We were proud to have the lead scientist Gabriel De La Fuente Oliver present a paper of his findings on the anti obesity compound, developed by ourselves fro an indigenous plant extract, at the European Convention of Comparative Veterinary Nutrition in Utrecht and an update planned for BEVA 2015. The following post explains why we think the research is so worthwhile and why we are committing another year and another trial to look closer at how the compound favours a gut population to promote leanness. From fat pads to feet- the descent into laminitis. ‘Cresty’ necks are unsightly lumps of fat found on the neck of an overweight or obese horse and there is a growing awareness amongst vets and horse owners that having a ‘cresty neck’ predisposes it to laminitis. Some breeds are more prone to having a ‘cresty’ neck than others, native breeds such as the Welsh, Connemaras, Highlands and Shetland ponies are among the more susceptible as they require less food with lower sugar/starch than many of the other breeds, they also have a natural leaning towards insulin resistance because they have evolved from an environment where food supplies are often scarce and available nutrients change from season to season. Susceptible ponies (and cross breeds) are called ‘good doers’ and they possess an insulin resistant genotype as a survival mechanism which gives them a natural leaning towards insulin resistance, a good thing as it helps them to survive their native harsh mountain/moorland environment. These ponies naturally have a higher level of insulin secretion and a slower glucose disposal rate which is a positive adaptation for sparse food rations. During the harsh winter conditions when glucose is unavailable or scarce the ‘good doer’ will switch to an alternative energy system to ensure survival and as the available food changes from grass to shrubs/herbage such as gorse, tree bark and marsh grass the metabolism will also switch to a more conservative system of energy use and storage which prevents any ingested glucose from entering the muscle and adipose tissue. Deprived of glucose the tissues then start to use another energy supply (lipids/triglycerides) allowing the dwindling but precious sources of glucose to support vital organs. ‘Good doers’ have lower insulin sensitivity and higher insulin secretion plus high circulating levels of triglycerides. This tendency towards insulin resistance is a natural efficient adaptation which also involves the ‘pay it forward’ insulin system which exists in the gut. The problems start when the ‘good doer’ clashes with the modern management system and change of environment, and switches to a diet containing too much sugar and starch from high quality hay and grass designed by modern farming methods as suitable for high milk yielding cattle, with no drop in the quality of nutrients through the winter months. ‘Good doers’ are more predisposed to laminitis but any horse receiving more calories than required for work will store the excess as adipose tissue and fat pads will soon appear as cresty necks, tail pads, shoulders, sheath etc. What happens next? The ‘cresty’ neck is not just a layer of fat but it is a hormone factory manufacturing at least 10 different types of hormones which set in place several mechanisms which eventually lead to the catastrophe of laminitis. In humans, adipose tissue around the stomach has been found to contain large amounts of chemicals which are inflammatory in nature, the same chemicals have been found in the ‘cresty neck’ and tail fat pads of horses. These inflammatory chemicals have a massive impact on health with multiple complex interactions between glucose and lipid metabolism, control of appetite and energy levels to name just a few. Countdown to Catastrophe 1. The first stage of the breakdown is the release of a chemical (MCP-1) from the fat pad to attract and recruit white blood cells (monocytes) from out of the blood stream into the adipose tissue . CP-1 is responsible for recruiting MCP-1 both can be found in blood tests but it may not been seen until obesity has been present for some time, this chemical is also breed specific to natives and cross breeds. The monocytes cause the fat cells to grow and to swell hence the hardness of a ‘cresty neck’ before an attack of laminitis. 2. Step two is the setting up of a low grade inflammation throughout the body, to achieve this effect the monocytes convert to macrophages and to a chemical called TNF-1 both alter the normal metabolism and signal the release of triglycerides from the adipose tissue which is a normal response to infection/inflammation and disease. Low grade inflammation results and chronic insulin resistance sets in. 3. The third step is the release of yet more insulin to deal with the transport of triglycerides, whilst in the adipose tissue IL-1 and IL-6 are produced and have a negative impact, producing greater insulin resistance, these immune cells also have an effect on the appetite and energy levels by producing a hormone called leptin. This hormone is often measured in a blood test as it is indicative of insulin resistance. Breakdown The final stage in the process is endocrinopathic laminitis caused by;- • High levels of circulating insulin (above 200 micro iu/ml) • A disrupted glucose supply to the foot. • High levels of triglycerides/lipids cause an altered blood flow to the foot. • Pro inflammatory chemicals TNF-1, IL-1, IL-6 which are influential in many diseases states in humans are anticipated to be part of the final breakdown of the hoof.
Posted on: Tue, 21 Oct 2014 11:06:22 +0000
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