Nutrition Exam 2

The student will be able to discuss the role of carbohydrate metabolism with respect to diabetes mellitus

Diabetes mellitus: alteration in cellular transport/metabolism of glucose

-insufficient insulin release

-lack of insulin receptors

-inability of receptors to transduce signal

The student will be able to differentiate between Type I and II diabetes with respect to felines and canines

Type I - insulin dependent

2 forms

-rare: no beta cells

-common: no insulin producing beta cells (autoimmune destruction)

IDDM is more common in dogs

Type 2 - insulin independent

Impaired insulin secretion AND receptor sensitivity

NIDDM is more common in cats and is potentially reversible

The student will be able to discuss unique digestive and metabolic peculiarities of carbohydrate metabolism in felines

Cats need low carb high protein, strict carnivores

The (2) student will be able to discuss goals of dietary therapy in treatment of feline and canine diabetes

Feline goals:

-modulate hyperglycemia

-delay gastric emptying

-delay CHO absorption

-feed to achieve lowest possible insulin dose

-low CHO, high protein

Canine goals:

-moderate fiber and CHO

-low fat

-normal or higher protein

Discuss why dietary fiber is non-digestible

Dietary fiber contains non-soluble carbohydrates

-cellulose

-lignin

-hemicellulose

requires fermentation

The student will be able to define ‘dietary fiber’ in the context of its chemical nature, physiological aspects, and within the context of feline/canine nutrition

Chemical:

The sum of all non-starch polysaccharides, non-digestible oligosaccharides, and lignin

Physiological:

All plant polysaccharides and lignin that are resistant to hydrolysis by endogenous secretions of the gastrointestinal tract

Nutrition:

Edible parts of plants or analogous carbs that are resistant to digestion and absorption in the small intestine

Differentiate between soluble and insoluble fiber types and understand the proposed modes of action

Soluble:

Pectins, gums, mucilages, beta-glucans, hemicelluloses

-increase water holding cap

-delay gastric emptying, slows transit time, delays glucose uptake

-modifies microbiome

-tends to be fermentable

Modes of Action:

-Fermentation by microbes produces VFAs > fuel source, lower pH, promote microbial growth

-Regulation of bowl movement > stool consistency, manage diarrhea

-Enhance nutrient absorption > slowing of digestion/absorption

-Enhance barrier function/gut integrity > anti-inflammatory

Insoluble

Cellulose, some hemicellulose, lignin

-decreased water holding cap

-increases fecal bulk

-decreases transit time

-decreases energy density of diet

-increases satiety

-decreased fermentability

Modes of Action

-increase passage rate

-decrease E. Coli, diarrhea

-increase fecal bulk

-enhance satiety

The student will be able to list and describe plant cell components

Starch - storage carb

Oligosaccharides - cell walls and membranes

Cell wall (soluble) - cell walls

Cell wall (insoluble) - cellulose/hemicellulose

Lignin - structural carb

Phenolics - defense mechanism

The (3) student will be able to discuss the difference between crude fiber and total dietary fiber analyses

Crude:

-underestimates dietary fiber

-should be abandoned

TDF:

-most accurate

-represents insoluble & soluble

-expensive, time consuming

The student will be able to discuss effects of fiber on growth performance, weight control, glycemic index and satiety

Growth performance:

-DF reduces energy intake

Weight control:

-restricts digestion/absorption, energy intake

-dilutes caloric content

Glycemic index

-Viscous fiber in SI acts as barrier to release of nutrients, slows absorption

Satiety

-gastric distention

-Work time/chewing

The student will be able to discuss fiber recommendations for feline and canine patients including factors that influence dietary fiber inclusion levels

Cats:

-lower fiber requirement, 1.5-4%

-Support digestive health, manage chronic conditions

Dogs:

-benefit from more fiber 2.5-5%

-GI health, weight management, satiety

The student will be able to list characteristics of ‘nutrient lipids’ and list the functions of lipids

Soluble in organic solvents

Energy source

Constituent of cell membranes

Fat-soluble vitamin transport

Corticosteroid hormones

Triacylgrlycerols are most important

Functions:

-supply metabolic energy by oxidation of FAs

-structural component of cell membranes

-lubricants

-signaling molecules

The student will be able to describe the structure of triglycerides and explain their biological significance

TAGs have 3 chains

Used for things

The student will be able to describe fatty acid characteristics:

a. Saturated vs. unsaturated fatty acids

b. FA that are most important nutritionally

c. Clinical implications for a fat deficient diet

d. Essential FAs

A) saturated fats only have single bonds in the chain, unsaturated fats have at least one double bond

B) 14 or more carbons long

C) delayed growth, dermatitis, kidney lesions, early death

D) Linoleic and alpha linoleic FAs

The student will be able to describe the pathway of de novo fatty acid synthesis, including:

a. The main function: synthesis of palmitate from glucose

b. Roles of: citrate, acetyl-CoA carboxylase, malonyl-CoA and the multifunctional enzyme fatty acid synthase

A) Synthesis of palmitate from glucose

B)

Citrate: upregulates

acetylene-CoA carboxylase: carboxylates acetyl CoA > malonyl CoA rate limiting

Malonyl CoA: needed to combine with acetyl-CoA for second step in FA synthesis

FA synthase: catalyzes a polypeptide w/ ACP (carrier of acrylic intermediates)

The student will be able to discuss short/long term regulation of de novo fatty acid synthesis

a. Nutritional influences: Fed vs. Fasted

b. Hormonal influences: Insulin vs. Glucagon

c. Metabolite influences: Citrate vs. Palmitate

 

Short-term (enzyme activity):

• Insulin ↑ synthesis (activates ACC)

• Glucagon ↓ synthesis (inhibits ACC)

• Citrate ↑ synthesis (activates ACC)

• Palmitate ↓ synthesis (feedback inhibition)

Long-term (gene expression):

• Fed state ↑ synthesis (insulin promotes lipogenic enzyme production)

• Fasted state ↓ synthesis (glucagon reduces lipogenic enzyme production)

Remember: ACC (acetyl-CoA carboxylase) is the rate-limiting enzyme.

Fed + Insulin + Citrate = ON

Fasted + Glucagon + Palmitate = OFF

The student will be able to explain the effects of omega-3 and omega-6 fatty acids on cell function and health, including:

a. Contribution ot the inflammatory response and other biological effects

b. Examples of eicosanoid molecules

c. Discussing why omega-3 fatty acid dietary supplementation may impact the clinical outcomes of EIPH

A) n-6 are pro inflammatory

N-3 are less inflammatory

B) linoleic acid, stearidonic acid

C) n-3 are considered anti-inflammatory as they are precursors to anti-inflammatory molecules. Higher diet in anti-inflammatory precursors > less inflammatory molecules in body

The student will be able to describe ketogenesis including the ketone bodies produced

When there are high rates of fatty acid oxidation, large amounts of acetyl CoA are produced in the liver

Normal conditions: low production

CHO shortage: high production

Body needs ketones for energy (BRAIN) when low on carbs

The student will be able to list the three main sources of acetyl CoA and the three main fates of acetyl CoA and how lipid metabolism is affected by glucose metabolism

Sources:

-oxidative decarboxylation of pyruvate

-oxidation of long-chain fatty acids

-oxidative degradation of amino acids

Fates:

-fatty acid synthesis

-Ketone body/cholesterol synthesis

-Oxidation in TCA

Less glucose metabolism leads to more lipid metabolism

The student will be able to describe lipid metabolism in the fed and fasted state

Fed

Dietary fat is hydrolyzed to FFAs and glycerol

FAs are stored as fat, used for energy, reesterfied in liver

Insulin stimulates lipoprotein lipase, FA and triglyceride synthesis

Fasted

Hormone-sensitive lipase is activated, fat is hydrolyzed to glycerol and FA

The student will be able to discuss Feline Idiopathic Lipidosis including how arginine and carnitine deficiency, and endocrine abnormalities may be involved in the etiology of the disease

Arginine: deficiency promotes hyperammonemia and encephalopathy

-promotes anorexia, perpetuates

Carnitine: need to transfer FA into mitochondria

Endocrine abnormalities: insulin deficiency

-lipidosis and gluconeogenesis are not inhibited

-accelerated lipidosis leads to hypertriglyeridemia and ketonemia

The student will be able to characterize and give an example of a protein belonging to the following functional categories: enzymes, hormones, structural, immunoproteins, transport proteins

Enzymes: Hydrolases

Hormones: GnRH

Structural: Actin

Immunoproteins: Immunoglobulins

Transport proteins: albumin

The student will be able to discuss the two major classes of plasma proteins (albumin and globulin) including how the plasma protein profile may be affected by dehydration, disease, and malnutrition

• Albumin: Maintains oncotic pressure; transports substances.

• Globulins: Immunity (antibodies), transport, inflammation.

• Dehydration: ↑ Both (concentration effect).

• Inflammation/disease: ↓ Albumin, often ↑ globulins.

• Malnutrition: ↓ Albumin due to inadequate protein/amino acids.

Remember: Albumin = fluid balance; Globulins = immunity.

The student will be able to list the 10 amino acids that are essential (indispensable) to most species

Phenylalanine

Valine

Threonine

Tryptophan

Isoleucine

Methionine

Histidine

Arginine

Leucine

Lysine

The student will be able to have a general understanding of protein (amino acid) absorption, protein quality, complementation, availability and disproportion (imbalance, antagonism)

Mostly absorbed as small peptides

Bioassays for protein quality

Proteins can complement each other, take advantage when making diets

Imbalances can cause detrimental effects

The student will be able to discuss protein turnover

1-2% of total body protein daily

Synthesis > degradation: anabolic

Synthesis < degradation: catabolic

The student will be able to list factors that affect animal amino acid requirements

Stage/level of production

Genetic factors

Health

Environment

Energy density

The student will be able to list the fates of amino acids

Protein synthesis

Synthesis of other nitrogenous compounds

Biological fuel

The student will be able to discuss reasons for protein digestion and compare/contrast exogenous and endogenoussources of protein

Facilitate uptake/absorption, resynthesize necessary proteins, immune process

Exogenous:

-animal/plant products

Endogenous:

-mucosal cells

-digestive enzymes/glycoproteins

The student will be able to discuss nitrogen balance as an indicator of net protein synthesis

Difference b/t N entering and N leaving the body

Positive balance:

-N uptake > excretion

-body protein increases

Negative balance:

-N excretion > intake

-defines dietary requirements

The student will be able to discuss the two key reactions in amino acid metabolism

Transamination

Aminotransferases transfer NH3 from AA to alpha-keto acid

Fully reversible

Needs PLP

Oxidative Deamination

Glutamate dehydrogenase Removes amino group from Glu

In mitochondria

Reversible, inhibited by ATP/GTP

The student will be able to list the two main stages of nitrogen disposal and the three main sources of ammonia

a. Ammonia is generated from:

i. Excess amino acids from the diet (Glutamate dehydrogenase-oxidative deamination)

ii. Catabolism of Glutamine by enterocytes

iii. From catabolism of peripheral tissue protein (e.g., muscle)

2 Stages:

-removal of amino group from AA

-formation of urea

The student will be able to discuss the ornithine cycle, including:

a. Rate-limiting reaction/enzyme

b. Sources of animo groups, entry into cycle

A) Formation of carbomoyl phosphate, needs carbomyl phosphate synthase I

B) Transdeamination (enters are step 1) and Transamination (enters at step 3)

The student will be able to summarize amino acid metabolism in both the absorptive and post-absorptive state

Absorptive

Large proportion of AA transaminated to alanine

Alanine released to portal circulation to liver

-protein synthesis

-Transamination

Post-Absorptive

Muscle breakdown of AA, transaminated to alanine and glutamine

The student will be able to characterize the ‘central dogma of molecular biology’

DNA > RNA > protein

The student will understand the Alanine cycle and its importance

Supplies glucose to muscle, removes ammonia from alanine/muscle

The student will understand the unique protein requirements of carnivores

a. Differences in aminotransferase activity

b. Increased amino acid requirements

A) strict carnivores have reduced aminotransferase activity

B) increased need for AA, main course of things

Protein-losing enteropathy

a. Causes

b. Clinical presentation

c. Dietary therapy

A) diseases affecting intestinal lymphatic drainage

-acute/chronic inflammatory diseases

B) Weight loss, panhypoproteinemia, hypocholesterolemia, hypocalcemia

C) high digest ability, low fat, high protein