Nutrition and Metabolism Flashcards
1
Q
what are the factors that affect BMR?
A
- surface area 2. gender/muscle content 3. activity level - muscular activity provides greatest variation between people (sedentary or active job) 4. age 5. pregnancy and lactation 6. anxiety 7. body temp (fever) 8. environmental temp 9. eating 10. thyroid hormones 11. depression
2
Q
what is the thermic effect of food
A
diet induced thermogenesis, metabolic rate increases after consumption of food bc digestion, absorption, distribution and storage of food needs energy
3
Q
effects of growth hormone on muscle and adipose and bone
A
- induces lipolysis in the adipocytes, increasing FFA in blood 2. muscle preferentially uses FFA which indirectly suppresses glucose oxidation in muscle (decrease glucose uptake), therefore, muscle increases protein synthesis (more glucose to use) 3. directly stimulates bone growth 4. indirectly stimulates bone growth by stimulating IGF-1
4
Q
effect of growth hormone on liver
A
because of increased FFA in blood, liver enhances fatty acid oxidation and ketogenesis, increases gluconeogenesis and glycogen synthesis, secretes IGF-1
5
Q
what is IGF-1
A
insulin-like growth factor, somatomedins, is secreted by the liver and binds to receptor on the liver and other tissues (bone)
6
Q
what do IGF-1 do?
A
- stimulates MAPK and ERK pathways 2. stimulates mitogenic cellular proliferation 3. stimulates bone growth
7
Q
direct anabolic effects of GH
A
- stimulates division of chondrocytes of cartilage 2. stimulates synthesis and secretion of IGFs (somatomedins)
8
Q
indirect anabolic effects of GH
A
IGFs stimulate osteoblast and chondrocyte activity to promote bone growth
9
Q
how does IGF stimulate bone growth?
A
binds to TK receptors
10
Q
how does GH stimulate chondrocyte division?
A
binds to TK receptors and activates MAPK/ERK pathway
11
Q
how does GH stimulate synthesis and secretion of IGFs
A
activates cytosine TK (JAK-STAT/Janus) signaling pathway
12
Q
where is GH made
A
somatotroph cells in the anterior pituitary
13
Q
how is GH regulated?
A
- hypothalamus releases GHRH or GHIH (inhibiting hormone) 2. depending on the ratio of GHRH/GHIH from hypothalamus, GH is released or not released
14
Q
what affects the GHRH/GHIH ratio from the hypothalamus?
A
exercise, nutrition, sleep, FFA
15
Q
another name for GH?
A
somatotropin
16
Q
another name for GHIH
A
somatostatin
17
Q
where is somatostatin released?
A
- hypothalamus 2. delta cells of pancreas
18
Q
what else does somatostatin inhibit?
A
- GH 2. insulin 3. TSH 4. glucagon
19
Q
what is the effect of somatostatin release?
A
- reduces nutrient absorption in the gut
20
Q
how does somatostatin reduce nutrient absorption in the gut
A
- prolongs gastric emptying 2. diminishes pancreatic exocrine secretion
21
Q
how do thyroid hormones affect metabolism?
A
indirectly by regulating other hormones like insulin, glucagon, epi/norepi
22
Q
how do thyroid hormones act on our cells?
A
their action mediated by nuclear receptors, so they have long term effects due to increased or decreased transcription of genes directly related to metabolism
23
Q
what is the most important effect of thyroid hormones?
A
catabolic and stimulation of energy expenditure
24
Q
how does T3 affect the liver?
A
- increase glycolysis 2. increases cholesterol synthesis 3. increase cholesterol conversion to bile acid/salts 4. increase sensitivity of hepatocytes to gluconeogenic and glycogenolytic actions of epinephrine
25
how does T3 affect the adipocytes?
1. sensitizes adipocyte to lipolytic action of epinephrine/norepi by increasing gene for beta adrenergic receptors 2. increases availability of glucose to fat cells
26
how does T3 affect the muscle cells?
1. increase glucose uptake 2. stimulate protein synthesis
27
how does T3 affect the pancreas?
promotes insulin release from Beta cells to increase glycolysis and glucose uptake (protein sparing)
28
what does it mean that T3 has a bipolar effect?
1. it increases Beta adrenergic receptors for epi/norepi action in adipose, increases lipolysis = catabolism 2. it increases insulin release in pancreas, increasing glucose uptake and glycolysis in muscles, sparing protein --\> protein synthesis = anabolism
29
how does T3 increase heat production?
stimulates ATP utilization and effecting the sympathetic nervous system to increase norepi release
30
how does NE stimulate heat production?
it increases thermogenin in brown adipose tissue that uncouples oxidative phosphorylation, causing heat production
31
explain the action of thermogenin
thermogenin acts as an uncoupler that makes holes in the inner mitochondrial membrane, letting protons through the hole without the ATP production, this increases O2 consumption and ATP synthase production, which generates more heat
32
describe hypothyroidism
low T3 or T4, causes slower metabolism, cold intolerance, and weight gain because of decreased ATP production from the decreased uncoupling of thermogenin
33
describe hyperthyroidism
overactive thyroid, more T3/T4, elevates BMR, feel warm, weight loss due to increased uncoupling of thermogenin and increased ATP production
34
what is gastrin
GI derived hormone, induces gastric acid secretion, inducing hunger
35
what is ghrelin
GI derived hormone, produces hunger by stimulating orexigenic neurons
36
what is motilin
GI derived hormone, stimulates gastric and pancreatic enzyme stimulation, inducing hunger
37
GI derived hormones that induce hunger
1. gastrin 2. ghrelin 3. motilin
38
GI derived hormones that reduce hunger
1. pancreatic polypeptde 2. peptide YY 3. secretin 4. cholecystokinin
39
what is pancreatic polypeptide (PP)
GI derived hormone, reduces gastric emptying and slows upper intestinal motility, makes you feel full
40
what is peptide YY (PYY)
GI derived hormone, inhibits gastric acid secretion, reduces hunger
41
what is secretin
regulates pancreatic enzyme secretion and inhibits gastrin release and secretion of gastric acid
42
what is cholecystokinin
satiety hormone, appetite suppressing effect on brain
43
what are the incretin hormones
1. glucagon like peptide 1 (GLP-1) 2. glucose dependent insulinotropic polypeptide (GIP) (secreted from gut, target of novel treatments for DM2)
44
what induces insulin?
1. increased blood glucose 2. GLP-1 and GIP
45
when are incretin hormones released?
after a meal by the gut, affects pancreas and becomes like glucagon or enhance secretion of insulin, they have a short half life and get degraded quickly
46
what do the incretin hormones do?
1. enhance synthesis and release of insulin 2. GLP-1 inhibits secretion of glucagon 3. regulates amount of nutrients ingested through their central action as satiety signals
47
how do GLP-1 agnoists work?
they bind to GLP-1 receptors and stimulate insulin secretion
48
how are incretin hormones broken down?
degraded quickly by dipeptidyl peptidase 4
49
how do DPP4 inhibitors work?
inhibit the degradation of GLP-1, prolonging the stimulation of insulin
50
what hormones do adipocytes secrete?
leptin and adiponectin
51
what does leptin do?
binds to its receptor in the hypothalamus and stimulates neurons that produce appetite suppressing hormones, stimulates satiety, increases energy expenditure
52
what does adiponectin do?
reduces blood FFA - produces a better glycemic control, improved lipid profile, reduced inflammation in diabetics
53
what are PPAR gamma agonists?
they increase adiponectin levels through binding to peroxisome proliferator activated receptor gamma (PPAR gamma) in the adipocytes. it increases the peroxisomes so FFA go into peroxisomal beta oxidation, decreasing blood FFA, decreasing insulin resistance in the muscle cells
54
what do adipokinase do?
TNFalpha, increase FFA, increase LPL activity, increased lipolysis, increased insulin resistance
55
explain pathway of leptin
1. leptin activates anorexigenic neurons in the arcuate nucleus 2. anorexigenic neurons express proopiomelanocortin (POMC) 3. proopiomelanocortin is a precursor of alpha melanocyte stimulating hormone aMSH
4. alpha MSH is released from POMC expressing anorexigenic neurons of the arcuate nucleus
5. alpha MSH binds to its receptors MC3-R and MC4-R at the paraventricular nucleus (PVN)
6. binding of alpha MSH activates the melanocortin signaling pathway
7. activation of the melanocortin pathway inhibits food intake and increases energy expenditure
56
what genetic mutations are associated with inherited obesity?
MC4-R receptor mutations, don't allow alpha MSH to bind and activate melanocortin signaling pathway = uninhibition of food intake, decreased energy expenditure
57
what is the most important pathway in inherited obesity?
melanocortin signaling pathway that reduces food intake and increases energy expenditure
58
why are the anorexigenic neurons in the arcuate nucleus important?
they not only suppress appetite, but also involved in the activation of the sympathetic nervous system = causes release of cortisol and thyroid hormones = increase BMR and energy expenditure
59
what NT stimulates the desire for carbs?
norepinephrine
60
what NT stimulates the desire for fats?
galanin
61
what NT stimulates the desire for protein?
endorphins
62
why are carbs considered to be protein sparing?
when intake of carbs is low, dietary AA are deaminated and the carbon skeletons are used to make glucose. complete absence of carbs leads to ketone body production. when eating carbs, that is used to make glucose, sparing protein deamination.
63
what is the RDA for carbs?
150g per day - based on the amt of glucose used in RBC and brain (depends on activity)
64
when would a person be in negative nitrogen balance?
increased protein degradation and excretion of N to use the carbon skeletons for gluconeogenesis
1. protein malnutrition
2. dietary deficiency of even 1 essential amino acid
3. starvation
4. uncontrolled diabetes
5. infection
65
when would a person be in positive nitrogen balance?
1. growth
2. pregnancy
3. convalescence (recovery phase of injury or surgery)
4. recovery from condition associated with negative nitrogen balance
66
what happens to excess protein that is consumed? the carbons
protein in excess is used as fuel, but is deaminated first.
1. carbons left are metabolized to pyruvic acid (glucogenic), acetyl CoA (ketogenic) or citric acid cycle to provide energy
67
what happens to the excess protein that is consumed? the amino group
2. NH2 become ammonia, which is converted to urea. usually accompanied by increased urinary calcium. increases risk of nephrolithiasis and osteoporosis
68
what is Kwashiorkor
inadequate intake of protein with adequate energy intake
69
symptoms of Kwashiorkor
1. patients have edema due to severely decreased synthesis of plasma proteins (albumin)
2. stunted growth
3. dry brittle hair
4. diarrhea
5. dermatitis
6. anorexia
7. enlarged fatty liver
70
what is marasmus
inadequate intake of both protein and energy
71
symptoms of marasmus
1. thin wasted appearance
2. arrested growth
3. extreme muscle wasting
4. weakness
5. anemia
72
what is the most common form of protein energy malnutrition?
PEM in the hospital setting where the patients are not eating well because of chronic/devastating illness, trauma, severe infection, or surgery (aka negative nitrogen balances)
73
what would you see in a patient in a hospital setting with PEM?
decreased plasma albumin and other plasma proteins
decreased cellular immunity/increased susceptability to infection
decreased wound healing
increased mortality
74
what is related to PEM that is not hair or plasma protein related?
sarcopenia - aka muscle loss due to aging or becoming less active or hormonal changes or poor nutrition
75
how do you fix sarcopenia?t
exercise and good nutrition
