Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

Physio > Nutrient Metabolism: Insulin And Glucagon > Flashcards

Nutrient Metabolism: Insulin And Glucagon Flashcards

1
Q

Phases of metabolism

A

. Absorptive phase: when substrates are invested

. Post-absorptive phase: what occurs btw meals

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

Absorptive phase

A

. Ingestion of food causes inc. levels of glucose, FA, ad AA
. Most tissues primarily oxidize FA at all times, but as glucose availability inc. glycolysis is inc.
. Substrates directed toward glycogen synthesis, triglyceride synthesis, and protein synthesis
. Glycogenolysis, lipolysis, gluconeogenesis, protein degradation, and FA oxidation are suppressed

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

Carbs in absorptive state

A

. Inc. availability inc. glycolysis
. Excess glucose converted to glycogen in mm. And liver or converted to long chain FA in liver
. Stimulation of glycolysis generates citrate and acetyl-CoA

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

Citrate role in metabolism

A

. Citrate is potent activator of FA synthesis
. High levels of malonyl-CoA from this inhibits carnitine palmitoyltransferase
. Directs FA away from oxidation and towards synthesis of TAG

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

Amino acids in absorptive state

A

. Stimulated to enter mm. And other tissues where they are synthesized into protein
. Excess protein converted by liver into FAs, incorporated into triglyceride, and stored in liver or adipose tissue

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

Fatty acids in absorptive state

A

. Enter liver and are converted to triglycerides
. Some stored there but most transported to peripheral tissues via lipoproteins
. In adipose and mm. Lipoprotein lipase cleaves FAs from glycerol backbone of TAG
. FAs diffuse into adipocytes where they are esterified w/ glycerol to form TAG again
. In skeletal mm. The FAs are oxidized for ATP

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

Post-absorptive state

A

. Need to maintain glucose levels about. 60 mg/100mK so brain uptake does not decline and become impaired
. Provides adequate FAs for other tissues to metabolize
. Glycogenolysis, gluconeogenesis, lipolysis, and protein breakdown are stimulated
. Glycolysis, glycogen synthesis, triglyceride synthesis, and protein synthesis are inhibited
. Once fasting is over gluconeogenesis will continue for several hours to rebuild hepatic glycogen stores

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

Obligatory users of glucose

A 
. Brain
. Nerves
. RBCs
. Intestinal mucosa
. Renal medulla 
. None regulated by insulin 
. Facilitated diffusion depends on glucose 
. High sensitivity transporters will continue to bring glucose into cell even at low plasma conc.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

Brain fuel in extreme prolonged starvation

A

. Ketones: b-hydroxybutyrate and acetoacetate

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

Carbs during postabsorptive state

A

. Glycogen stores in liver and mm. Catabolized to glucose
. Mm. Glycogen is metabolized to lactate that can enter blood and convert into glucose in liver (mm. Lacks G6P to released glucose directly into bloodstream)
. Glycogen stores are small and deplete quickly
. If fasting continues generation of glucose occurs via gluconeogenesis glom lactate, pyruvate, AAs, and glycerol
. Occurs in liver first and then in prolonged fasting it also occurs in kidney

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

Protein in post-absorptive state

A

. In prolonged fasting AAs used as substrate for gluconeogenesis
. Primarily Ala and Glu

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

Fat in post-absorptive state

A

. Lipolysis releases long chain FAs from adipose that are then used in most body tissues.
. Randle effect: elevated FAs inhibit glycolysis promoting FA use as fuel
. Inside cells transport gets FAs into mitochondria and the beta-oxidation inside mitochondria converts FAs into acetyl-CoA
. Acetyl-CoA is converted to CO2, H2O, and ATP
. In liver after prolonged fasting FAs converted into ketones

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

Transport system of FAs into mitochondria

A

. Acyl-CoA exchanges CoA for carnitine catalyzed by carnitine palmitoyltransferase I (CPT I) in mitochondrial membrane
. In mitochondria interior, acylcarnitine is reconverted to acyl-CoA by CPT II and oxidized

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

Ketones

A

. After few hrs fasting ketogenesis in liver is initiated
. Enhanced by low insulin:glucagon ratio
. Serves as alternate substrate for most tissues except liver
. When fasting for several days, ketones reach critical level and are transported into CNSS for ATP production to dec. glucose amt needed and limiting protein breakdown as source of glucose
. FAs and ketones can stimulate insulin secretion that limits lipolysis and glucagon secretion to prevent ketone conc. From getting too high

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

How long can adult survive w/o food if they have water?

A

. 50-75 days

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

Cells in islets of langerhans

A

. Alpha: glucagon (polypeptide)
. Beta: insulin (protein)
. D: somatostatin (peptide)
. F: pancreatic polypeptide

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

Insulin synthesis

A

. In beta cells in islets
. 2 polypeptide chains (alpha and beta) joined via disulfide bridges
. Synthesized as preproinsulin and cleaved to proinsulin
. Converted to insulin and c-peptide in golgi

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

Stimulus for insulin secretion

A

. Glucose enters beta cells via GLUT 2 to be metabolized and generate ATP
. Inc. ATP conc. Inhibit ATP-sensitive K channels in plasmalemma which depolarized cells activating VG- Ca channels
. Ca entry activated Ca release from ER activating exocytosis of insulin and C-peptide

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

Sulfonylurea drugs

A

. Close ATP-sensitive K channels to stimulate insulin secretion

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

Diazoxide

A

. Opens ATP-sensitive K channels to hyperpolarize cell and inhibit insulin secretion

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

Adrenergic stimulation on insulin effect

A

. Stimulation of alpha 2 receptors on beta cells inhibits insulin secretion
. Overexpression of alpha 2 receptors can cause DM II
. Inhibition by catecholamines is thought to protect against hypoglycemia in exercise

22
Q

Pattern of insulin secretion

A

. Biphasic
. Initial rapid release attributed to release of pre-synthesized hormone
. If plasma glucose remains elevated, decline of this initial inc. is followed by slower rise in plasma insulin (synthesis of new hormone)

23
Q

Nutrients regulated by insulin

A

. Glucose primarily
. FAs
. AAs

24
Q

Only situation both glucagon and insulin are stimulated at same time

A

. High protein carb free meal

. Elevation in plasma AAs stimulates both hormones

25
Q

Somatostatin effect on insulin

A

. Inhibits it

26
Q

Overall effect of insulin

A

Lower plasma glucose, AA, and FA concentrations

27
Q

Insulin interaction w/ target cells

A

. Insulin receptor composed of alpha and beta subunits
. Alpha assoc. w/ autophosphorylation of Tys kinase on intracellular site on beta subunit
. TRK phosphorylated other proteins in cells to activate or inactivate metabolic enzymes
. Some tissues has insulin modulating intracellular conc. Of other second messengers (cAMP, inositol phosphate (IP3), and DAG

28
Q

Triglyceride synthesis

A

. Promoted by insulin
. Glucose uptake into adipose
. Activates TAG synthesis enzymes and inhibits Hormone-sensitive lipase (HSL)
. Induces synthesis of lipoprotein lipase that is exported from adipocytes to endothelial cell

29
Q

Lipoprotein lipase

A

. Catalyzes hydrolysis fo TAGs releasing FFAs for entry into adipose tissue
. Inhibited by insulin in muscle bc those FFAs are immediately oxidized for fuel when freed

30
Q

Effects of insulin on protein

A

. Inc. uptake of AAs via active transport in target tissues
. Stimulates protein synthesis and dec. level AA in plasma
. Protein synthesis also inc. by transcription stimulation
. Insulin inhibits proteolysis to reduce protein breakdown and inhibit gluconeogenesis in liver
. Makes insulin an anabolic hormone

31
Q

How insulin is helpful in treating hyperkalemia

A

. Stimulates NA-K ATPase and cellular uptake of PO4 and Mg from extracellular fluid
. When insulin is given w/ glucose it stimulates K transport into cells lowering plasma K conc.
. Lowers cell excitability

32
Q

Are glucagon cells inhibited by insulin release?

A

Yes

33
Q

Insulin metabolism

A

. Liver and kidney
. Half is extracted and degraded and never reaches systemic circulation
. Of circulating insulin, 4-% is filtered by kidneys and then degraded in tubular cells so very little is actually excreted
. Half life is 5 to 8 minutes

34
Q

Glucagon synthesis

A

. Synthesized as large precursor molecule that is cleaved to active molecule before storage
. Released by Ca-induced exocytosis of large dense-core vesicles
. Initiated by Ca-sensing protein synaptotagmin-7
. Once in circulation the glucagon is not bound to plasma protein

35
Q

Glucagon mechanism of action

A

. Interacts w/ plasmalemal receptor to release. cAMP that mediates biological effect on target cells

36
Q

Glucagon effect on carb metabolism

A

. Wants to inc. bloody lucose
. Inhibition of glycogen synthesis and stimulation of glycogenolysis and stimulation of hepatic gluconeogenesis
. Glucagon has little to no effect on glucose use in peripheral tissues

37
Q

Glucagon effect in fat metabolism

A

. Minimal effects on adipose tissue
. May act on adipose when glucagon is very high (insulin deficiency) to stimulate lipolysis
. In liver: directs FAs toward beta-oxidation and ketogenesis

38
Q

Glucagon effect on protein metabolism

A

. Stimulation of AA uptake by liver and conversion of AA into glucose

39
Q

Glucagon secretion regulation

A

. Dec. in plasma glucose conc. Stimulates it (70 mg/dl)
. Arg stimulates both glucagon and insulin to prevent hypoglycemia following insulin stimulation by high protein meal
. PNS via ACh stimulates insulin and glucagon as do gastrin, pancreozymin, cholecystokinin, and gastric inhibitory peptide
. Somatostatin inhibits it
. Insulin secretion directly inhibits it

40
Q

Glucagon metabolism

A

. In liver and kidney
. 50% released from pancreas is removed by liver never reaching systemic circulation
. Circulating glucagon is filtered and metabolized by kidney and no glucagon is excreted in urine
. Plasma half life is short (5 min)

41
Q

Insulin:glucagon ratio

A

. Ratio in plasma is most important determinant of overal metabolic state
. High ratio: insulin dominates
. Lower ratio: glucagon dominants

42
Q

Counter-regulatory hormones to insulin

A

. E, cortisol, and GH
. Similar to glucagon
. Inc. plasma glucose
. Play role in control during starvation, stress, and exercise

43
Q

What does epinephrine stimulate metabolically?

A

. Gluconeogenesis
. Glycogenolysis
. Inhibition of insulin-dependent glucose uptake

44
Q

What goes growth hormone stimulate metabolically?

A

. Gluconeogenesis
. Protein breakdown
. Inhibition of insulin-dependent glucose uptake

45
Q

What does cortisol stimulate metabolically?

A

. Gluconeogenesis
. Protein breakdown
. Inhibition of insulin-dependent glucose uptake

46
Q

DM I

A 
. No or almost no insulin secretion 
. Onset in childhood
. 10-50% total diabetes
. Beta-cells destroyed 
. Not usually obese
. Genetic factors are involved 
. Rapid symptom development, start when over 90% of beta cells are destroyed
. Complete destruction seen when there is absence fo C-peptide in serum  
. Presence of ketoacidosis if untreated 
. Treatment: insulin and diet
47
Q

DM II

A

. Insulin is normal ,elevated, or dec.
. Onset in adulthood usually
. 80-90% total diabetics
. Caused by reduced sensitivity of target cells to insulin
. Yes obese
. Yes genetic/environmental factors involved
. Slow development of symptoms
. Rarely have ketoacidosis
. Treatment: weight loss, diet, oral medication

48
Q

Effect of inadequate insulin on carbs

A

. Glucose uptake in insulin-dependent tissue is depressed and glycogen synthesis is inhibited
. Glycogenolysis and gluconeogenesis are enhanced in liver
. Blood glucose conc. Inc. and eventually appears in urine
. Presence of glucose in tubular filtrate will osmotically slow water and electrolyte reabsorption producing diuresis that can result in severe dehydration and hypotension

49
Q

Inadequate insulin effect on protein

A

. Dec. AA uptake and protein synthesis in mm.
. Overall catabolic state produced
. Plasma levels AA rise and provide fuel for gluconeogenesis in liver and ketone formation
. Protein degradation inc. excretion of urinary N and produces neg. nitrogen balance

50
Q

Inadequate insulin effect on lipids

A

. Dec. TAG synthesis and enhances TAG lipase activity in adipose that inc. FAs in blood
. Liver converts FAs to triglyceride (hyperlipidemia) and ketones that can result in ketonemia, ketouria, and ketoacidosis
. Assoc. w/ mild hyperkalemia as intracellular K and extracellular H exchange places, but this can cause an overall. K deficit as extra K in plasma is excreted due to osmotic diuresis

51
Q

Metabolic syndrome

A 
. Abdominal obesity
. Inc. TAGs
. Dec. HDL
. presence of small dense LDL
. Inc. bp 
. Insulin resistance
. Inc. coagulability

Physio (62 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions