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  • Writer's pictureSarah L Rhoades, DVM

Insulin Dysregulation and Metabolic Syndrome


Even mules can suffer from insulin dysfunction, metabolic syndrome, and laminitis.
Mules too, can suffer from metabolic syndrome and laminitis.

How can something so beautiful be so dangerous?


It’s March – time when that magic moment occurs, where the world announces a season of new life in the shade of green, everywhere. New grass.


It’s difficult to view such beauty in the world as having the potential to carry such danger – but it is a danger that many are sadly familiar with. There are few things as heartbreaking as watching a beloved companion undergo an event so painful as a severe laminitis episode.


A description I will often give people: if you can imagine what it would feel like to have someone partially rip your fingernails from their attachment… and then have to walk on them, bearing the entirety of your weight… you can imagine how painful this process is to a horse.


Why do some horses develop laminitis or founder and others not?


Would it surprise you to learn sometimes thin horses can develop the metabolic derangements that lead to laminitis or founder?


Probably more important to all of it is the question: How can I avoid this situation entirely? What can I do to prevent metabolic syndrome and laminitis?


Because without a doubt, this is one situation where an ounce of prevention is worth a pound of treatment and then some.


The Physiology of Insulin Metabolism

After a meal, sugars and starches are absorbed into the blood stream raising blood glucose concentrations.
Figure 1 - Glucose is absorbed into the blood.

You can’t have a discussion about Insulin Dysregulation, Metabolic Syndrome, or Endocrinopathic Associated Laminitis without also discussing the physiology of Insulin Metabolism. (And to be fair the names for the subset of these associated processes is endless - even I have to go back, check and recheck the current terminology – so let me apologize if I missed an outdated change somewhere in the body of this post.)


Your body, and the body of every mammal, absolutely depends on glucose in order to function – it’s the main source of energy cells utilize. What’s more, your body puts an inordinate amount of effort into tightly regulating the

In response to meal consumption and rising glucose blood concentration, the pancreas releases the hormone insulin into the blood.
Figure 2 - The pancreas releases insulin.

specific concentration of glucose in your blood into a tiny range. The mammalian body does not like it when blood glucose gets too high or too low – when either is observed on serum chemistry there is usually something very wrong going on at that point - it means that the body’s normal regulating mechanisms have been entirely overcome.


When you eat a meal, the simple sugars and starches it contains, get absorbed into the blood stream, which abruptly raises blood glucose levels (Figure 1). The mammalian body has a wonderful set of signaling pathways that trigger the pancreas to release insulin in preparation for and response to that meal (Figure 2).


Insulin then interacts with the various cells of the body, signaling them to take in additional glucose from the

Insulin act on cell surface receptors, signaling those cells to take in blood glucose effective maintaining blood glucose concentration.
Figure 3 - Insulin signal cells to take in glucose

blood, which effectively lowers and maintains the blood glucose concentration (Figure 3).


Here’s where the problems derive:


The more sugar and starch a mammal consumes, the more insulin the pancreas secretes, the more insulin the body’s cells are exposed to. When this occurs on a repeated, chronic basis, those cells begin to fundamentally ignore the signal of insulin (not literally of course, there’s some biochemistry and cell biology involved here, but we won’t get into that). The take home point is: the cells of the body become resistant to the effects of insulin – which

With chronic high exposure, cells begin to downregulate surface receptors and become less responsive to the effects of insulin.
Figure 4 - Cells stop responding to Insulin

give us our terms Insulin Resistance and the newer, more current term, Insulin Dysregulation (Figure 4).


We already said tight control over blood glucose levels is vitally important to the body – so what does the body do when insulin secretion doesn’t lower blood glucose enough? The pancreas secretes more insulin. And more. And more. (Figure 5).


In humans, the pancreas eventually peters out and just can’t do it anymore: insulin secretion stops entirely, blood glucose levels then rise uncontrollably. We call this Type II diabetes and it has profound effects on the body as many are aware.

In horses, the pancreas releases more and more insulin until blood glucose levels are normal.
Figure 5 - The pancreas releases more insulin

Horses never reach that state, they instead progress from a state of Insulin Resistance or Insulin Dysregulation to Metabolic Syndrome.


Of most notable and direct concern is laminitis – these horses just keep producing more and more insulin in an effort to control their body’s blood glucose concentration, until that insulin triggers a laminitic even (Figure 6).


Metabolic Syndrome can be simply understood as the ultimate progression of Insulin Dysregulation – it is characterized by three points: the presence of Insulin Resistance (or a high blood insulin concentration), laminitis (which can be acute severe, or mild chronic), and regional fat adiposity (a cresty neck and/or enlarged fat pads). On that last note, even horses with an overall thin body condition score will often suffer from a degree of regional fat adiposity, it just may be more subtle in appearance.


There are many consequences to this – it is an absolute endocrine nightmare: chronic, system wide inflammatory state that can manifest or exacerbate a wide range of other diseases including osteoarthritis, chronic obstructive pulmonary disease (COPD), and it is speculated Equine Cushing’s disease (PPID) can also be instigated and accelerated by this process.


These events probably start small, in fact, they probably don’t even get noticed – but rather manifest themselves in other chronic changes: growth rings on the dorsal hoof wall, a dished dorsal hoof wall, flattened feet, stretching and bruising of the white line, and difficulty ambulating over hard surfaces without shoes.

Chronic elevated insulin levels result in the lamina of the equine hoof becoming inflamed and weakened. The lamina begin to stretch, tear, and the pull of the Deep Digital Flexor Tendon causes rotation of the coffin bone.
Figure 6 - The equine hoof's relationship with insulin

Eventually, though, without intervention a severe laminitic event precipitates – the effects of which only compound the significant metabolic endocrinopathy that caused it.


See, when these horses become painful, they stop moving as much. And this is a problem: movement and exercise release adrenaline/epinephrine, which diverts blood flow to the musculature, and signals those cells to take in more glucose to meet increased metabolic demands. More simply put, epinephrine allows the body to reduce blood glucose levels independently of insulin. Orthopedic pain, such as laminitis reduces the horse’s ability and tendency to utilize this pathway only compounding the effects of the syndrome.


Diagnosis, Early Treatment and Prevention

Diagnosis of insulin dysregulation, metabolic syndrome, and Equine Cushing’s Disease (PPID) can be done off a thorough history, clinical exam, and blood work.


Some of the things I look for on routine wellness evaluation including estimating a body condition score, monitoring a patient’s weight with a weight tape, inspecting the patient for signs of regional adiposity (abnormal fat deposits, cresty neck, etc.), inspecting his feet to look for signs of changes such as abnormal growth rings, a dished dorsal hoof wall, inspect his white line to look for signs of bruising and stretching, hoof tester response, I may ask questions about his history and any recent changes to his diet and activity, etc. I may recommend additional testing based off those physical exam findings.


This is one disease process I feel annual and biannual wellness monitoring can benefit greatly: the earlier this disease process is interrupted, the more success husbandry changes will have on its progression if it even develops at all. There is often times something we can do, changes we can make to help and because of this, it’s an important disease process that inspired me to write my wellness plans.

For most of these horses a weight loss and calory restriction, vitamin and mineral supplementation, and exercise program is imperative to reduce the metabolic derangements occurring. For the exceptional thin horses afflicted by it, diet changes that involve shifting dietary calories from the traditional grains high in sugar and starch, to fats and proteins. Some horses have genetics working profoundly against, but even for those guys, while we may not be able to stop the disease process, we can improve the circumstances and slow its progression.


Interested in our Wellness Plans? Check those out here.


Want to learn more? Here are some informative articles for your viewing pleasure!


El Museo de Maya en Cancun, Mexico.

Sarah L Rhoades, DVM




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