Post by bellajack on Mar 30, 2007 7:56:08 GMT -1
Report on The Royal Veterinary College Laminitis Conference 24th May 2007
Part 2
How Problems In The Gut Trigger Laminitis In The Foot.
The speaker for this section was:
Jonathon Elliott MA VetMB PhD CertSAC DECVPT MRCVS
He completed his PhD in vascular pharmacology in1989 and is now Professor of Clinical Pharmacology at The Royal Veterinary College and is Vice Principal of Research. He has won awards for his contributions to companion animal medicine, particularly in the area of equine laminitis.
The link between events in the gastrointestinal tract and the foot is still a mystery, although the common pathway to the separation that occurs in the foot due to laminitis seems to be brought about by activation of enzymes called Matrix Metalloprotienase (MMP) and represents an extremely exaggerated response to injury. The question is what triggers this and how is it linked to consumption of carbohydrates?
MMP’s are important enzymes in normal tissue growth and the resident cells in the foot produce them to support the continuous growth of the hoof.
Excessive MMP activity occurs in the developmental and acute phases of laminitis and is responsible for destroying the membrane that bonds the laminae in the foot leading to separation of the pedal bone from the hoof wall.
There are 3 theories as to how these MMP’s are activated:
1) Bacteria derived exotoxins activate MMP’s.
2) Gut derived products trigger inflammation in the foot, leading to MMP activation.
3) Gut derived products trigger vascular disturbances leading to vasoconstriction and ischaemia- reprofusion injury (blood supply to the foot gets compromised and then blood rushes back, like putting a tourniquet on your leg and taking it off again, only much worse because of the lack of expansion of the hoof wall) part of which involves MMP activation. The blood vessels in the foot are highly susceptibly to the vasoconstrictory effects of these substances and the effects of the reduced blood, oxygen and glucose supply that results from vasoconstriction. This has been compared to Raynaud’s Disease in man (impaired blood supply to hands and feet that can lead to amputation) and advances in treatment of this condition could help advance laminitis treatment in the future.
These theories are not mutually exclusive, but none explains why some horses are so much more susceptible to laminitis than others. Recent evidence suggests a strong link between the insulin resistant type of horse and increased susceptibility to vasoconstriction and laminitis.
Carbohydrate overload leads to more of the Gram-positive bacteria that ferment carbohydrate in the hind gut. This lowers the pH in the hind gut (acidosis) and increases the permeability of the gut wall. This allows the entry of undesirable substances into the circulatory system (endotoxins and too many amines) which cause vascular (blood vessel) problems in susceptible horses and trigger MMP activation leading to failure of the foot.
Thus both inflammatory and ischaemic (results of reduced blood supply) stimuli could trigger MMP activation and cause the foot to fail and there is evidence that all 3 theories may contribute to the pathophysiology (the disturbance of the processes underlying normal function) of pasture induced laminitis.
I hope that this makes some sort of sense. I am sorry that it is so complex. I know that it has made my brain hurt! Thank god for a veterinary dictionary!
Next exciting episode ‘Metabolic Predisposition to Laminitis – Obesity and Insulin Resistance.’ It is a bit easier to follow – promise!
Part 2
How Problems In The Gut Trigger Laminitis In The Foot.
The speaker for this section was:
Jonathon Elliott MA VetMB PhD CertSAC DECVPT MRCVS
He completed his PhD in vascular pharmacology in1989 and is now Professor of Clinical Pharmacology at The Royal Veterinary College and is Vice Principal of Research. He has won awards for his contributions to companion animal medicine, particularly in the area of equine laminitis.
The link between events in the gastrointestinal tract and the foot is still a mystery, although the common pathway to the separation that occurs in the foot due to laminitis seems to be brought about by activation of enzymes called Matrix Metalloprotienase (MMP) and represents an extremely exaggerated response to injury. The question is what triggers this and how is it linked to consumption of carbohydrates?
MMP’s are important enzymes in normal tissue growth and the resident cells in the foot produce them to support the continuous growth of the hoof.
Excessive MMP activity occurs in the developmental and acute phases of laminitis and is responsible for destroying the membrane that bonds the laminae in the foot leading to separation of the pedal bone from the hoof wall.
There are 3 theories as to how these MMP’s are activated:
1) Bacteria derived exotoxins activate MMP’s.
2) Gut derived products trigger inflammation in the foot, leading to MMP activation.
3) Gut derived products trigger vascular disturbances leading to vasoconstriction and ischaemia- reprofusion injury (blood supply to the foot gets compromised and then blood rushes back, like putting a tourniquet on your leg and taking it off again, only much worse because of the lack of expansion of the hoof wall) part of which involves MMP activation. The blood vessels in the foot are highly susceptibly to the vasoconstrictory effects of these substances and the effects of the reduced blood, oxygen and glucose supply that results from vasoconstriction. This has been compared to Raynaud’s Disease in man (impaired blood supply to hands and feet that can lead to amputation) and advances in treatment of this condition could help advance laminitis treatment in the future.
These theories are not mutually exclusive, but none explains why some horses are so much more susceptible to laminitis than others. Recent evidence suggests a strong link between the insulin resistant type of horse and increased susceptibility to vasoconstriction and laminitis.
Carbohydrate overload leads to more of the Gram-positive bacteria that ferment carbohydrate in the hind gut. This lowers the pH in the hind gut (acidosis) and increases the permeability of the gut wall. This allows the entry of undesirable substances into the circulatory system (endotoxins and too many amines) which cause vascular (blood vessel) problems in susceptible horses and trigger MMP activation leading to failure of the foot.
Thus both inflammatory and ischaemic (results of reduced blood supply) stimuli could trigger MMP activation and cause the foot to fail and there is evidence that all 3 theories may contribute to the pathophysiology (the disturbance of the processes underlying normal function) of pasture induced laminitis.
I hope that this makes some sort of sense. I am sorry that it is so complex. I know that it has made my brain hurt! Thank god for a veterinary dictionary!
Next exciting episode ‘Metabolic Predisposition to Laminitis – Obesity and Insulin Resistance.’ It is a bit easier to follow – promise!