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Physiology > Metabolism > Flashcards

Metabolism Flashcards

0
Q

Insulin’s Job

A

store fuel

lower blood glucose

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1
Q

Fuel homeostasis

A

not a constant b/c supply & demand change.

must have the right amount of fuel to live well.

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2
Q

Glucagon, Epinephrine, Growth Hormone, & Cortisol’s Job

A

increase blood glucose

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3
Q

How is metabolism regulated?

A

locally and hormonally

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4
Q

Local Metabolism Regulation

A

serves needs of individual cells

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5
Q

Hormone Metabolism Regulation

A

defends entire organism

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6
Q

Energy Expenditure

A
  • Basal metabolic rate (minimal amt): 60-70%
  • Dietary thermogenesis (food intake) & obligatory thermogenesis (maintaining body temp) = 5-15%
  • Physical Activity = 20-30%
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7
Q

What can alter metabolic rate?

A

disease, growth, aging, pregnancy, lactation

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8
Q

What determines utilization of different nutrients?

A

cell’s needs and capabilities

ex: cells w/ few-no mitochondria can’t use AA & FFA & must use anaerobic glycolysis

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9
Q

Brain and Heart do not

A

store energy

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10
Q

Brain requires

A

glucose & can use ketones (doesn’t like to though)

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11
Q

Heart requires

A

glucose & can use FAs & ketones

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12
Q

Glucose is exported only from

A

the liver! (some from kidneys though)

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13
Q

Mechanisms by which liver can give off glucose

A
  • gluconeogenesis (make glucose)

- release glucose from glycogen (fastest way)

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14
Q

Where are most of the body’s energy reserves?

A

fat

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15
Q

Brain & glucose

A
  • obligate glucose user
  • doesn’t require insulin
  • requires glucose concentration gradient
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16
Q

4 Metabolic Phases

A

Digestive, Interdigestive, Fasting, Strenuous

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17
Q

Key inputs to making ATP

A

glucose, FFA, AA, Ketones

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18
Q

What are the key fuel storage forms?

A

Glycogen, AA, Fat

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19
Q

Glucose is

A

major final conversion product of carb. metabolism

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20
Q

Glucose Transport into cells

A

by GLUTs (Na independent facilitated diffusion)

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21
Q

GLUTs are

A

2-way glucose transporters based on gradients

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22
Q

Glucose transport across cell mem. vs. Glucose transport in GIT/kidney

A

DIFFERENT

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23
Q

Glucose Uptake

A

greatly influenced by [insulin] present

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24
Q

Glucose Trapped in cell by

A

hexokinase or glucokinase

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25
Q

glucokinase location

A

liver or pancreatic B cells

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26
Q

Hexokinase location

A

not in liver or pancreatic B cells

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27
Q

Glycolysis

A

Conversion of glucose into pyruvate for storage

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28
Q

liver enzymes involved in glycolysis’ irreversible reactions

A

glucokinase, phophofructokinase, pyruvate kinase

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29
Q

Gluconeogensis

A

must circumvent the 3 irreversible reactions of glycolysis

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30
Q

Local Glycolysis Regulation

A
  • high levels of low energy substrate locally stimulate glycolysis
  • high levels of ATP, substrate, or end products of glycolysis inhibit it
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31
Q

Hormonal Glycolysis Regulation

A

Insulin & Glucagon

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32
Q

Insulin promotes glucose storage by

A

stimulating ^ in making glucokinase, phosphofructokinase, & pyruvate kinase => conversion

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33
Q

Glucagon promotes use of glucose by

A
  • decreasing formation of glucokinase, phophofructokinase, and pyruvate kinase in fasting phase or diabetes 1
  • it mobilizes glucose to ^ blood [glucose]
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34
Q

Where is the most ATP made from glucose?

A

when it’s metabolized through TCA & os. phos.

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35
Q

Where is the least ATP made from glucose?

A

glucose metabolized to lactate (anaerobic)

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36
Q

FFA release

A

hormone sensitive lipase catalyze release of FFA from TAG (triglycerides)

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37
Q

Hormone Sensitive Lipase Activators

A

catecholamines, glucagon, cortisol, growth hormone

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38
Q

hormone sensitive lipase inhibitor

A

insulin

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39
Q

insulin stimulates

A

lipoprotein lipase

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40
Q

how are FA’s stored in fat?

A

TAGs/triglycerides

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41
Q

Pathways for FFA in hepatocyte

A
  1. Complete oxidation for energy
  2. Formation of triglyceride
  3. Ketone body production
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42
Q

FFA utilization

A
  1. FFA released by lipolysis & enter circulation bound to albumin
  2. FFA enter mitochondria via CARNITINE
  3. FFA undergo B-oxidation to yield ACoA or ketones
  4. TCA
  5. Ox. Phos.
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43
Q

AA utilization

A
  1. Transamination (in liver)
  2. Conversion to intermediates in TCA, ACoA, or pyruvate
  3. TCA
  4. Ox. Phos.
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44
Q

Types of AA

A

Glucogenic

Ketogenic

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45
Q

Ketone Body Utilization

A

Ketones made in liver & exported to circulation/used by tissues for energy by conversion to ACoA -> TCA -> ox. phos.

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46
Q

Where can ketones not be used?

A

liver

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47
Q

ketoacidosis

A

excessive ketone body production (occurs often w/ diabetes)

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48
Q

When are ketones formed?

ketogenesis

A

during starvation or excessive ACoA formation (with imbalance b/n flow of FFA into liver & TCA capacity to use AcCoA) or TCA is inhibited

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49
Q

3 Ketone Bodies

A

Acetoacetate, 3-Hydroxybutyrate, Acetone

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50
Q

Acetoacetate ->

A

dissociates into acetoacetic acid

metabolizable

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51
Q

3-Hydroxybutyrate ->

A

dissociates into betahydroxybutyric acid

metabolizable

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52
Q

acetone is

A

non-metabolizable.

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53
Q

Lactate formation

A
  • in anaerobic conditions

- uses both products of glycolysis so glycolysis can continue w/o O2

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54
Q

Lactate converted back to pyruvate…

A

when aerobic conditions exist (locally or in liver) with energy usage

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55
Q

Cori Cycle

A

lactate from exercising muscle goes to liver & is converted to glucose which enters blood to feed brain

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56
Q

Blood lactate levels and emergency medicine

A

lactate levels measured as indicator of prognosis or response to therapy

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57
Q

TCA Cycle

A
  • mechanism for converting carbs, FA, & AA into USEABLE ENERGY
  • occurs in mitochondria
  • need O2
  • makes FADH2 & NADH
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58
Q

Oxaloacetate

A

important TCA intermediate used to make glucose w/ ATP

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59
Q

Important Step b/n Glycolysis & TCA

A

Pyruvate -> ACoA

by pyruvate dehydrogenase complex. thiamine required

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60
Q

TCA Regulation

A
  • local reg. only
  • ATP & reaction products inhibit
  • low energy phosphates & substrates stimulate it
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61
Q

Oxidative Phosphorylation

A
  • occurs in mitochondria
  • requires O2, NADH, FADH2,
  • makes the most ATP
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62
Q

What are the body’s energy stores?

A

Glycogen, Gluconeogenesis, Triglycerides (fat), protein

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63
Q

Glycogen location

A

liver & muscle

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64
Q

Where does blood glucose come from?

A

diet, gluconeogenesis (slow), and glycogenolysis (rapid)

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65
Q

Which glycogen storage organ shares?

A

ONLY liver

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66
Q

Liver glycogen

A

maintains blood glucose levels

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67
Q

muscle glyogen

A

fuels muscle activity

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68
Q

What happens if liver is at max. glycogen storage?

A

excess glucose become FA

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69
Q

Local Glycogen regulation

A
  • build up of glucose promotes glycogen synthesis & inhibits glycogenolysis
  • high [ATP] inhibit glycogenolysis
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70
Q

Hormonal Glycogen regulation

A
  • insulin promotes glycogen synthesis

- glucagon & epinephrine promotes glycogenolysis

71
Q

glycogenolysis

A

glycogen breakdown

72
Q

Gluconeogenesis

A

-formation of moderate amounts of glucose in liver
(longer than glycogenolysis)
-requires energy to bypass irreversible steps

73
Q

Gluconeogenesis occurs because

A
  • glucagon ^ PEPCK synthesis & decreases Pyruvate Kinase synthesis
  • low insulin favors AA mobilization and fat catabolism to provide intermediates & fuel for it
74
Q

Gluconeogenesis Stimuli

A
  • low carb stores
  • low blood glucose levels
  • release of glucocorticoids from adrenal CORTEX
  • release of catecholamines (ep, norep)
75
Q

Gluconeogenesis substrates

A

-OAA (oxaloacetate)
-Glycerol
-Lactate
-AA carbon skeletons
(ruminants = proprionate)

76
Q

Fats travel through circulation as

A

lipoprotein or chylomicrons

77
Q

Lipoprotein Lipase

A

releases FAs & glycerol to adipose tissue, sk. m. or cardiac m.

78
Q

Liver & fat processing

A

it isn’t fast at processing fat

79
Q

When can fat accumulation in liver occur?

A

when lipoprotein formation is impaired

80
Q

Protein as energy substrate

A

no a preferred source of energy long term

only used in survival mode

81
Q

Key hormones involved in metabolism

A

insulin, glucagon, epinephrine, norepinephrine, & their actions

82
Q

Main players in fuel homeostatis

A

brain, liver, sk. m., & fat

83
Q

brain requires

A

constant availability of glucose from blood

84
Q

Goal of Glucagon, Catecholamines, Cortisol, & Growth hormone

A

to mobilize fuel (catabolism)

85
Q

Insulin’s Goal

A

to store fuel & promote anabolism

86
Q

Endocrine Pancreas Islets contain

A

alpha, beta, and delta cells

87
Q

alpha cells release

A

glucagon

88
Q

beta cells release

A

insulin

89
Q

delta cells release

A

somatostatin

90
Q

Insulin controls

A

upper limit of blood glucose & FFA levels

91
Q

How does glucose limit upper level of blood glucose & FFA levels?

A

metabolic effects on carbs & lipid metabolism & protein synthesis

NET effect: reduced blood glucose & FFA levels (promotes storage) & promotes protein synthesis

92
Q

Consequences of no Insulin

A

Severe hyperglyemia & Dyslipidemia

Diabetes Mellitus

93
Q

Insulin & Carb Metabolism

A

^ glycogen synthesis, glycolysis, and # of GLUTs (^ glucose uptake)
inhibits glycogenolysis, gluconeogenesis

94
Q

Insulin & Lipid Metabolism

A

inhibits hormone sensivitive lipase
+ lipoprotein lipase

NET: decreased circulating FFA levels

95
Q

Insulin and Protein Synthesis

A

+ AA uptake, activates transcription factors that promotes protein synthesis

96
Q

Insulin secretion stimulated by:

A
  1. Glucose

2. AA, FFA, Ketoacids, K, Parasympathetic ns, GI hormones

97
Q

Insulin secretion inhibited by

A

fasting, exercise, sympathetic ns.

98
Q

Why is K included on the list of Insulin secretion stimuli?

A

because when insulin & dextrose are given to an animal with high [K], the insulin will bring down blood [K] and save the animal

99
Q

Insulin is what type of hormone?

A

PROTEIN!

100
Q

implications of insulin being a protein hormone

A
  • must be injected

- must not be heated or shaken too much or it’ll be denatured

101
Q

What degrades insulin?

A

insulinase enzyme in liver, kidney, & other tissues

102
Q

Fact about insulin release

A

it isn’t constant but is oscillating

-meaning must test levels over time & for administration times

103
Q

How are exogenously administered insulins categorized?

A

by onset of activity and duration of effect

104
Q

Glucagon hormone type

A

peptide

105
Q

Glucagon’s primary purpose

A

counter-regulatory hormone to insulin

106
Q

Glucagon prevents

A

hypoglycemia during a fast

107
Q

Glucagon & Carb Metabolism

A

decrease glycogen synthesis, glycolysis
^ glycogenolysis, gluconeogenesis

(^ glucose production)

108
Q

Glucagon & Lipid Metabolism

A

+ lipolysis, uptake of FFA

- TAG synthesis

109
Q

Glucagon & Protein Synthesis

A

^ AA uptake in liver (aka more fuel for gluconeogenesis)

110
Q

Glucagon stimulated by

A
  1. Low Glucose & Sympathetic N.S.

2. AA & exercise

111
Q

Glucagon inhibited by

A

insulin

112
Q

Epinephrine & Norepinephrine released in response to

A
  • stress
  • hypoglycemia
  • exercise
113
Q

hypoglycemia is sensed by

A

hypothalamus which initiates sympathetic response

114
Q

Norepinephrine released from

A

adrenal medulla and postgang. sympathetic neurons

115
Q

Epinephrine released from

A

adrenal medulla

116
Q

Sympathetic innervation to pancreas can cause

A

glucagon release regardless of blood glucose levels

117
Q

Norepinephrine & Epinephrine effects

A
  • direct metabolic ones
  • stimulating glucagon release
  • inhibiting insulin
118
Q

Insulin decreases

A

glycogenolysis, gluconeogenesis, ketogenesis, lipolysis

119
Q

Glucagon & Epinephrine increase

A

glycogenolysis, gluconeogenesis, ketogenesis, lipolysis

120
Q

Hypoglycemia

A

occurs when blood [glucose] falls below acceptable levels

121
Q

Body’s reaction to Hypoglycemia

A

hypothalamus senses it => sympathetic response => ep. & norep. release => glucagon release (direct/indirect form) => cortisol release => blocks insulin

122
Q

Hypoglycemia Symptoms

A
  • early: related to adrenergic stimulation (hungry, grumpy, ^ Heart rate, sweating)
  • profound: weakness
  • severe: seizures, coma, death
123
Q

Clinical Examples of Hypoglycemia

A
  • insulinoma

- insulin overdose

124
Q

hypoglycemia range

A

can normally be large

125
Q

Insulinoma (tumors) treatment options

A

-surgery, prednisolone (^ blood sugar when it remains low), insulin blocking drug

126
Q

Pancreatic Somatostatin

A

peptide hormone made in pancreas, hypothalamus, & gut

127
Q

Somatostatin inhibits

A

insulin & glucagon

128
Q

Somatostatin’s actions

A

decrease GI absorption, secretion, motility, & assimilation of nutrients

129
Q

Somatostatin stimulated by

A

glucose, AA, FFAs glucagon, GI hormones, sympathetic stimulation

130
Q

Suggested Role of Somatostatin

A

to ^ time period over which food nutrients are assimilated into blood & to decrease rate of utilization

131
Q

Absorptive/Fed State

A

high [insulin], high insulin:glucagon ratio

132
Q

Organ with biggest role in fed state =

A

liver!

133
Q

Why does the liver the biggest role in the fed state?

A

it serves a the nutrient distribution center after meal

134
Q

Liver in Fed State

A
  • not insulin dependent BUT insulin sensitive which stimulates glucokinase
  • ^ glucose uptake, glycogen synthesis, glycolysis, FA synthesis, TAG synthesis, AA degredation
  • decrease gluconeogenesis & no maintenance of large protein stores
135
Q

Excess of anything is

A

converted to fat!

136
Q

Fat in Absorptive/Fed State

A

-^ Glucose uptake, glycolysis, FA synthesis, TAG synthesis,

137
Q

In the fed state, insulin does ___ in fat

A
  • promotes lipoprotein lipase expression

- suppresses hormone sensitive lipase activation

138
Q

in fed state, fat ____ share

A

doe not

139
Q

Skeletal M. in Absorptive/Fed State

A

^glucose uptake, glycogen synthesis, AA uptake & protein synthesis
-does NOT uptake fat

140
Q

In fed state, skeletal muscle _____ share

A

does NOT

141
Q

preferential energy source for skeletal m in fed state

A

glucose

142
Q

Brain in Absorptive/Fed State

A
  • Glucose uptake isn’t insulin dependent
  • no glycogen, TAG stores
  • protein bound FA can’t cross blood-brain barrier
143
Q

Brain ____ shares

A

NEVER!

it is selfish

144
Q

Fasting State

A

low insulin

low Insulin:glucagon ratio

145
Q

The fasting state mobilizes

A

glucagon

146
Q

the fasting state sets into motion an

A

exchange of substrates among liver, brain, sk. m., & fat

147
Q

The exchange of substrates in the fasting state is guided by what 2 priorities?

A
  1. Maintain blood glucose levels

2. Mobilize energy stores (fat = most important)

148
Q

Liver’s Primary Goal in the Fasting State

A

maintenance of blood glucose

the ONLY organ that does this!

149
Q

Liver in the fasting State

A

^ Glycogen degradation, gluconeogenesis, FA oxidation, Ketone body production

150
Q

ketone body production

A
  • unique to liver

- ketones = fuel for peripheral tissues but not liver

151
Q

During Fasting, the liver only exports

A

ketone bodies and glucose

152
Q

Adipose in Fasting State

A
  • decreases glucose uptake, lipoprotein lipase activity

- ^ TAG degradation to release FFA into blood, hormone sensitive lipase activity

153
Q

Hormone Sensitive Lipase

A

degrades TAGs & decreases glucose absorption

154
Q

FFA aren’t reuptaken by adipose when in circulation in fasting state because

A

insulin is low therefore lipoprotein lipase activity is decreased

155
Q

Skeletal M. in Fasting State

A
  • decreased glucose uptake
  • ^protein degradation (which ^ even more if cortisol is high)
  • can use ketones and FFA for energy
  • sacrifices glucose so brain can have it
156
Q

Brain in the fasting state

A
  • doesn’t change from fed state except it will use ketones if absolutely necessary
  • glucose = preferred fuel
  • relies on blood glucose
157
Q

Brain’s use of ketones slows

A

the need for protein breakdown of muscle to fuel gluconeogenesis

158
Q

Diabetes

A

metabolic disease due to an absolute or relative deficiency of insulin (or both)

159
Q

Absolute Insulin deficiency

A

not enough insulin produced

160
Q

Relative insulin deficiency

A

cells aren’t responsive to insulin produced

161
Q

Clinical signs of Diabetes

A

polyuria/polydipsia, weight loss, polyphagia, hyperglycemia, glucosuria, hyperlipidemia, catabolic effect, ketoacidosis, blindness, neuropathy

162
Q

Type 1 Diabetes

A
  • BETA cells are destroyed (no insulin made)
  • low levels of insulin
  • insulin therapy needed
  • undernourishment & ketosis
  • more common in dogs
163
Q

Type 2 Diabetes

A
  • Insulin resistance
  • high levels of insulin at first & cells become unresponsive to insulin
  • associated with obesisty
  • may respond to diet & exercise
  • usually not associated with ketosis
  • more common in cats
164
Q

Cats with diabetes

A
  • different than dogs with diabetes

- can restore their insulin

165
Q

Equine Metabolic Syndrome Characteristics

A
  • Obesity or regional adiposity
  • Insulin resistance (high [insulin]) which causes ->
  • Laminitis

& thyroid levels may be low

166
Q

Equine Metabolic Syndrome can occur with

A

Cushings

167
Q

General Treatment Options of Uncomplicated Diabetes

depends on species & diabetes type

A

insulin, oral hypoglycemic drugs, diet, weight management, exercise, address underlying conditions, monitoring

168
Q

Somogyi Phenomenon

A

rebounding high blood sugar that is responsive to low blood sugar
(one reason blood glucose curves are important)

169
Q

Somogyi Phenomenon occurs due to

A
  • insulin overdose

- counterregulatory hormones responding to insulin overdose

170
Q

Major counterregulatory hormones involved in the Somogyi Phenomenon

A

Glucagon, Epinephrine, Cortisol

171
Q

Diabetic Ketoacidosis is seen more with

A

Type 1 diabetes

172
Q

Clinical Signs of Diabetic Ketoacidosis

A

Ketonemia, Ketonuria, Metabolic acidosis, diabetes symptoms, depressing, vomitting, anorexia, fluid & electrolyte disturbances

*may be due to concurrent diseases

173
Q

Types of Fluid & Electrolyte Disturbances in Diabetic Ketoacidosis

A

hyponatremia, hypokalemia, hypovolemia, hyperosmolarity (if glucose is high enough)

174
Q

Insulin, Glucagon, & Epinephrine in Diabetic Ketoacidosis

A
  • Greater imbalance between Insulin & others.
  • less insulin & much more counter-regulatory hormones present
  • no insulin for cells to uptake glucose to get energy
175
Q

During exercise, what happens to these hormones?

A

glucagon increases, insulin decrease, catecholamines increase

Physiology (10 decks)

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