1
Q
Blood glucose curve after a meal is ingested
A
2
Q
What is the fasting blood glucose?
A
4.5-5 mmol/l
3
Q
What are the process that increase and decrease after CHO-containing meal is ingested
A
↑GI absorption
↓Glycogenolysis
↑Glycolysis
↓Gluconeogenesis
Insulin release
4
Q
What are the processes that occur 2 after a meal is ingested
A
Decay slope-> High Insulin : ↑Tissue uptake ↑Glycogenesis
Causes blood glucose levels to drop
5
Q
When is glucgon start to be released after ingesting a meal?
A
2.5 h
6
Q
What is the steady phase of the blood glucose curce
A
4h after a meal
↓Insulin:Glucagon
↑ Glycogenolysis
↑Gluconeogenesis
7
Q
Between which values do we regulate our blood glucose
A
we regulate our glucose in the blood between 4.5-7.8 mmol.l
8
Q
What are the glucose blood level processes controlled by?
A
insulin to glucagon ratio
9
Q
What initially increases as a response to a meal?
A
- Insulin
- Glucose
- Lactate
- Pyruvate
lactate and pyruvate are glycolysis intermediates
- Triglycerides
- Alanine
- BCAA
- Total Amino Acids
- I:G
10
Q
What initially decreases in the blood as a response to a meal
A
- Glucagon
- Free Fatty Acids
TG are released by lipolysis durign a fast to make energy
insulin inhibits lipolysis
as FA are attached to glycerol, thus we see an decrease in both
- Ketoacids
- Glycerol- insulin inhibits lipolysis-> decrease in free fatty acids and glycerol
- Urea Nitrogen- inhibitory effect of insulin on protein breakdown
protein breakdown levels are the highest during fasting
11
Q
Glucose, lactate, pyruvate response to a meal
A
12
Q
TG, Free FA and ketone bodies response to a meal
A
13
Q
Glycerol, Alanine and BCAA response to a meal
A
14
Q
Total amino acids and urean nitrogen response to a meal
A
15
Q
Does ingestion of fat lead to an insulin release?
A
no
16
Q
Do CHOs only result in inuslin release?
A
CHO do have the highest effect on insulin release, some AA however also result in insulin release
17
Q
How doe blood glucose levels in circulation differ in an individual with insulin resistance from a normal patient
A
in people with insulin resistance blood glucose response will be higher and will remain high for a longer period of time
18
Q
What is reactive hypoglycemia
A
Also known as postprandial hypoglycemia, drops in blood sugar are usually recurrent and occur within four hours after eating
associated wiht insulin resistance, and results from overproduction of insuln
19
Q
When do blood glucose levels normally start to drop after a meal?
A
1 hour after a meal
20
Q
What is insulin resistance associated with?
A
With high BMIs
21
Q
What dictates energy storage
A
ratio of insulin:glucagon
22
Q
How much energy does brain need?
A
The brain needs ≈500 kcal of water-soluble fuels (usually glucose) per day.
23
Q
Describe the events of the first 24h of fast
A
first 24h of fasting in someone who expends 2000kcal/day:
- TG will be released from fat stores-> FA + glycerol will be released
- FA will be taken up by muscle and liver
- Glycerol will be used by the liver to be converted to glucose. FA will be used for energy by liver by b-oxidation
- Protein will be released from muscles-> liver will do gluconeogenesis-> makes glucose
- Muscle provides amino acids and also provides alanine which will be used as a precursor for glucose
- lactate-pyruvate is being released from tissues that use glycolysis (RBC, skin, renal medulla) will be released from the use of glucose. It will then be reconverted to glucose via cori cycle
24
Q
What are the methods of glucose production in short -term fast
A
- Liver converst substrates from lactate, pyruvae, alanine cycles are converted to glucose
- Glycerol form FA release from adipose tissue is converted to glucose in the liver
- Glygcogenic AA from muscles
25
What are glucogenic precursors?
glycerol, amino acids, lactate-pyruvate, alanine, glycogen in the liver
26
What is the production of ketones determined by?
by the amount of FA in the circulation \> the rate of supply of FA to the liver triggers ketoacedosis
this is mainly regulated by insulin and glucagon at early fast state
27
What are the effects of low insulin levels in a short-term fast?
* insulin being low, allows lipolysis to occur at a high rate (insulin normally inhibits lipolysis);
* low insulin will also allow protein breakdown to occur (insulin inhibits protein breakdown)
* glycogenolysis is stimulated by low insulin and high glucagon as well as stimulating gluconeogeneis from AA and glycerol
28
WHat are the outputs of ketones prodcued by the liver
breath, urine and energy supply for the brain
29
is lipolysis rate ever increasing?
No, after reachign a certain poitn, it will occur only at a certian rate
30
When will ketones be excreted in urine
when ketone concentration will reach a certain level in the circulation
31
What will stimulate glycolysis in long-term fast?
more impact of catecholamines and GH in response to prolonged fasting/stress-\> they will stimulate glycolysis
32
When does gluconeogenesis start to decline
After day ~6
33
When is liver glycogen start to be used
Around 4 hours after the meal when glucose levels in the blood drop
34
When do we use liver glycogen at a max rate?
4-8h after a meal
35
What will be the sources of glucose 12h after a meal
mix of glycogen and gluconeogenesis
36
will gluconegenic processes ever stop durign fasting?
no, they will just occur at low rates
37
Origin of blood glucose 0-4h; 4-16h; 16-28h; 2-24 days and 24-40 days after a meal
0-4h: exogenous
4-16h: glycogen; hepatic gluconeogenesis to a lower extent
16-28h: hepatic gluconoegenesis; glycogen to a lower extent
2-24 days: Gluconeo- genesis, hepatic and renal
24-40 days: Gluconeo- genesis, hepatic and renal
38
Tissues using glucose 0-4h; 4-16h; 16-28h; 2-24 days and 24-40 days after a meal
0-4h: all
4-16h: all exept liver (it will use FA); Muscle and adipose tissue at diminished rates
16-24h: All except liver. Muscle and adipose tissue at rates intermediate between 4h and 24 days
2-24 days: Brain, RBCs, renal medulla. Small amount by muscle (mostly will use FA)
24-40 days: Brain at a diminished rate RBCs, renal medulla
39
Major fuel of brain 0-4h; 4-16h; 16-28h; 2-24 days and 24-40 days after a meal
0-4h: Glucose
4-16h: Glucose
16-28h: Glucose
2-24 days: Glucose, ketone bodies (at lower rates)
24-40 days: ketone bodies, glucose (at lower rates)
40
Name ketone bodies
Acetoacetate, β-hydroxybutyrate
41
How are ketone bodies excreted?
Excreted via lungs (acetone from acetoacetate) and kidneys
42
What are the implications of ketone bodies?
* When ketones are excreted via kidneys they must be “salted”/ buffered out which involves the loss of either Na, K, H, or NH4
* Ideally NH4 (ammonia) is excreted because it is a waste product
* BUT K is the preferred ion to be excreted-\> hypokalemia
43
normal __ function is important during ketone diets and sufficient __ intake
normal kideny function is important during ketone diets and sufficient water intake
44
How do insulin levels change through out the fast?
Decrease
45
How do glucagon levels change through out the fast?
Increases, then decreased and stabilizes
46
How does ins:gluc ratio change through out the fast?
Decreased
47
How do fatty acid levels change through out the fast?
increase
48
How do lactate and alanine levels change through out the fast?
are pterry much stable (occur at constant rate)
49
Describe weight loss rate durign prolonged fasting
rapid at first
after a week weight loss occurs at "lnear rate"
early wight loss-\> protein is used as an energy store-\> water is lost\> rapid weigth loss
deeper into a fast-\> fat is used as a fuel-\> lipolysis occurs at a constant rate-\> linear weight loss
50
Urinary Nitrogen Constituents: normal vs starvation for several weekd\s
under normal conditions most of our nitrogen is excreted in urea
small amount form ammonia and others
Starvation:
* urea component is decreased, no more nitrogen is coming from the diet but also due to muscle sparing-\> less urea is produced
* more ammonia in terms of nitrogen excretion as kidney is producing some glucose as well through gluconeogenesis
* kidney’s ability to make glucose is more important in long starvation
* by producing glucose, kidney produces more ammonia
* more ammonia is excreted in oder to buffer the keto acids in the urine
51
Why do we need higher water intake in starvation
Ammonia is toxic-\> more water is needed to dilute it in the urine
52
Ketosis vs ketoacidosis: ketone levels
ketosis (less than 3 mmol) has been reached- but not ketoacedosis
ketoacedosis - 10+ mmol of ketones in the circulation, doesn’t normally occur in starvation; occurs in diabetes
ketoacedosis is dangerous, ketosis isn’t if renal function is normal
53
Is ketosis or ketoasidosis dangerous?
ketoacedosis is dangerous, ketosis isn’t if renal function is normal
54
What is the relationship between enerhy intake/expenditure and nitrogen balance
even if you consume enough protein, but don’t consume enough energy, you may still not reach NB
if you consume a lot of energy, you will reach NB faster or with less protein in the doet
55
What is the relationship between fat mass and weight loss (forbes predictions)
PREDICTION I:
During fast, obese individuals will lose less nitrogen (hence less LBM) than will thin people
PREDICTION II:
The fatter the subject the less the contribution of LBM to total weight loss on energy restricted diets
56
Cardiovascular and Renal changes due to Severe Weight Loss
* Decreased cardiac output, heart rate, BP, blood volume- medical supervision is required, especially if they are taking medications that lower blood pressure
* Increased tachycardia (compensatory mechanism)- observed in the beginning
* stress on kidney (acid/base balance)
57
immune function changes due to Severe Weight Loss
* Decreased T-cell function/lymphocytes - measures through decreased T-cell function, decreased lymphocyte count
* Decreased cytokines
58
Gastrointestinal Function chnages due to severer weigth loss
* Decreased Lipid absorption – steatorrhea (more fat in the stool)
* Decreased gastric, pancreatic and bile secretion/production
* Decreased Villous surface area- GI tract is affected as less food is coming in-\> villus surface is affected-\> malabsorption, especially lipids are poorly absorbed
59
Electrolyte chnages due to severe weigth loss
• Potassium losses (LBM and intracellular losses) (K is used to buffer keto acids)
60
CNS functions chnages due to severe weigth loss
brain function is affected
these are reversible
61
What is the FTO gene?
at mass and obesity–associated gene (FTO). Though FTO has the strongest link to obesity, the relative risk of 1.2–1.3 still remains small.
62
Why is a wrigt loss of 5% considered to be metabolically important?
is considered clinically important,as many cardiovascular risk factors (e.g., elevated blood pres- sure, glucose and lipids) may improve with weight loss of this magnitude.
63
is brain able to store energy?
no
64
which organs serves as a reservoir for excess calories
liver
65
what is the primary glucose source at 24h of fasting
hepatic gluconogenesis
66
What is the primaary brain region involved in the homestatic control of food intake.
The ARC (arcuate nucleus) of the hypothalamus is the primary brain region involved in the homoeostatic control of food intake.
67
What are the 2 groups of nerurones in ARC region? What do they produce and what are the effects?
Neurons which co-express **NPY** (neuropeptide Y) and **AgRP** (agoutirelated peptide) stimulate food intake, whereas neurons expressing **POMC** (pro-opiomelanocortin) have the opposite effect
68
what are the hormones involved in long-term regulation of energy balance? Which ones are involved in short-term regulation of energy balance
Long term: leptin (from adipose tissue) and insulin (from the pancreas)
Short term: short-term signals send information to the brain on a meal-to-meal basis and include hormones from the gastrointestinal tract and pancreas, such as ghrelin, CCK (cholecystokinin), GLP-1 (glucagon-like peptide-1), amylin, PP (pancreatic polypeptide) and PYY (peptide YY)
69
What is te preferential substrate for energy in those subjects, who lost weight? What does it mean for those individuals
Carbs is the preferential substrate
lower fat oxidation
70
What are the adverse effects of excess cortisol?
leads to weight gain, particularly central adiposity
71
How does leptin result in reduced food intake?
Leptin acts in the hypothalamus to reduce food intake and increase energy expenditure by reducing the expression of AgRP and NPY, and stimulating that of POMC
72
What is addison's disease
also known as chronic adrenal insufficiency; a rare endocrine disorder in which the adrenal glands do not produce enough steroid hormones; some common symptoms include fatigue, dizziness, muscle weakness, weight loss, difficulty in standing up, vomiting, anxiety, diarrhea, headache, sweating, changes in mood and personality, and joint and muscle pains
73
What is amylin
a hormone synthesized by pancreatic b cells that contributes to glucose control dur- ing the post-prandial period
74
macrosomia
condition of abnormally large infants whose mothers have diabetes
75
WHy do kidenys have to work extra hard durign a fast?
kidneys try to regulate acid/base balance
NUTR 344
flashcards
Decks in class (22)
# Cards
-
Nutritional Assessment72
-
NA part 2180
-
Obesity111
-
Obesity 275
-
lesson 552
-
Popular diets51
-
Hypertension176
-
Intuitive eating28
-
Dislipidemias222
-
Dysphagia150
-
Cardiovascular Disease (CVD) with a focus on Secondary Prevention100
-
Cystic fibrosis38
-
COPD, Respiratory and Nutrition Disorders84
-
Diabetes Introduction74
-
Metabolic syndrome- ??16
-
Diabetes Physical exercise advice & Pharmacological Management67
-
Diabetes diet calculations: choices and meal plan55
-
Nutrition and cancer84
-
Cancer Pathophysiology and Cachexia88
-
Nutritional assessment and approach in cancer88
-
final revision112
-
Diabetes nutritional approach57
