BIOL 0800 Reading- Chapter 16 Flashcards Preview

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Flashcards in BIOL 0800 Reading- Chapter 16 Deck (105):
1

What is the absorptive state?

When ingested nutrients enter the blood from the GI tract

2

What is the postabsorptive state?

When the GI tract has no more nutrients, and the body's own stores supply energy

3

What is the different in absorption of carbs/amino acids vs fats?

Fats are absorbed first through the lymph, rather than the blood, in the form of chylomicrons

4

What is the body's main energy source during the absorptive state?

Glucose

5

What is the major consumer of glucose? Why?

Skeletal muscle, because it makes up the majority of the body mass

6

What mostly happens to glucose in adipocytes?

Turned into triglycerides to be stored as fat: as alpha-glycerol phosphate and fatty acids

7

What happens to glucose in the liver?

Either turned into glycogen or fatty acids/alpha-glycerol phosphate for storage as triglycerides; triglycerides then packaged into VLDLs for transport to bloodstream

8

What happens to glucose in the skeletal muscles?

Used up, or turned into glycogen for energy storage for later

9

What is a VLDL?

Very low density lipoprotein: combination of lipid and protein made in the liver from glucose

10

What happens to VLDLs in the bloodstream?

Hydrolyzed monoglycerides by lipoprotein lipase for entry into capillaries (otherwise, too big)

11

Where is lipoprotein lipase located?

On the blood-facing side of the capillary walls, especially in adipose tissue

12

What happens to the VLDL after the lipoprotein lipase in the capillaries disintegrate it into monoglycerides (glycerol plus fatty acid) and fatty acids?

Fatty acids go into adipocytes to be rebound with alpha-glycerol phosphate to reform into triglycerides; monoglycerides taken up by the liver for metabolism

13

What happens to absorbed lipids in the blood stream?

Broken down by lipoprotein lipase in adipose-tissue capillaries; fatty acids go into adipocytes for combination with alpha-glycerol phosphate to be stored as triglycerides

14

Why is glucose critical for lipid absorption?

Because the adipocytes have no other way to get alpha-glycerol phosphate but from breaking down glucose: need it to combine with fatty acids to make triglycerides

15

What are the three sources of fatty acids in the adipose-tissue triglycerides?

1) glucose enters adipocytes, broken into FAs; 2) glucose enters liver, converted to VLDLs, enters adipocytes, broken into FAs; 3) lipids enter lymph and then adipocytes, broken into FAs

16

Which cells use/produce cholesterol?

Most cells use it, but cells in the liver and GI tract lining can produce cholesterol to enter the blood

17

What happens to cholesterol in the liver?

Some secreted into bile to the GI tract; most metabolized into bile salts for secretion into SI

18

What is the major cholesterol-control organ?

The liver!

19

How does ingested cholesterol inhibit liver cholesterol synthesis?

Inhibits the enzyme HMG-CoA reductase: critical for liver cholesterol synthesis

20

How does cholesterol usually circulate?

As part of different lipoprotein complexes: chylomicrons, VLDLs, HDLs, and LDLs

21

What are the main cholesterol carriers?

LDLS: deliver cholesterol to the body

22

How do LDLs bring cholesterol to the body?

Bind to receptors, taken in by endocytosis, release cholesterol to tells

23

How do HDLs function in terms of cholesterol transport?

Remove cholesterol from blood/tissue; deliver to liver for secretion into bile/conversion to bile salts; ALSO deliver cholesterol to steroid-producing endocrine cells

24

What kind of lipoprotein complex carries cholesterol to steroid-producing endocrine cells?

HDLs

25

What is a major indicator for propensity for atherosclerosis?

Ratio of LDL to HDL: want the number to be low; more HDL than LDL

26

How does estrogen affect cholesterol levels?

Decreases them because lower LDL and raises HDL

27

What happens to some amino acids after absorption, by way of the liver?

Used in liver for protein synthesis; OR converted to alpha-keto acids by deamination

28

What is an alpha-keto acid?

A deaminated amino acid; removed amino groups used to form urea in the liver

29

What happens to alpha-keto acids after they are synthesized from amino acids?

Enter into Krebs cycle to be catabolized for liver cell energy; can be converted into fatty acids to produce fat in liver

30

What happens to most AAs after absorption?

Enter other cells to synthesize proteins

31

What marks the shift from absorptive to postabsorptive?

Stops the net synthesis of glycogen, fats, and protein; starts the net catabolism of glycogen/fats/protein

32

What are the two main ways the body postabsorptively provides glucose?

Through blood glucose sources, or through "sparing," or fat utilization

33

What are three main mechanisms for postabsorptively providing blood glucose?

Glycogenolysis, lipolysis, or protein breakdown

34

What happens during glycogenolysis?

Breakdown of liver/skeletal muscle glycogen by different pathways

35

How does glycogenolysis occur in the liver?

Breakdown into glucose 6-phosphate, conversion into glucose

36

What is the body's first line of defense to maintain plasma glucose?

Hepatic glycogenolysis

37

How does glycogenolysis occur in the skeletal muscles?

Breakdown into glucose 6-phosphate, which undergoes glycolysis to produce ATP, pyruvate, and lactate; ATP and pyruvate used by muscle cell, lactate enters bloodstream for metabolism into glucose by liver

38

How does lipolysis contribute to blood glucose?

Lipolysis in adipocytes breaks triglycerides into glycerol and FAs; glycerol converted in liver to glucose

39

How does protein breakdown contribute to blood glucose?

Breakdown into AAs, into bloodstream to liver; AAs converted by alpha-keto acid pathway into glucose for release to blood

40

What is the essential step in the switch from blood glucose to glucose sparing?

Lipolysis: liberation of glycerol and FAs from triglycerides in adipocytes; NOW depends on the FFAs in circulation

41

How do FFAs provide energy after being liberated from triglycerides during lipolysis?

Undergo beta-oxidation to yield H+ and acetyl CoA; acetyl CoA enters the Krebs cycle to be catabolized into CO2 and H2O

42

How does the liver's glucose sparing differ?

When it uses its FFAs to make acetyl CoA, it catabolizes the acetyl CoA into ketones instead of entering them into the Krebs cycle; provides and important energy source

43

What are the two most important controls of transition from absorptive to postabsorptive?

Insulin and glucagon

44

Where do insulin and glucagon come from?

Islet of Langerhans in pancreas; alpha cells for glucagon, beta cells for insulin; (also includes delta cells for somatostatin, just as released from hypothalamus; may act as a paracrine factor for inhibition of glucagon/insulin)

45

What is the most important controller of organic metabolism?

Insulin!

46

What is the major cause of absorptive-state events vs postabsorptive-state events?

Increased insulin vs decreased insulin

47

How does insulin act on cells?

Binds to receptors, triggers transduction pathways that influence plasma membrane transport proteins and intracellular enzymes

48

How does insulin affect muscle cells and adipocytes?

Triggers vesicles with GLUT-4 inside to bind with the membrane to provide more glucose transporters to the membrane

49

How does insulin act by multiple actions to increase glucose storage in muscle cells?

Increases glycogen storage by: increasing number of glucose transports to increase intracellular glucose; stimulating the glycogen synthase enzyme; inhibiting the glycogen phosphorylase enzyme

50

How does insulin act by multiple actions in increase protein storage in muscle cells?

Same way as with glucose: increases ability of amino acids to enter the cell, stimulates ribosomal synthesis of AA into protein, inhibits catabolism of proteins

51

What is a major controlling factor for insulin secretion? How?

Plasma glucose concentration: increased glucose stimulates beta cells in islet of Langerhans to produce insulin

52

How does increased insulin act on the liver and adipocytes and muscle?

In liver, ceases glucose output and increases glucose uptake; in adipocytes/muscle, increases glucose uptake

53

What others factors besides increased plasma glucose stimulate insulin secretion?

Increased plasma AAs

54

What is the main hormonal control of insulin secretion?

Incretins: released by endocrine GI cells in response to eating; amplify insulin response to glucose

55

What is the importance of the actions of incretins (hormonal control) on insulin?

Feedforward control to glucose regulation; increased secretion of insulin without a proportional increase in glucose; prevents glucose absorption overload on kidneys; also allows insulin to decrease even if lots of glucose, to prevent hypoglycemia

56

What are two important incretins?

GLP-1 and GIP

57

Describe nervous control of insulin secretion.

Stimulated by autonomic neurons: parasympathetic neurons activation increases insulin; second feedforward regulation of insulin secretion; inhibited by sympathetic neurons or increase in epinephrine

58

How does parasympathetic vs sympathetic/epinephrine influence insulin secretion?

Parasymp = stimulate, symp/Epi = inhibits

59

What are five important glucose-counterregulatory controls?

Glucagon, EPI, sympathetic nerves, cortisol, and GH

60

What kind of hormones are insulin and glucagon?

Peptide hormones

61

What are the three main actions of glucagon?

Increased glycogen breakdown, increase gluconeogenesis, increase ketone synthesis

62

What happens to glucagon/insulin with a reduction in circulation glucose levels?

Increased glucagon, decreased insulin

63

How does the nervous system affect glucagon secretion?

Increased by sympathetic, decreased by parasympathetic

64

How does EPI (or symp nerves) affect nutrient metabolism directly, in addition to inhibiting insulin and stimulating glucagon?

Stimulates glycogenolysis in liver/skeletal muscle; stimulates gluconeogenesis in the liver; stimulates lipolysis in adipocytes

65

How does EPI affect adipocytes?

Stimulates hormone-sensitive lipase enzyme: catabolizes triglycerides into FAs and triglycerides for energy use (FAs) or gluconeogenesis precursor (glycerol)

66

How does cortisol interact with fasting?

Permissive role: maintains concentrations of key liver/adipocyte enzymes to allow gluconeogenesis and lipolysis; in high concentrations: can reduce sensitivity to insulin (maintains plasma glucose levels during fasting)

67

How does GH affect glucose levels?

Anti-insulin effects: make adipocytes more responsive to lipolytic stimuli, increases hepatic gluconeogenesis, reduces ability of insulin to stimulate glucose uptake by muscle and adipose tissues

68

Which hormones (glucagon, EPI, cortisol, GH) affect glycogenolysis?

Glucagon, EPI

69

Which hormones (glucagon, EPI, cortisol, GH) affect gluconeogenesis?

Glucagon, EPI, cortisol, GH

70

Which hormones (glucagon, EPI, cortisol, GH) affect lipolysis?

EPI, cortisol, GH

71

Which hormones (glucagon, EPI, cortisol, GH) affect inhibition of glucose uptake by adipocytes/skeletal muscle?

Cortisol, GH

72

Why does fasting hypoglycemia cause increased sympathetic stimulation and dizziness/etc?

Because low levels of glucose in the bloodstream stimulate glucagon, which is stimulated by sympathetic/EPI; dizziness because not enough glucose is reaching the brain

73

How is availability for glucose for energy increased during exercise?

Increased glycogenolysis in the liber, increased adipocyte lipolysis

74

How does insulin/glucagon control interact in exercise?

Decreased insulin, increased glucagon: mediated by increased sympathetic input, increased EPI, increased GH and cortisol; similar to stimulation of the glucose-counterreg controls during fasting

75

How does glucose concentration differ between fasting and exercise, if the insulin/glucagon controls are all pretty similar between the two?

With fasting, glucose uptake by muscle/adipocytes is decreased, but with exercise, glucose uptake is increased: muscle contraction causes more glucose to enter the cells

76

What percentage of energy released from organic molecules appears as heat rather than work?

~60%

77

What is a calorie?

The amount of heat required to raise the temperature of one gram or water by a degree (14.5 to 15.5)

78

What are the most important determinants of BMR?

Thyroid hormones (T3 and T4)

79

Why are thyroid hormones so integral to BMR?

Calorigenic effect: increase oxygen consumption and heat production of most body tissues except for brain

80

Why does EPI exert a calorigenic effect?

Stimulation of glycogen and triglyceride catabolism: increase metabolic rate with EPI, so greater heat production

81

What is food-induced thermogenesis?

How the ingestion of food rapidly increases the metabolic rate after eating

82

What substance produced the greatest food-induced thermogenesis effect?

Protein, then carbs/fat

83

Where does most of the increased heat production of food-induced thermogenesis come from?

Processing of absorbed nutrients by the liver

84

What factor can increased metabolic rate most?

Altered skeletal muscle activity: physical activity

85

What is leptin?

Hormone from adipocytes and released in proportion to the amount of fat in the adipose tissue; acts on hypothalamus to reduce food intake; inhibits the release of neuropeptide Y

86

What is neuropeptide Y?

Hypothalamic neurotransmitter that stimulates appetite

87

What hypothalamic hormone does leptin inhibit? What does this do?

Neuropeptide Y: stimulates appetite

88

What are the two main functions of leptin?

To inhibit neuropeptide Y (thus inhibiting appetite) and to stimulate the metabolic rate

89

What is the significance of the fact that leptin stimulates metabolic rate for starvation?

During starvation, adipocytes shrink (because triglycerides removed for use): less fat means less leptin secreted ; no more inhibition of neuropeptide Y, so appetite increases and BMR decreases

90

What is ghrelin?

Peptide hormone synthesized/released from stomach endocrine cells; increases GH release and increases hunger by stimulating NPY, stimulates fat breakdown, increases gastric motility/acid production

91

What are the four main functions of ghrelin?

Growth hormone release, increased secretion of NPY, decreased fat breakdown, increased gastric motility/acid production

92

What is the formula for BMI?

Weight in kg / square of height in m

93

What brain structure is the control center for temperature regulation?

Hypothalamus]

94

What kind of nervous output controls temperature regulation from the hypothalamus?

Sympathetic to sweat glands, skin arterioles, adrenal medulla; motor neurons to skeletal muscles

95

What is the first muscle response to changes in core body temperature?

Decreased temperature = shivering thermogenesis: increase skeletal muscle contraction through efferent motor nerve stimulation; Increased temperature = decreased in basal muscle contraction

96

How does increased core body temperature affect metabolism?

Increases because higher temperatures increase thermal motion of dissolved molecules, so faster expenditure of ATP; generates heat itself, so limited reduction of heat when core temp was increased :(

97

What happens during chronic cold exposure?

Nonshivering thermogenesis: increase in metabolic rate/heat production not due to increased muscle activity

98

What causes nonshivering thermogenesis?

Increased adrenal section of EPI and increased sympathetic activity to adipose tissue, with some thyroid hormone too

99

How does nonshivering thermogenesis work in infants?

Have brown adipose tissue: responsive to TH, EPI, and sympathetic nervous system: lots of uncoupling proteins that make metabolism less efficient, which generates heat instead of ATP to maintain body temperature

100

How do uncoupling proteins work to increase heat production?

Uncouple oxidation from phosphorylation and make metabolism less efficient: produce less ATP, more heat

101

Production of sweat is stimulated by what nerves?

Sympathetic nerves: using ACh

102

What is the thermoneutral zone?

The range of environmental temperatures that the body can regulate itself for with skin blood flow alone; 25-30* C, 75-86* F

103

What are EPs, endogenous pyrogens?

Chemical messengers released from macrophages that act on thermoreceptors to increase the thermal set point, causing fever

104

What is the immediate cause of thermal resetting for fever?

Synthesis and release of prostaglandins

105

What are endogenous cryogens?

Chemical messengers released to reset the body back to its normal set point after a fever breaks; include vasopressin and glucocorticoids