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ACVIM SAIM (2023) > Metabolism > Flashcards

Metabolism Flashcards

1
Q

90-95% of serum copper is bound to __

A

Ceruloplasmin

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2
Q

What enzymes are copper an integral part of (co-factor)?

A

Superoxide dismutase
cytochrome-c oxidase
lysyl oxidase
tyrosinase
monoamine oxidase

transported from the liver bound with ceruloplasmin

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3
Q

Most iron in the body is in the form of __

A

Hemoglobin

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4
Q

There are __ iron atoms per molecule of hemoglobin

A

4

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5
Q

__ is secreted in bile that aids in iron absorption

A

Apotransferrin

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6
Q

Where is iron absorbed?

A

Small intestine - absorption is slow

If a large quantity is ingested, only a small amount is absorbed and the rest will be excreted

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7
Q

Apotransferrin in bile reaches the duodenum via the __

A

Bile duct

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8
Q

Apotransferrin binds to free iron to form __

A

Transferrin

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9
Q

How does transferrin reach plasma?

A

Ferric iron (Fe3+) converted to Ferrous iron (Fe2+) by duodenal cytochrome B

Ferrous iron taken into duodenal epithelial cells by DMT1 synporters (also bring in an H+ ion)

Inside the cell, ferrous iron binds to apoferritin to form ferritin for storage, or will be exported into the bloodstream via ferroportin

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10
Q

What molecule binds ferrous iron in the blood for transport?

A

Apotransferrin

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11
Q

Where in the body is excess iron deposited for storage?

A

Liver
Bone marrow

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12
Q

The majority of iron in cells is stored in what form?

A

Ferritin

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13
Q

Small quantities of iron are stored in the insoluble form known as __

A

Hemosiderin

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14
Q

Apotransferrin is made in the __ and transported in __

A

Made in the liver, transported in bile

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15
Q

What are the positive acute phase proteins?

A

C-reactive protein
Serum amyloid A
Haptoglobin
Alpha-1-acid glycoprotein
Ceruloplasmin
Ferritin
Hepsidin
Alpha-2 macroglobulins
Fibrinogen

Major in dogs: SAA, C-RP

Major in cats: SAA +/- haptogloglobin

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16
Q

What are negative acute phase proteins?

A

Albumin
Transferrin

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17
Q

Total iron binding capacity (TIBC) is a DIRECT/INDIRECT measure of what?

A

Indirect measure of serum transferrin

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18
Q

Why are cats obligate carnivores?

A

They cannot synthesize arginine, it must be present in their diet and arginine is available in meat sources only

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19
Q

What are the essential amino acids in dogs and cats?

A

Acronym: PVT MATT HILL
Phenylalanine
Valine
Tryptophan
Methionine
Arginine
Threonine
Taurine (CATS)
Histidine
Isoleucine
Leucine
Lysine

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20
Q

Arachadonic acid deficiency in cats causes __

A

Insufficient platelet aggregation
Poor reproductive performance

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21
Q

What causes lipemic serum?

A

Increased triglycerides (either as chylomicrons or VDLDs)

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22
Q

Supranatant of serum may appear creamy due to

A

chylomicrons

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23
Q

If the lower part of spun serum is cloudy, that suggests

A

VLDL

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24
Q

Lipemic serum falsely increases what values

A

Bilirubin
Hemoglobin
MCH
MCHC
TP by refractometer
Platelet count

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25
Q

Lipemic serum falsely decreases what values

A

Na
Cl
K (lesser extent)

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26
Q

Which lipoprotein has the highest protein content?

A

HDL - about 50% is protein, has much smaller concentrations of cholesterol and phospholipids

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27
Q

What happens after 0-12 hours of starvation

A

Decreased insulin/glucagon ratio
Hepatic glycogenolysis supports euglycemia, but only enough stores to provide energy for ~1/2 day

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28
Q

What happens with 12-48 hours of starvation

A

Glycogen depleted at this point
Glucocorticoids and norepinephrine levels increase
Release of free fatty acids (FFA) and glycerol from fat
Release of amino acids (breakdown of branch chained aa) from muscle and utilization via hepatic gluconeogenesis

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29
Q

What happens with >48 hours of starvation

A

Induction of ketogenic enzymes
Production of ketones from FFA and protein sparing
Shift to renal gluconeogenesis using glutamine as substrate

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30
Q

Provision of calories and protein reverses starvation by __ and __

A

Restoring glycogen and adipose stores

Promoting protein anabolism

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31
Q

Enterocytes in the small intestine prefer __ as a source of metabolic fuel

A

Glutamine

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32
Q

Colonocytes prefer __ as a source of metabolic fuel

A

Butyrate

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33
Q

How is butyrate formed for use by colonocytes

A

Fermentation of luminal carbohydrates

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34
Q

What happens to the gut in the absence of fuel sources

A

Gut epithelium slows growth and replication
Mucosal billows epithelium no longer replaced

This results in mucosal atrophy, necrosis, and increased risk of bacterial translocation across abnormal gut barrier

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35
Q

Definition of hypermetabolic starvation

A

Ill or traumatized animal that is absolutely or relatively starved and has increased needs for energy

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36
Q

What are the three stages of protein depletion in starvation

A

Initial rapid protein depletion

Greatly slowed protein depletion

Rapid protein depletion shortly before death

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37
Q

What happens in initial rapid protein depletion

A

Easily mobilized proteins are used for direct metabolism or for conversion of glucose, then metabolism of glucose (mainly by the brain)

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38
Q

What happens in greatly slowed protein depletion

A

Readily mobilized protein stores have been depleted, and the remaining protein is not as easily removed which leads to slowed protein use. Gluconeogenesis will also slow down. This leads to the beginning of excessive fat utilization (ketosis). 2/3 of the brain’s energy will be derived from ketones in this state, mostly BETA-HYDROXYBUTYRATE

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39
Q

What happens in rapid protein depletion shortly before death

A

Fat stores are almost completely depleted so protein is the only remaining energy source. They enter another stage of rapid depletion. Death occurs when proteins are half their normal levels

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40
Q

After how long in starvation do vitamin deficiencies develop, and which vitamins are especially affected?

A

1 week

Water soluble vitamins like B and C are particularly affected

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41
Q

When during starvation do branched chain amino acids (leucine, isoleucine, valine) get used?

A

Final stage of rapid protein depletion before death

During starvation, muscle activity decreases, but branched chain amino acids remain in muscle cells to provide a source of energy for the muscles

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42
Q

Is refeeding syndrome more likely with high carbohydrate or high protein diets?

A

High carbohydrate

To avoid refeeding syndrome, feed a diet similar to what the body was using (fat and protein)

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43
Q

The amino acid __ is a major cofactor for the Krebs cycle and pentose phosphate pathway

A

Thiamine

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44
Q

Thiamine deficiency leads to

A

Cessation of neuronal oxidative metabolism and switch to anaerobic energy production

Buildup of lactic acid leads to myelomalacia especially of grey matter

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45
Q

What are clinical signs of thiamine deficiency?

A

Central vestibular disease
Ventroflexion in cats
Cardiac hypertrophy in dogs

46
Q

What are some causes of thiamine deficiency?

A

Feeding meat preserved with sulfites
Feeding a diet high in thiaminases (fish)

47
Q

What is the predominant fasting plasma lipoprotein in dogs?

A

VLDL

48
Q

How long is TPN good for?

A

Not good after 48 hours (refrigerated), only good for 24h outside of fridge

49
Q

Does TPN commonly increase BG?

A

Yes, mildly

50
Q

Which protein source has the lowest purine content?

A

Vegetable

(Animal has intermediate, glandular tissue has highest)

51
Q

What are some essential fatty acids in cats and dogs?

A

Linoleic acid - all mammals
Arachadonic acid - cats (deficiency leads to lack of platelet aggregation)
Gamma-linoleic
+/- alpha-linoleic, eicosapentanoic acid, docosahexonoic acid

52
Q

Two active glucose transporters and locations?

A

SGLT1 - enterocytes, renal tubular cells
SGLT2 - renal tubular cells

53
Q

Passive glucose transporters and locations

A

GLUT1 - glial cells
GLUT2 - renal tubular cells, hepatocytes, enterocytes, pancreatic beta cells
GLUT3 - neurons
GLUT4 - muscle cells, adipocytes

54
Q

Define metabolizable
energy (ME).

A

ME of a nutrient is the amount of energy available to the animal after taking into account losses from digestion (nutrients in foods are not 100% digested),
urine losses, and losses in exhalation of gases.

55
Q

Average ME for protein vs fat vs CHO in whole food vs commercial dog food?

A

Protein & CHO: 3.5kcal/g (dog food), 4kcal/g (whole food)

Fat : 8.5kcal/g (dog food), 9kcal/g (whole food).

56
Q

Recommendations for minimum dietary protein intake in working dogs?

A

22-24% ME

(25-28% or higher if maintaining muscle, extreme working envt)

57
Q

What energy sources do dogs use predominantly during low, moderate & intense exercise?

A

Exercise at </=40% of max aerobic capacity: predominantly fat (aerobic metabolism)

40-70%: CHO (from protein oxidation) & fat

> 70% (e.g. sprinting): glucose (anaerobic metabolism)

58
Q

Causes of hypercobalaminemia in dogs & cats?

A

Dogs - overall 3% incidence of high B12. DDx chronic GI signs (48%), hypoA (uncommon)
Cats - chronic enteropathy (65%), acute/chronic pancreatitis (24%), cholangiohepatopathy, gastric lymphoma (6%), hyperT (3%).

59
Q

Short chain fatty acids
- Produced by which bacteria?
- Name the main SCFAs.
- Name 5 key roles.

A

Ruminococcus, Faecalibacterium, Turicibacter - ferment dietary CHO to SCFAs.

Butyrate, acetate, propionate.

Roles:
* Nutrients
* Regulate satiety
* Anti-inflammatory properties
* Regulate intestinal motility
* Downregulate intestinal pH to create an environment that is not suitable for pH-sensitive enteropathogens.

60
Q

Dietary copper - what forms are available, and which form is recommended?

A

Copper sulfate recommended, more bioavailable vs copper oxide.

61
Q

Describe copper metabolism.

A

Copper absorption occurs in the upper SI via membrane transporters –> transported to liver in free & protein-bound forms –> uptake by hepatocytes –> added to transcriptional products, bound to metallothionein or cupriproteins for storage, OR shuttled to canaliculi for bile elimination.

62
Q

Describe roles of copper.

A

Required for function of the following metalloenzymes:
- Lysyl oxidase - essential for molecular cross-linking of collagen & elastin
- Cytochrome c oxidase - essential for electron transport chain that generates ATP –> mitochondrial energy generation
- Copper–superoxide dismutase - role in antioxidation, dismutates superoxide anions that otherwise cause oxidative damage to local protein & lipid cell constituents.

63
Q

AAFCO recommendation for minimum daily copper intake for maintenance adult dog diet?
How does this compare to prescription copper restricted diets?

A

1.83 mg/1,000 kcal = ~Cu intake of ~0.067 mg/kg/day

(0.9 to 1.1 mg/1,000 kcal, ranging from approx 0.04 to 0.07 mg/kg/d)

64
Q

What is a disadvantage of feeding a hepatic diet to dogs with copper storage/necroinflammatory liver disease vs dogs with PSS or HE? (Hint: copper & protein content)

A

Most dogs with CSH or NIH don’t have hepatic failure or HE - so protein restriction is not ideal as these patients can be expected to have heightened nitrogen turnover secondary to inflammatory cytokines & catabolism.

65
Q

What is a disadvantage of feeding a hepatic diet to dogs with copper storage/necroinflammatory liver disease vs dogs with PSS or HE? (Hint: copper & protein content)

A

Most dogs with CSH or NIH don’t have hepatic failure or HE - so protein restriction is not ideal as these patients can be expected to have heightened nitrogen turnover secondary to inflammatory cytokines & catabolism.

66
Q

Consequences of phosphorus deficiency? (Name 3)

A

Hemolytic anemia
Decreased mobility
Metabolic acidosis

67
Q

Consequences of phosphorus deficiency? (Name 3)

A

Hemolytic anemia
Decreased mobility
Metabolic acidosis

68
Q

What dietary factors may affect phosphorus bioavailability?

A

Form of phosphorus (inorganic salts more available than organic)

Dietary Ca content (Ca:P ratio) - high Ca:P ratio (1.5-2:1) results in less increase in serum P

Dietary Mg content - high dietary Mg content (>0.32g/1000kcal ME) reduces P intestinal absorption by 13%. Unknown mechanism

69
Q

What dietary factors may affect phosphorus bioavailability?

A

Form of phosphorus (inorganic salts more available than organic)

Dietary Ca content (Ca:P ratio) - high Ca:P ratio (1.5-2:1) results in less increase in serum P

Dietary Mg content - high dietary Mg content (>0.32g/1000kcal ME) reduces P intestinal absorption by 13%. Unknown mechanism

70
Q

Apart from neurological signs, what does mucopolysaccharidosis (liposomal storage disease) typically cause?

A

Skeletal & ocular changes.

71
Q

What IV drug can be used to activate lipoprotein lipase? How does it work?

A

Ettinger

Heparin, used in a liproprotein lipase activity test.

Heparin activates lipoprotein lipase (LPL) by releasing LPL from vascular endothelium where it is normally anchored.
Also activates hepatic lipase (HL). Overall enhances plasma lipolytic activity & elevates FFA levels.

72
Q

What are the roles of adiponectin? What is the effect on obesity on it?

A

Ettinger Chap 176

Adiponectin = synthesized by mature adipocytes.
Roles vary depending on organ. Increases insulin sensitivity, lowers serum glucose [ ], reduces liver & muscle triglyceride concentrations.
Anti-inflammatory & insulin-sensitising hormone.

Serum concentrations are decreased with obesity (possibly inhibition by inflammatory cytokines)&raquo_space; results in insulin resistance.

73
Q

What is leptin & its effects? What is its status in obese cats?

A

Adipokine; appetite suppressant & modulates insulin sensitivity.
Obese cats are leptin-resistant (high circulating leptin [ ] but less response)

74
Q

Glycogen storage diseases - types, breeds affected, CSx?

A

Glycogen storage dz – deficient or defective activity of the enzymes responsible for metabolizing glycogen.

  • Type Ia = Maltese (von Gierke dz); deficiency in glucose-6-phosphatase (gene mutation)
  • Type II = Lapland dogs (Pompe dz); deficiency of lysosomal acid a-glucosidase
  • Type III = GSD and Curly-coated retrievers (IIIa) (Cori’s dz) deficiency of glycogen debranching enzyme amylo-1,6-glucosidase&raquo_space; Curly coated affects liver and muscle (AGL gene)
  • Type IV in Norwegian Forest cats (Anderson’s dz), deficiency in glycogen branching enzyme  glycogen accumulation in skeletal m, cardiac m, nervous system
  • Type VII = English springer spaniel (Tauri’s dz) deficiency in PFK&raquo_space; hemolytic anemia, hemoglobinuria
75
Q

Tryptophan
- Metabolic pathways & roles
- Significance in which diseases

A

Allenspach VCNA 2021 PLE review
- Essential AA in dogs/cats, largely absorbed in SI
- 2 main metabolic pathways in host:
1. Kynurenine pathway (90%) = energy metabolism: precursor for kynurenine
2. Serotonin pathway (5%) (90% in ENS, 10% in brain): metabolized to serotonin
- Melatonin pathway (pineal gland, GIT)&raquo_space; metabolized to melatonin
3. Small % reaches colon&raquo_space; metabolized by luminal bacteria to metabolites (indole, skatole indicant, tryptamine ‘SIT’).
- Microbial metabolites play an essential role in counteracting intestinal inflammation (induce anti-inflammatory cytokines e.g. IL-22).

PLE, canine CIE

76
Q

What are the major roles of leptin & where are its receptors located? What factors can influence circulating leptin levels?

A

Type of adipokine.
Roles
- Suppress appetite
- Inhibit apoptosis (mitogen)
- Stimulate angiogenesis
- Pro-inflammatory, modulate T cell responses
- Repro - incr during puberty, causes FSH & LH release
- Pro-thrombotic
- Inhibits adiponectin (opp effects)

OB-R in hypothalamus (satiety centre), also hematopoietic SCs

77
Q
A

Circadian rhythm
Amt of fat mass (linked to BW) - increases leptin expression but causes ‘leptin resistance’
Food (post prandial levels = 2-3x fasting levels)
Breed (Shelties higher)
GCS tx (dex incr, pred no effect, methylpred high dose suppress but low dose incr)

78
Q

What are the top 2 major endogenous sources of angiotensinogen?

A

1 white adipose tissue (WAT)

#2 Liver

79
Q

What is SOCS-3 and its effects? What factors induce SOCS-3 expression?

A

Supressor of cytokine signaling 3. Negative regulator of insulin expression –> induces insulin resistance.
Expression induced by leptin, insulin(?), resistin (these are increased in obesity)

80
Q

Where is ghrelin produced and what are its effects? Name a drug that potentiates its effects?

A

Produced by oxyntic glands within the gastric fundus.
Orexigenic (hunger) hormone. Fasting produces acylated active form&raquo_space; crosses BBB & binds to receptor&raquo_space; stimulate appetite & GH synthesis
Capromorelin (ghrelin agonist)

81
Q

What nutrients do cats have higher requirements for?

A

Arachidonic acid
Niacin, B12, pyridoxine, vit A, D
AA - taurine, arginine, methionine, lysine

82
Q

Which part of the GI lymphoid system does oral tolerance to food antigens occur?

A

M (microfold) cells of the Peyers patches

83
Q

What hematologic abnormality & clinical sign may be noted in cats with adverse food reactions and at what %?

A

20-50% peripheral eosinophilia
30% peripheral lymphadenopathy

84
Q

Food elimination diet - how long for GI signs vs dermatologic signs?

A

GI signs only: 2-4 wks
Skin signs: 8-12 wks

85
Q

How are hydrolysed protein diets beneficial for CE?

A

Reduces MW & shape of protein, reduces allergenicity & antigenicity as hydrolysate is too small to cause X-linking of IgE on mast cells, preventing degranulation.

86
Q

What is a common nutritional deficiency noted in unbalanced home-prepared or raw diets? What CSx does this cause?

A

Low Ca-P ratio. Ca +/- vit D deficiencies.
Young animals - long bone abnormalities; adults - bone resorption of mandible & maxilla –> rubber jaw. Nutritional 2’ hyperPTH

87
Q

Melanin (disguised as wheat gluten in diets) - toxic effects?

A

Crystals in renal tubules > AKI

88
Q

What pathogen recognition receptor can dietary fat effect have an effect on? What are the immunological effects?
Which other stimulus similarly binds to this PRR?
What dietary supplementation can inhibit this receptor?

A

TLR-4 (expressed on adipocytes, IELs, Mp, Np)
TLR-4 activation > COX-2 derived cytokines > NFKB > TNF-a > pro-inflammatory.
LPS endotoxin binds to TLR-4 & has similar potency to saturated LCFAs.
O3FA (e.g. DHA)

89
Q

Is dietary fat linked to pancreatitis in cats?

A

Poorly described as risk factor, but anecdotally yes (hyperlipidemia also potential risk factor)
Best to avoid high fat diets in cats with pancreatitis

90
Q

What is the hallmark feature of cancer cachexia? What immune system & biochemical changes are implicated?

A

Weight loss that cannot be reversed by increasing food intake.
Inflammatory cytokines (TNF-a, IL-6) + biochemical changes (glucose intolerance, increased lipolysis, hyperlactatemia (< common))

91
Q

What is the hallmark feature of cancer cachexia? What immune system & biochemical changes are implicated?

A

Weight loss that cannot be reversed by increasing food intake.
Inflammatory cytokines (TNF-a, IL-6) + biochemical changes (glucose intolerance, increased lipolysis, hyperlactatemia (< common))

92
Q

What metabolic complications can occur with parenteral nutrition (highlight those that are most common)?

A

Common - hyperTG, hyperglycemia
Also hyperNH3, hyperBIL, azotemia, incr ALKP, electrolyte derangements. Sepsis (3-12%)

93
Q

What essential AA do crystalline AA solutions (e.g. Travasol) used for parenteral nutrition lack? Is this a major clinical concern?

A

Taurine.
Usually not a concern as used for short term (up to 10d) only)

94
Q

Name 1 proposed adverse effect & 1 relative contraindication of IV lipid infusions.

A

AE - immunosuppression (impairs reticuloendothelial system; suppress Np & Lc function). But studies have not correlated lipid use & increased rates of infections.
Relative contraindication - hyperTG. Lipid infusions have not been shown to worsen pancreatitis or increase pancreatic secretion (so safe to give in these patients), BUT acc to human guidelines, markedly reduce or eliminate lipid component if TG >400mg/dL (4.2mmol/L)&raquo_space; aim to maintain normal serum TG.

95
Q

What are the different forms of vitamin K & where are they absorbed?
What is the main source of vitamin K in cats & dogs?

A

Vitamin K1 - diet. Absorbed in the proximal SI & requires bile for absorption (being fat soluble).

Vitamin K2 - bacterial synthesis in the intestinal tract. Absorbed in the ileum and colon. Main source of vit K.

96
Q

Why is atherosclerosis rare in dogs & cats compared to people?

A

High [HDL] cholesterol but lack cholesterol ester transfer protein (CETP) enzyme responsibel for reverse cholesterol transport.

97
Q

What cardiac changes may be observed in obese dogs? Is this reversible?

A

LV hypertrophy. Reversible with weight loss.

98
Q

What are the potential effects of obesity on glomerular health? Reduction in which urinary biomarkers were observed following weight loss in obese dogs?

A

Increased renal blood flow, filtration fraction & GFR; increased renal mass & glomeruli diameter w/o concurrent expansion of podocytes > could form gaps & lead to loss in protein filtration selectivity.
Obesity also stimulates RAAS > glomerular hypertension.

Markers - UPC, urine albumin, USG, homocysteine, cystatin C, clusterin (tubular marker).

99
Q

What effects does obesity have on RAAS & cardiac disease in dogs & cats?

A

Increased fat mass > increased adipose-derived angiotensinogen increases plasma angiotensinogen > increased AT-II > incr aldosterone.
High fat diets may also cause Na retention.

100
Q

What effects does obesity have on RAAS & cardiac disease in dogs & cats?

A

Increased fat mass > increased adipose-derived angiotensinogen increases plasma angiotensinogen > increased AT-II > incr aldosterone (cardiac remodelling)
High fat diets may also cause Na retention.

101
Q

How does EPA (O3FA) help to preserve lean muscle?

A

Interferes with ubiquitin-dependent protein degradation pathway

102
Q

How do acid-base derangements contribute to protein imbalance & muscle wasting?

A

Acidosis perpetuates insulin resistance > influences signaling pathways that trigger reduction of phosphoinositide 3-kinase (PI3K) activity > up-regulates the ubiquitin proteasome pathway (key pathway for protein degradation).
(Common animal proteins are metabolised to acid residues)

103
Q

What clinical manifestations does taurine deficiency cause in cats?

A

DCM (not all cats develop)
Central retinal degeneration
Hepatic lipidosis (taurine def limits lipoprotein synthesis needed for lipid metabolism and transport in the liver)

104
Q

Where are apolipoproteins found and what types are there?
Which ones activate a) lipoprotein lipase, b) lecithin cholesterol actyltransferase and c) chylomicrons?

A

Found in amphophilic membrane (with phosphlipids & free cholesterol) as part of lipoprotein molecule. Types A, B, C, E
Apolipoprotein C II - LPL co-factor (found on surface of CMs)
Apolipoprotein A1 - LCAT
Apolipoprotein B48 - chylomicrons

105
Q

Describe the roles of the following enzymes:
1 Lipoprotein lipase
2. Hepatic lipase
3. Lecithin cholesterol acyltransferase (LCAT)
4. Diacylglycerol acyl transferase 2

A
  1. LPL
    - On vascular endothelium. Hydrolysis of TG to FFA + glycerol in circulation - for CM & VLDLs.
    - Needs apolipoprotein C-II (on cell surface of CMs & VLDL) for activation.
    - For VLDLs > forms CM remnants, LDL.
  2. Hepatic lipase
    - Hydrolysis of TG & phospholipids
    - Facilitates liver uptake of TG & phospholipids from CM & VLDL remnants
    - On endothelium of hepatic sinusoids, some extra-hepatic tissues.
    - Converts VLDL to LDL (tgt with LPL)
    - Converts HDL2 to HDL3
  3. LCAT
    - Role in reverse cholesterol transport
    - Activated by Apo A1
    - Circulates in blood mainly bound to HDL > acts on HDL to convert cholesterol from tissues into cholesterol esters for incorporation into HDL molecules.
    - Esterifies and sequesters cholesterol in HDL > returns cholesterol is returned to liver.
  4. Diacylglycerol acyl transferase 2 = enzyme that catalyses conversion of diglycerides to TG
106
Q

What is the normal role of hormone sensitive lipase and where is it located? What physiologic/pathologic factors activate or decrease its activity?

A

I/C enzymes (within adipocytes). Cleaves FAs from intracellular TG. Activated by phosphorylation.
Essentially a physiologic response to provide energy from FA during fasting.
Factors - activated by insulin deficiency, ACTH, GCS, GH, thyroid hormone, catecholamines (NAd, Epi). Bolded = impt hormones.

107
Q

What factors increase vs decrease LPL activity?

A

Increase - heparin, insulin & thyroid hormone
(NB Insulin has opp effects on HSL - decreases HSL activity)

Decrease - GCS, inflammmatory cytokines (e.g. acute panc)

Heparin release test can be used to assess LPL activity (give IV heparin, check TG at baseline & 15min, LPL defect > no rise in TG)

108
Q

List some breeds that are prediposed to:
- Primary hyperTG
- Primary hyperchol

A

HyperTG - Mini Schnauzers, Beagles
Hyperchol - Briards, Dobermans, Rotties

109
Q

What bloodwork values may be affected by lipemia?

A

Increased - bile acids, TBIL, TP
Decreased, Na, K, Cl, crea
Increased/decreased LE, glucose

110
Q

What are treatment recommendations & goals for hyperTG in dogs/cats?

A
  1. 1st line low fat diet: dietary fat <12% DM (20% ME basis) OR <20g fat/1000kcal ME; lower if already on lower-fat diet. NB cats <24% fat
  2. Omega3 FAs (DHA, EPA) - GI
  3. Fibrates - PPARa agonist, LP activation, inhibits diacylglycerol acyl transferase 2, stim FA oxidation. AE: cholelithiasis, panc, GI, LE incr, azotemia > myalgia.
  4. Niacin (B3) - AE: LE incr, myotox, hepatotox, increase BG, erythema, puritus
  5. Soluble fibre - interferes with enterohepatic reabsorption of BAs
    Aim TG <400-500mg/dL
111
Q

What are treatment recommendations & goals for hyperCHOL in dogs/cats?

A

Tx overlaps with that for hyperTG
PLUS
1. Statins - reversible inhibitors of hydroxymethylglutaryl coenzyme A (HMG-CoA) reductase – enzyme catalyzing rate-limiting step for cholesterol synthesis. AE: GI (V+, D+, hyporexia), myopathy, rhabdomyolysis, hepatotox. NOT to be given with fibrates
2. Cholestyramine

ACVIM SAIM (2023) (19 decks)

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