metabolism, digestion Flashcards

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1
Q

Metabolic rate

A

a. Best index of total physiological state b. Rate of energy utilization: tells us how hard an animal is working to meet both internal and external demands

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2
Q

metabolism is a function of what 4 things?

A

Basal Metabolic Rate (BMR) + Activity + special biological processes (ex: reproduction) + TEF (Thermal Effect of Food—digestion)

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3
Q

when you’re thinking of standard metabolic rate; in what zone does stable metabolic rate occur?

A

thermal neutral zone

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4
Q

discuss the energy costs thermal neutral zone vs lower, upper critical temp

A

LCT and below: shivering costs energy (calories) UCT and above: sweating costs calories TNZ: adjustments here cost nothing Within TNZ make adjustments with posture and blood around skin without causing increase in metabolism. We are endotherms so try to regulate body temp at constant level. Outside TNZ your metabolic rate increases

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5
Q

what are the types of thermogenesis you would see?

A

shivering , or nonshivering aka burning brown fat

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6
Q

what are dogs equivalent of sweating? how does it work?

A

panting. rapid shallow breaths allow animal to breathe out heat from upper respiratory track. Takes place at resonant frequency of chest cavity

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7
Q

Below LCT and above UCT metabolic rate does what?

A

increases

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8
Q

Non-shivering thermogenesis

A

babies, hibernating animals using brown adipose tissue (BAT). It is innervated by sympathetic nervous system. We release norepinephrine and it acts on receptor (beta 3 adrenergic receptor) on BAT to turn it on. BAT has special protein (UCP1—uncoupling protein #1) which is expressed in the inner mitochondrial membrane and it uncouples oxidative phosphorylation. Won’t make ATP, instead it just generates heat. Blood gets warmed by BAT and then that gets circulated throughout the body 1. As adults, we have White adipose tissue (WAT) is in clavicle area and retroperitoneal area. In this, there is beige fat which is BAT that can be turned on if needed. It is “recruitable” and can make heat. 2. Initially found in rodents put in cold environments and they recruit beige fats 3. Active beige cells vary inversely with obesity

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9
Q

Things that influence our metabolic rate

A

activity, diet, body weight

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10
Q

Highest metabolic rate an individual can have is due to :

A

exercise

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11
Q

when you have Resting MR and then introduce activity and see how much MR increases, that Increase is called:

A

oxidative metabolic scope . 4.3x in most people

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12
Q

what role does creatine play in metabolism

A

creatine phosphate holds phosphates and then donates those phosphates to ADP to make a lot of ATP

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13
Q

difference between human and alligator metabolism?

A

in humans oxidative metabolic scope is much higher; alligators oxidative scope is much lower

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14
Q

beige fat

A

white adipose tissue that can turn to brown

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15
Q

why would you turn beige fat into brown fat?

A

brown fat does thermogenesis- burns fat to produce energy

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16
Q

Indirect calorimetry:

A

oxygen in, oxygen out; change in O2. measures metabolic rate (This is the type of calorimetry we use) change in oxygen / time gives you metabolic rate.

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17
Q

Initial Way for direct calorimetry:

A

Put an animal in a bomb calorimeter and as it eats it gives off heat and warms the water around it—find change in temp of water. Know volume of water. Know specific heat of water and then find heat given off by metabolism

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18
Q

RQ/ respiratory exchange rate

A

CO2/O2. an RQ of 0.7, that corresponding to fat, would signal someone who is diabetic; can only breakdown fat, not carbs (carbs are 1.0)

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19
Q

what is oxygen debt?

A

O2 debt; your metabolic rate remains elevated after exercise stops; metabolism still has a lot of catch up to play. Lots of lactic acid, need to run cycles.

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20
Q

What limits our metabolic scope?

A

central limit (aka oxygen delivery 2 tissue) GI abilities oxygen utilization with tissues all three can be improved with exercise.

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21
Q

describe what influences the central limit

A

Cardiovascular function, Respiratory changes # capillaries

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22
Q

what is Thermal effect of food: TEF?

A

% of energy utilized to make something metabolically available to body

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23
Q

Describe varying TEF’s of carbs, fat, protein

A

protein: 30% fat: 12% carbs: 5% aka protein burns the most efficiently

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24
Q

what is the ancel keys study?

A

in the minnesota study, people went from 3200 to 1800 calories a day for 6 months; keys noted the severe psychological effects. “democracy is not possible while people are hungry.”

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25
Q

Describe the various changes occur when you lose 10% of your body fat in one of these diets

A

what happens is that body decreases metabolic rate/energy expenditure per kilogram body weight -Decrease in sympathetic tone; sympathetic nervous system (fight or flight responses) . We tone that down. -increases parasympathetic tone- also autonomic nervous system- turns on for rest + digestion. -Decrease thyroid hormones – TH elevates metabolic rate! And we just dropped it. -Skeletal muscle; contractions 20% more efficient. Get more efficient at getting energy – use less anerobc, more aerobic. People who have dieted expend 300 kcal per day less while dieting- than what they were doing before. So u eat less calories but u burn less calories and it never goes away!!!! You will have a low metabolism for life likely

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26
Q

Females need __ body fat to be able to reproduce

A

15

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27
Q

why might caloric restriction cause animals to live longer?

A

protein turnover increases. Utilizing some of ur body protein for energy . Less protein with macromolecular damage aka . Non-enzymatic glycosylation (sugars that attach to proteins in no nenzymatic fashion, sugars sticking to proteins making them less functional.) also turnover more oxidative damaged ones (from reactive oxygen species) so basically u turnover some bad proteins and have more healthy proteins left. Also, less DNA damage from ROS. 2: sintuins; proteins expressed with Caloric restriction; act on histones , increase DNA stability.

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28
Q

name some other molecular effects of caloric restriction

A

influence hormone IGF1 (insulin-like growth factor 1) that is invovled in growth. So caloric restriction decreases growth. Affects energy metabolism in cell : AMP protein kinase (turns ADP into ATP) increases Mtor- (mammalian target of rapamyicin) a kinase , enzyme that phosphorylates things, involved in cell growth + metabolism.

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29
Q

does caloric restriction work on older/adult primates?

A

no, had to start from birth. does work on rodents for making them live longer

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30
Q

name some biological factors that can lead to obesity

A
  1. Leptin signals fullness- lack of leptin can lead 2 obesity 2. FTO gene- mutation causes u to retain too much fat 3. Microbiome- gut may play a role. Theres something in their gut that makes them obese- put fecal transplant into mice, mouse becomes obese! 4. Epigenetics- diet/smoking can alter expression of a whole range of genes. Infants born small for gestational age very likely to become obese- mom had poor protein diet while pregnant, kid holds on to fat too much
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31
Q

T/F: Humans don’t make vitamin C but everyone else can

A

true

32
Q

Peristalsis

A

muscle movement that moves food thru GI tract

33
Q

how does peristalsis work?

A

a. Circular smooth muscle near mucosal side that contracts in towards the food in the tract b. Bands of longitudinal smooth muscle that contract back and forth

34
Q

why is GI tract so sticky? what are the uses of this stickines- basically what does our GI tract do?

A
  1. Sticky property because it is mostly made of glycoproteins 2. Works as a lubricant 3. Provides physical protection along wall of the gut 4. Resistant to digestive enzymes so can’t be broken down easily 5. Helps form the fecal mass 6. Amphoteric so act as either acid or base (acts as a good buffer)
35
Q

when you digest food, how far down do you go? to nothingness?

A

digest all the way down to carbon-carbon bonds; leave those intact , use for energy

36
Q

describe the steps of the general digestion pathway

A

mouth -> esophagus -> stomach -> small intestine -> large intestine

37
Q

what key event occurs during mastication? (chewing)

A

salivary glands contain amylase enzyme, breaks down + lubricates food

38
Q

what happens in the esophagus?

A

ii. Food goes into esophagus where there is sphincter muscles (very tight) formed by smooth muscle. Use peristalsis to get food actively pushed through esophagus. Chest cavity is at lower pressure than atm so we use sphincter muscles so there is no problem with pressure

39
Q

how do we make acid in the stomach?

A

a. G Cells make hormone gastrin which activates gastric pits
b. Enterochromaffin-Like cells (ECL) make histamine which stimulates gastric pits. Histamine receptor in gastric pit is different than one for immune responses.
c. Gastric pits which have various cells types (in the stomach lining)
i. Parietal cells make HCl (pH 2-3 in stomach) and intrinsic factor (helps absorb vitamin B12)
ii. Chief cells make pepsinogen (zymogen—enzyme precursor so you don’t digest the cell proteins where it is made) which then gets activated by HCl into pepsin
iii. Goblet cells make the mucus to protect from HCl

40
Q

what is the stomach’s primary function- what does it digest?

A

Involved in digestion of proteins mostly (hardest to digest)—Secrete HCl and enzyme pepsin to denature proteins and kill foreign bacteria. Can’t absorb much in your stomach except things that are highly lipid soluble like alcohol.

41
Q

how much can the stomach expand?

A

from 200 mL to 2L (10x!!)

42
Q

enzyme responsible for protein breakdown

A

pepsin

43
Q

when food enters the stomach it stimulates the secretion of ____.

A

HCL

44
Q

name of acid-secreting cells in stomach

A

parietal cells

45
Q

what are the stomach’s three tasks?

A
  1. store the swallowed food and liquid. This requires the muscle of the upper part of the stomach to relax and accept large volumes of swallowed material.
  2. mix up the food, liquid, and digestive juice produced by the stomach. The lower part of the stomach mixes these materials by its muscle action. (The mixture is referred to as chyme.)
  3. empty its contents slowly into the small intestine.
46
Q

Food leaves stomach and goes through_____ to get to duodenum

A

pyloric sphincter

47
Q

function of liver in digestion during duodenum stage?

A

Liver: makes bile which emulsifies fat

48
Q

function of gallbladder during duodenum stage of digestion?

A
  1. Gallbladder: stores the bile and then when the gallbladder is stimulated it releases bile which goes into pancreatic duct and then to duodenum
49
Q

how does small intestine do absorbtion?

A
  1. Vili in the small intestine and folding (folds of keckering) that increases surface area dramatically
  2. In each vili there are capillaries that take Carbs and proteins to liver and there are lacteals that take fats to lymph system
  3. Vili has brush border membrane with glycoproteins to even further increase surface area. Slows down movement of all food in gi tract so the cells can WORK
  4. Epithelial cells are enterocytes
50
Q

what are trypsin and chymotrypsin?

A

pancreatic enzymes that digest proteins

51
Q

what is pancreatic lipase?

A

breaks down fats

52
Q

exocrine vs endocrine pancreas:

A

exocrine secretes bicarbonate to neutralize chyme, and digestive enzymes : (amylase (carbs) lipase (fats) etc) trypsinogen (enzyme that will turn into trypsin in the duodenum and eventually break down proteins)

  1. Endocrine pancreas: little islands of tissue in the pancreas that make insulin (glucose into glycogen) and glucagon (glucose breakdown) secreted into blood
53
Q

•uncoupling protein #1

A

how brown adipose tissue generates heat;

  • Uncouples oxidative phosphorylation
  • Allows hydrogen ions to cross membrane by themselves (not coupled to ATP generation)
  • Tissue gets warm
  • Increase temperature in BAT

Bring in blood flow, use that to circulate heat

54
Q
A
55
Q

name 3 possible ways that caloric restriction could help you live longer

A

•protein turnover increases. Utilizing some of ur body protein for energy . Less protein with macromolecular damage

  1. turnover more oxidative damaged ones (from reactive oxygen species) so basically u turnover some bad proteins and have more healthy proteins left. Also, less DNA damage from ROS.
    3: sintuins; proteins expressed with Caloric restriction; at leas 7 sintuins- some go to nucleus some 2 mitochondira, cytosol etc. act on histones , increase DNA stability
56
Q

what happens when food hits the stomach?

A

chyme in stomach; GI is highly innervated (lots of nerves)

upon food detection gastric pits secrete hcl, pepsinogen

acid: protein denaturing

pepsinogen becomes pespin, does protein breakdown

goblet cells secrete mucus to protect stomach lining

57
Q

•Small intestine connected by ___ to body wall

A

mesentery

58
Q

summary of liver functions

A

first stop for all nutrients

secretes bile

glucose + fat metabolism

insulin + glucagon

secretes bile salts

59
Q

The body need to conserve bile salts. Note the pathway used to reabsorb the bile salts.

A

We recycling bile salts. After they do job in duodenum/small intestine we reabsorb bile salts while we absorb fat and then the bile salts split off and go back to the liver via hepatic portal vein. Our ability to make bile isn’t that great so recycling is CRITICAL

60
Q

What developmental process is most detrimentally affected (as seen in many third world countries) when sufficient nutrition is not available during third trimester of pregnancy? Would you expect general organogenesis (formation of heart, liver, eyes, etc.) to also be affected by poor nutrition at this stage? Why or why not?

A

brain development would be the biggest issue; mental retardation, personality issues

organs are first/second trimester

61
Q

Give a name for the failure to close up the tube at the caudal end, and explain how the position of the developmental error (along the length of the tube) can affect the outcome.

A

lack of closure tail end ; spina bifida.

further up = more severe issues

62
Q

function of gallbladder

A

stores bile

63
Q

describe what occurs when food hits stomach

A

G-cells activated, (local action) produce

Gastrin-> wakes up parietal cells -> produce HCL

can also produce histamine, more acid production

64
Q

what does vagus nerve do when food hits?

A

vagus -> gastrin -> parietal cells

65
Q

what stimulates gastric phase

A

distension

66
Q

vagus nerve prompts what?

A

vagus -> gastric -> parietal cells

67
Q

describe the process of absorption of glucose in small intestine

A

Na+, glucose in (GLT1) . Na+ higher outside cell but we keep pumping it in; push out into blood via Na/K pump.

GLUT5 brings shit in too. GLUT2 lets all this glucose out into the blood stream. *low affinity*

68
Q

describe process of protein absorption in intestine

A

Na+ in, along with amino acids, peptids, via symporter

Na+ out via Na + / K+ pump

endocytosis (bring in whole proteins)

69
Q

describe the process of fat absorption and circulation

A

bile salts -> TG + lipases (micelles) -> break down TG into FFA’s -> add lipoproteins, pack into chylomicron -> exocytosis into lymph system -> venuous, heart, arteriol, tissues

70
Q

cephalic phase

A

food in mouth; nervous system activates; 30% HCL. ACH, VIP in effect

activates salivary glands, parietal cells

71
Q

gastric phase

A

triggered by food in stomach

60% of hcl secretion

G cells; gastrin release

ECL cells; histamine

72
Q

intestinal phase of digestion

A

when food enters duodenum.

release secretin, CCK

secretin: releases bicarbonates

CCK: release digestive enzymes + bile, slows down release of acid from gastric pit

73
Q
A
74
Q

what is the liver’s role as related to fat?

A

liver exports fats, takes in cholesterol

75
Q
A