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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

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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

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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

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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

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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

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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

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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

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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.
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9
Q

Brain fuel in extreme prolonged starvation

A

. Ketones: b-hydroxybutyrate and acetoacetate

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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

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11
Q

Protein in post-absorptive state

A

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

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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

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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

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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

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15
Q

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

A

. 50-75 days

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16
Q

Cells in islets of langerhans

A

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

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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

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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

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19
Q

Sulfonylurea drugs

A

. Close ATP-sensitive K channels to stimulate insulin secretion

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20
Q

Diazoxide

A

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

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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
Somatostatin effect on insulin
. Inhibits it
26
Overall effect of insulin
Lower plasma glucose, AA, and FA concentrations
27
Insulin interaction w/ target cells
. 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
Triglyceride synthesis
. 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
Lipoprotein lipase
. 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
Effects of insulin on protein
. 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
How insulin is helpful in treating hyperkalemia
. 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
Are glucagon cells inhibited by insulin release?
Yes
33
Insulin metabolism
. 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
Glucagon synthesis
. 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
Glucagon mechanism of action
. Interacts w/ plasmalemal receptor to release. cAMP that mediates biological effect on target cells
36
Glucagon effect on carb metabolism
. 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
Glucagon effect in fat metabolism
. 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
Glucagon effect on protein metabolism
. Stimulation of AA uptake by liver and conversion of AA into glucose
39
Glucagon secretion regulation
. 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
Glucagon metabolism
. 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
Insulin:glucagon ratio
. Ratio in plasma is most important determinant of overal metabolic state . High ratio: insulin dominates . Lower ratio: glucagon dominants
42
Counter-regulatory hormones to insulin
. E, cortisol, and GH . Similar to glucagon . Inc. plasma glucose . Play role in control during starvation, stress, and exercise
43
What does epinephrine stimulate metabolically?
. Gluconeogenesis . Glycogenolysis . Inhibition of insulin-dependent glucose uptake
44
What goes growth hormone stimulate metabolically?
. Gluconeogenesis . Protein breakdown . Inhibition of insulin-dependent glucose uptake
45
What does cortisol stimulate metabolically?
. Gluconeogenesis . Protein breakdown . Inhibition of insulin-dependent glucose uptake
46
DM I
``` . 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
DM II
. 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
Effect of inadequate insulin on carbs
. 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
Inadequate insulin effect on protein
. 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
Inadequate insulin effect on lipids
. 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
Metabolic syndrome
``` . Abdominal obesity . Inc. TAGs . Dec. HDL . presence of small dense LDL . Inc. bp . Insulin resistance . Inc. coagulability ```

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