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Physiology > Energy Balance/Metabolism (Day 2) > Flashcards

Energy Balance/Metabolism (Day 2) Flashcards

1
Q

What is the primary control mechanism of metabolism?

A

endocrine system

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2
Q

Endocrine cells in ____ secrete _____ and ____

A

pancreas

insulin and glucagon

a-cells: secrete glucagon
b-cells: secrete insulin

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3
Q

What happens to insulin during a meal?

A

Fasting: decreased glucose, decreased insulin, increased glucagon

Fed: increased glucose, increased insulin, decreased glucagon

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4
Q

What happens during the anabolic state?

A

Fed state: INSULIN dominates

Increased:
glucose uptake
glycogenesis
glycolysis
lipogenesis
TG storage
protein synthesis
Decreased: 
BG 
glycogenolysis
gluconeogenesis
FA oxidation
TG hydrolysis
protein catabolism
ureogenesis
ketogenesis
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5
Q

What happens during the catabolic state?

A

Fasting/starving state: GLUCAGON dominates

Increased:
BG
glycogenolysis
gluconeogenesis
FA oxidation
TG hydrolysis
protein catabolism
ureogenesis
ketogenesis
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6
Q

What stimulates insulin release?

A
  • increased plasma glucose
  • increased plasma AAs
  • incretin release from SI (in response to CHO coming in)
  • parasympathetic, vaguely-mediated reflexes originating in liver
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7
Q

What inhibits release of insulin?

A
  • sympathetic stimulation: norepinephrine (ex. fight or flight)
  • stress: epinephrine, cortisol from adrenal gland (fasting = form of stress)
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8
Q

Cellular mechanisms of insulin action

A
  1. insulin binds to receptor w/tyrosine kinase activity
  2. phosphorylation-mediated activation of IRSs
  3. coupled to diverse array of signal transduction cascades
  4. increased glucose uptake/utilization, increase expression of anabolic genes
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9
Q

How does insulin activate glucose uptake?

A

by inducing translocation of GLUT4 to cell membrane

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10
Q

What stimulated glucagon release?

A
  • decreased plasma glucose
  • increased plasma AAs (ex. if dietary protein increases, but dietary glucose decreases)
  • increased sympathetic activity
  • increased epinephrines release from adrenal
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11
Q

What inhibits glucagon release?

A
  • increased plasma glucose
  • increased parasympathetic activity
  • increased plasma insulin
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12
Q

Cellular mechanisms of glucagon action

A

Receptor couple to GTP binding protein

  1. activated AC produces cAMP
  2. cAMP produces PK (protein kinase)
  3. PK phosphorylates P’ase kinase (activation) and glycogen synthase (inactivation)
  4. P’ase kinase phosphorylates glycogen phosphorylase (activation
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13
Q

Diabetes

A

dysfunctional hormonal control of metabolism
–> characterized by a chronic, persistent catabolic state (body thinks it’s starving)

Hyperglycemia due to inadequate insulin secretion, decreased response to insulin, or both

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14
Q

How do we Dx diabetes?

A

Measure:

  1. fasting levels of glucose in plasma
  2. kinetics of glucose removal after defined oral glucose load –> glucose tolerance test
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15
Q

Gut Microglora

A

largest population of microbes in body

-play a regulatory role in metabolic/immune pathways: interactive host-microbiota metabolic, signaling, immune-inflammatory axes connecting gut/liver/muscle/brain

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16
Q

How do artificial sweeteners affect glucose?

A

they induce glucose intolerance by altering gut microbiota

17
Q

Diabetes Type 1

A

• formerly called juvenile-onset diabetes
• most severe form
• failure of pancreatic β-cells to produce/release insulin
• Incompletely understood autoimmune destruction of β-cells,
associated with genetic and/or environmental factors
• treatment: exogenous administration of insulin—resolves gluco-
regulation, but other complications (e.g. peripheral vascular disease) persist

18
Q

Diabetes Type 2

A

• formerly adult-onset diabetes, now insulin-resistant diabetes
• accounts for about 90% of cases of diabetes worldwide
• precise cause uncertain, but is associated with obesity-induced inflammation
• progressive: insulin resistance in target cells –> compensatory
hypersecretion of insulin –> eventual loss of β-cell function
• tissues with most prominent insulin resistance: skeletal muscle, liver, adipose

19
Q

Diabetes Consequences

A
  • muscle protein breakdown
  • ketoacidosis
  • hyperglycermia
  • increased thirst
  • overeating
  • glucosuria
  • dehydration
  • microvascular disease
  • macrovascular disease
  • myocardial dysfunction
20
Q

Insulin resistance –> T2D

A

partly a response to obesity-induced inflammation originating from adipose tissue under conditions of increasing fat content

21
Q

Obesity-induced inflammation compromises…

A

compromises insulin-dependent processes throughout body

22
Q

Obesity/insulin-resistance can produce…

A

can produce significant derangements in body lipid/lipoprotein metabolism –> CV disease or athlersclerosis

23
Q

What is a lipoprotein?

A

Large complex of lipid and proteins which serve as the transport vehicles for lipids (TG, cholesterol, cholesterlyl esters)

  1. chylomicrons
  2. VLDL
  3. IDL, LDL
  4. HDL
24
Q

Chylomicrons

A

produced by/released by intestine

transports dietary lipids in body - INCREASED TG

25
Q

VLDL

A

produced by liver

transports endogenous lipids - INCREASED TG

26
Q

IDL, LDL

A

derived from VLDL during it’s plasma passage/metabolism

transport cholesterol to periphery - INCREASED CHOLESTEROL

27
Q

HDL

A

precursor produced by liver, picks up cholesterol from peripheral tissues, transports it to liver

“reverse cholesterol transport” - INCREASED CHOLESTEROL

28
Q

Lipoprotein metabolism

A

healthy state depends on high HDL/low LDL

low HDL/high LDL = atherosclerosis

29
Q

Dysfunctional lipoprotein metabolism can lead to atherosclerosis

A

Insulin resistance:

  1. promotes VLDL production/secretion from the liver
  2. decreases expression of liver LDL receptor (increased production/decreased disposal)
    - -> increased VLDL in plasma = increased TG and increased LDL
  3. decreases plasma HDL
30
Q

What is athersclerosis cause by?

A

elevated LDL –> increased amounts taken up in artery walls

excess LDL taken up by blood vessels –. lipid deposition in arty walls –> chronic inflammation

31
Q

Metabolic Syndrome

A

cluster of risk factors for diabetes and CV disease

Physiology (29 decks)

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