4 Metabolic Disorders Related To Carbohydrate Metabolism

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 glucose

Fat reserves mobilized Partial oxidation of FFA to ketone bodies

Free fatty acids (FFA) released

Liver uptake of 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

CHO supply

Lactic acid production Systemi c acidosis

Rumen pH

Rumeniti 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

Acidosis

Portal blood

Live r

Rumenitis Bacteria Rumen bacteria

Liver abscesses

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 per day 



Excretion of dogs is 110 mg/kg BW

-0.75

/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 lowprotein diet 

 

No need for carnivore to conserve protein Cat has evolved to have increased protein metabolism:  



Dependent on high-protein diet as a result

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