
not: fatty acids from TGs

33
Q

glut-4

A

protein transporter stimulated by insulin to go to muscle cell wall and take in glucose for glycogenesis (storage)

34
Q

glut-2

A

transports glucose, fructose or galactose out of enterocytes and into bloodstream (afterwards they will then be transported to the liver by the portal vein where they will be turned into glucose or glycogen)

35
Q

glut-6? (or glucose-6-phosphatase)

A

present in the liver cells, but not muscle cells. once glucose enters the liver and muscle cells, hexokinase turns glucose into glucose-6-phosphate, which cannot enter the bloodstream. glut-6 (glucose-6-phosphatase) turns g-6-phosphate back into glucose so that it can leave the liver and enter the bloodstream again. once in the muscle tissue, glucose cannot leave because it’s now g-6-phosphate and can’t turn back.

36
Q

use of glycogenolysis vs gluconeogenesis (for glucose output from the liver)

A

at rest: glycogenolysis is 60% and gluconeogenesis is 40%
-gluconeogenesis increases with skipped meals, starvation, prolonged low carb intake, and during exercise (because liver glycogen becomes depleted)

37
Q

RDA of carbs

A

130 g/day for adults and children

38
Q

AMDR for carbs (acceptable macronutrient distribution range)…expressed as total % of intake

A

45%-65% of daily energy intake

39
Q

UL/AMDR of added sugars (% total energy intake)

A

less than 10% of total kcals

40
Q

3 layers of stomach muscle:

A
  • longitudinal
  • oblique
  • circular
41
Q

sodium-glucose transporter

A

transporter that brings glucose and galactose into enterocytes along with sodium

42
Q

glut-5

A

transporter used to bring fructose into the enterocyte (as opposed to sodium-glucose transporter for glucose and galactose)

43
Q

which transporter is used to bring glucose and galactose into the enterocytes?

A

sodium-glucose transporter

44
Q

which transporter is used to bring fructose into the enterocyte?

A

glut-5

45
Q

which transporter is used to bring glucose, galactose and fructose out of enterocytes and into the bloodstream?

A

glut-2

46
Q

which transporter accepts glucose into the muscle cells?

A

glut-4

47
Q

where is the majority of glucose stored? (think of the 3 fates of glucose)

A

in the skeletal muscle (90%)

48
Q

describe the whole process of monosaccharide absorption and glucose blood regulation

A

glucose and galactose enter the enterocytes via glucose-sodium transporters. fructose enters via glut-5. once in the enterocytes, all three monosaccharides need to be carried out of the enterocytes into the bloodstream via glut-2. once in the bloodstream, they get transported to the liver via the portal vein, where they will be made into glucose or glycogen. From the liver, they have 3 fates: immediate use, storage as glycogen in the liver and muscle tissue, or storage as fatty acids and triglycerides in the adipose tissue/liver.

-once in the liver, glucose is turned into glucose-6-phosphate. in order to enter the bloodstream again it needs to be turned back into glucose via glucose-6-phosphatase. if it stays in the liver, then it’s turned into glycogen and fatty acids/TGs.

from there:

  • immediate use: glucose gets broken down into 2 pyruvate (+2 ATP), is converted into acetyl CoA (+CO2 …and electrons?)–or lactate to be later converted back into glucose–and goes through the krebs cycle to combine with oxaloacetate (sp) and then lose 2 carbons again (+CO2, ATP, and more electrons). then electrons are transported by NADH and FADH2 to the electron transport chain to make more ATP (+ATP), and empty electrons are put into an oxygen basket in the mitochondria and combined with hydrogen to make water (+H2O).
  • storage as glycogen in muscle cells (glycogenesis) (90%): when there is too much glucose in the bloodstream, insulin is triggered. beta-cells in the pancreas release insulin into the bloodstream. insulin bind to insulin receptors on the walls of the muscle cells. this triggers transduction and glut-4 transporter in the muscle cell is brought to the muscle cell wall. once glut-4 is on the muscle cell wall, it’s able to accept glucose into the muscle cell. Once in the muscle tissue, glucose combines with hexokinase to make glucose-6-phosphate. this cannot leave, because there is no presence of glucose-6-phosphatase to turn it back into glucose. Once glucose is in the muscle cell, it can be used or turned into glycogen (glycogenesis).
  • stored as glycogen or fatty acids/TGs in liver. as glycogen that’s glycogenesis. as fatty acids, that’s lipogenesis. fatty acids combine with glycerol to make TGs (esterification). this happens with excess sugar intake, and especially with excess fructose intake. This is because the liver and muscle tissue only has so much capacity for glycogen storage. when this capacity is reached, excess glucose is used for lipogenesis. this can lead to non-alcoholic fatter liver disease.
  • what about the opposite, in cases of hypoglycemia? in this case, glycogenolysis happens (breaking down of glycogen to be made into glucose) as well as gluconeogenesis (making of new glucose molecules from substrates that are not carbs). these are both stimulated by the presence of glucagon in the bloodstream, which is secreted by alpha-cells in the pancreas. these are also (to a lesser extent) stimulated by cortisol and epinephrine, which are both secreted by the adrenal gland. the substrates for gluconeogenesis are: glycerols from TGs, amino acids, lactate, and pyruvate. substrates do not include fatty acids.
49
Q

where is the pancreas located?

A

posterior to the stomach

50
Q

what types of cells is the pancreas made of?

A

acinar cells (exocrine, 95% of pancreatic cells), beta and alpha cells in islet of langerhans (endocrine, 2-5% of pancreatic cells)

51
Q

what types of cells do the islet of langerhans produce? are they endocrine or exocrine?

A

alpha and beta cells: endocrine

52
Q

what hormones do alpha and beta cells produce?

A

alpha: glucagon
beta: insulin

53
Q

is insulin catabolic or anabolic?

A

anabolic

54
Q

is glucagon catabolic or anabolic?

A

catabolic

55
Q

diabetes mellitus

A

a group of metabolic diseases characterized by hyperglycemia

56
Q

what are the three types of diabetes

A

1, 2 and gestational

57
Q

which type of diabetes accounts for 90-95% of cases? which type accounts for 5%?

A

90-95: type 2

5: type 1

58
Q

what is a normal blood glucose concentration?

A

70-100 mg/dl (-1)

59
Q

what are the four types of diabetes diagnostic tests?

A

Hemoglobin A1C (measures average blood sugar levels over past 3 months), fasting blood sugar test, glucose tolerance test, random blood sugar test

60
Q

what is type 1 diabetes?

A

an autoimmune disease that destroys pancreatic b cells, which means you can’t produce insulin and lower glucose levels in blood

61
Q

what is one way to measure type 1 diabetes that doesn’t measure type 2 diabetes?

A

an autoantibodies test

62
Q

what is type 2 diabetes?

A

when chronically high levels of blood sugar lead to constant insulin output and make insulin receptors non-responsive (insulin resistance)

63
Q

what does not occur in the skeletal muscles in the case of diabetes mellitus?

A

skeletal muscles are not sending glut-4 to the cell wall, allowing for the acceptance of glucose into the muscle cells

64
Q

what tissues are not insulin dependent? why (how)?

A

the brain and skeletal muscle during exercise. skeletal muscle is not insulin dependent during exercise because muscle contractions translocate glut-4 receptors into the membrane without needing an okay from insulin receptors.

65
Q

which of the glut receptors are most abundant?

A

glut-4

66
Q

what is the opposite of insulin resistance?

A

insulin sensitivity

67
Q

what type of tissue is the primary site of insulin resistance?

A

muscle

68
Q

what is insulin sensitivity?

A

enhanced ability of cells to respond to insulin, results in improved uptake of glucose. increases with exercise.

69
Q

what are the three categories of chronic diabetes complications? (and one extra)

A
  • macro-vascular (atherosclerosis, heart attacks and strokes)
  • microvascular (small vessel disease like diabetic retinopathy)
  • neuropathy (nerve damage–affects legs before hands)
70
Q

risk factors for type 2 diabetes

A

excess fat, age, (ethnicity 🤨), genetics, lack of physical activity

71
Q

what is a complication of extreme hyperglycemia (besides insulin resistance)?

A

hyperglycemia damages organs and can be deadly

72
Q

what is a consequence of extreme hypoglycemia?

A

can lead to loss of consciousness and even death.

73
Q

what are ways to treat/manage diabetes?

A
  • diet, exercise and medications
  • complex carbs/manage timing of carbs
  • exercise increases insulin sensitivity

NS Preliminary Exam (9 decks)

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