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