Metabolic Disorders

Related to Carbohydrate
Metabolism
Metabolic Disorders Related
to Carbohydrate Metabolism
 Ketosis
 Acidosis
 Laminitis (founder)
 Liver abscesses
 Gastric ulcers
 Diabetes
Ketosis/Pregnancy Toxemia
 Adipose response to low blood
glucose
Low blood Fat Free fatty
glucose reserves acids (FFA)
mobilized released

Partial
oxidation of Liver
FFA to ketone uptake of
bodies FFA
Ketosis
 Dairy cows
 Occurs most often following calving
 Increased glucose demands to support lactation
 Body fat is mobilized to meet energy demands, but
TCA cycle ‘backs up’
 Over conditioned cows

 Pregnant ewes
 Last third of gestation
 Fetus takes up space and reduces capacity of
intestine
 Caused by inadequate energy intake
 Mortality can be as high as 80%
 Twin lamb disease
Ketosis
 Clinical signs
 Abrupt drop in milk production (dairy cows)
 Loss of appetite
 Sweet smelling breath (acetone)
 Weight loss

 Treatment
 Propylene glycol
 Glucagon injections
 Dextrose infusion
Ketosis Prevention
 Avoid excess body fat on females
 Increase concentrate feeding
gradually
 Avoid abrupt ration changes
 Acidosis in Ruminants
 Decreased pH of body fluids

Lactic acid
CHO supply Rumen pH
production

Systemi
c Rumeniti
acidosis s

Laminiti
s
Laminitis
 Lameness due to lactic acidosis
 Chronic inflammation of hoof
 Abnormal growth
 Inadequate perfusion of laminae
 Degeneration of bond between hoof
and bone
 Liver
Abscesses

High
Grain Diet Rumen
Portal
blood Live
Acidosis r

Rumenitis

Bacteria Liver
abscesses
Rumen bacteria
Gastric Ulcers
 Occurs primarily in horses and pigs
 Causes
 Stress
 High concentrate diets
 Finely ground grain
 Implications
 Decreased appetite & growth
 Dull hair coat
 Lethargic
Monogastrics
 Under-feeding carbohydrates:
 Weight loss

 Over-feeding carbohydrates:
 Obesity
 Diarrhea
 Diabetes
 Diabetes insipidus
 Excessive urination, water loss
 Due to shortage of antidiuretic hormone (ADH)
 ADH causes H2O reabsorption in the kidney

 Diabetes mellitus
 Lack of insulin or lack of insulin response
 Blood glucose is not metabolized or utilized
 Loss of glucose in urine
 Ketosis can occur, shift from CHO to fat metabolism
Diabetes
 Type I
 Pancreas islet cells destroyed
 Decreased production of insulin

 Type II
 Non-insulin dependent
 Insulin receptors less functional

 Gestational
 Occurs in pregnant woman
Glucose in Cats
 True carnivore
 VERY little carbohydrate in normal
diet
 Must rely on gluconeogenesis
 No VFA’s like herbivores
 Rely on AA’s as source of carbon
 Enzyme Adaptation
 Most mammals have the ability to
adapt enzyme activity to protein
intake
 Conservation of AA when consuming
low-protein diets
 Catabolism of AA when consuming
high-protein diets
 Rat enzyme activity can increase 2.75
to 13.0 fold
 Enzyme Activity
 High activity of alanine and aspartic transaminases
 Constant AA catabolism

 Urea cycle enzymes have high activity

 Particularly high arginase activity
 Cat cannot conserve N from the body pool
 Cats excrete 360 mg urinary nitrogen/kg body weight -0.75

per day

Excretion of dogs is 110 mg/kg BW /d
-0.75

 No adaptation to changes in protein intake

 Catabolize a substantial amount of protein, particularly
after a meal
 Catabolism regardless of meal’s protein content
 Carnivorous Diet
 No selection pressure to adapt to low-
protein diet
 Dependent on high-protein diet as a result
 No need for carnivore to conserve protein
 Cat has evolved to have increased protein
metabolism:
 AA catabolism
 Irreversible rate of urea synthesis
 Increased protein needs for maintenance
Advantages of High AA
Catabolism
 Immediate capability of cat to use
AA as a source of energy
 Gluconeogenic enzymes are
constantly active
 Quickly convert C-backbone of AA to
energy