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Physiology > BIOL 0800 Reading- Chapter 16 > Flashcards

BIOL 0800 Reading- Chapter 16 Flashcards

1
Q

What is the absorptive state?

A

When ingested nutrients enter the blood from the GI tract

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2
Q

What is the postabsorptive state?

A

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

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3
Q

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

A

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

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4
Q

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

A

Glucose

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5
Q

What is the major consumer of glucose? Why?

A

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

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6
Q

What mostly happens to glucose in adipocytes?

A

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

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7
Q

What happens to glucose in the liver?

A

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

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8
Q

What happens to glucose in the skeletal muscles?

A

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

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9
Q

What is a VLDL?

A

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

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10
Q

What happens to VLDLs in the bloodstream?

A

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

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11
Q

Where is lipoprotein lipase located?

A

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

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12
Q

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

A

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

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13
Q

What happens to absorbed lipids in the blood stream?

A

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

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14
Q

Why is glucose critical for lipid absorption?

A

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

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15
Q

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

A

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

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16
Q

Which cells use/produce cholesterol?

A

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

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17
Q

What happens to cholesterol in the liver?

A

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

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18
Q

What is the major cholesterol-control organ?

A

The liver!

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19
Q

How does ingested cholesterol inhibit liver cholesterol synthesis?

A

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

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20
Q

How does cholesterol usually circulate?

A

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

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21
Q

What are the main cholesterol carriers?

A

LDLS: deliver cholesterol to the body

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22
Q

How do LDLs bring cholesterol to the body?

A

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

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23
Q

How do HDLs function in terms of cholesterol transport?

A

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

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24
Q

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

A

HDLs

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25
Q

What is a major indicator for propensity for atherosclerosis?

A

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

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26
Q

How does estrogen affect cholesterol levels?

A

Decreases them because lower LDL and raises HDL

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27
Q

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

A

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

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28
Q

What is an alpha-keto acid?

A

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

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29
Q

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

A

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

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30
Q

What happens to most AAs after absorption?

A

Enter other cells to synthesize proteins

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31
Q

What marks the shift from absorptive to postabsorptive?

A

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

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32
Q

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

A

Through blood glucose sources, or through “sparing,” or fat utilization

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33
Q

What are three main mechanisms for postabsorptively providing blood glucose?

A

Glycogenolysis, lipolysis, or protein breakdown

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34
Q

What happens during glycogenolysis?

A

Breakdown of liver/skeletal muscle glycogen by different pathways

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35
Q

How does glycogenolysis occur in the liver?

A

Breakdown into glucose 6-phosphate, conversion into glucose

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36
Q

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

A

Hepatic glycogenolysis

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37
Q

How does glycogenolysis occur in the skeletal muscles?

A

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

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38
Q

How does lipolysis contribute to blood glucose?

A

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

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39
Q

How does protein breakdown contribute to blood glucose?

A

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

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40
Q

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

A

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

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41
Q

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

A

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

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42
Q

How does the liver’s glucose sparing differ?

A

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

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43
Q

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

A

Insulin and glucagon

44
Q

Where do insulin and glucagon come from?

A

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
Q

What is the most important controller of organic metabolism?

A

Insulin!

46
Q

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

A

Increased insulin vs decreased insulin

47
Q

How does insulin act on cells?

A

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

48
Q

How does insulin affect muscle cells and adipocytes?

A

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

49
Q

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

A

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

50
Q

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

A

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
Q

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

A

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

52
Q

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

A

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

53
Q

What others factors besides increased plasma glucose stimulate insulin secretion?

A

Increased plasma AAs

54
Q

What is the main hormonal control of insulin secretion?

A

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

55
Q

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

A

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
Q

What are two important incretins?

A

GLP-1 and GIP

57
Q

Describe nervous control of insulin secretion.

A

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

58
Q

How does parasympathetic vs sympathetic/epinephrine influence insulin secretion?

A

Parasymp = stimulate, symp/Epi = inhibits

59
Q

What are five important glucose-counterregulatory controls?

A

Glucagon, EPI, sympathetic nerves, cortisol, and GH

60
Q

What kind of hormones are insulin and glucagon?

A

Peptide hormones

61
Q

What are the three main actions of glucagon?

A

Increased glycogen breakdown, increase gluconeogenesis, increase ketone synthesis

62
Q

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

A

Increased glucagon, decreased insulin

63
Q

How does the nervous system affect glucagon secretion?

A

Increased by sympathetic, decreased by parasympathetic

64
Q

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

A

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

65
Q

How does EPI affect adipocytes?

A

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

66
Q

How does cortisol interact with fasting?

A

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
Q

How does GH affect glucose levels?

A

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
Q

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

A

Glucagon, EPI

69
Q

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

A

Glucagon, EPI, cortisol, GH

70
Q

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

A

EPI, cortisol, GH

71
Q

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

A

Cortisol, GH

72
Q

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

A

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
Q

How is availability for glucose for energy increased during exercise?

A

Increased glycogenolysis in the liber, increased adipocyte lipolysis

74
Q

How does insulin/glucagon control interact in exercise?

A

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
Q

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

A

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
Q

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

A

~60%

77
Q

What is a calorie?

A

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

78
Q

What are the most important determinants of BMR?

A

Thyroid hormones (T3 and T4)

79
Q

Why are thyroid hormones so integral to BMR?

A

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

80
Q

Why does EPI exert a calorigenic effect?

A

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

81
Q

What is food-induced thermogenesis?

A

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

82
Q

What substance produced the greatest food-induced thermogenesis effect?

A

Protein, then carbs/fat

83
Q

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

A

Processing of absorbed nutrients by the liver

84
Q

What factor can increased metabolic rate most?

A

Altered skeletal muscle activity: physical activity

85
Q

What is leptin?

A

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
Q

What is neuropeptide Y?

A

Hypothalamic neurotransmitter that stimulates appetite

87
Q

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

A

Neuropeptide Y: stimulates appetite

88
Q

What are the two main functions of leptin?

A

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

89
Q

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

A

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
Q

What is ghrelin?

A

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
Q

What are the four main functions of ghrelin?

A

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

92
Q

What is the formula for BMI?

A

Weight in kg / square of height in m

93
Q

What brain structure is the control center for temperature regulation?

A

Hypothalamus]

94
Q

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

A

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

95
Q

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

A

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

96
Q

How does increased core body temperature affect metabolism?

A

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
Q

What happens during chronic cold exposure?

A

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

98
Q

What causes nonshivering thermogenesis?

A

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

99
Q

How does nonshivering thermogenesis work in infants?

A

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
Q

How do uncoupling proteins work to increase heat production?

A

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

101
Q

Production of sweat is stimulated by what nerves?

A

Sympathetic nerves: using ACh

102
Q

What is the thermoneutral zone?

A

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

103
Q

What are EPs, endogenous pyrogens?

A

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

104
Q

What is the immediate cause of thermal resetting for fever?

A

Synthesis and release of prostaglandins

105
Q

What are endogenous cryogens?

A

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

Physiology (13 decks)

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