AS detailed in our last article, fat sensitivity is a common reported finding to our nutritional helpline, but often one incompletely investigated.
Often these cases are lumped into the “pancreatitis plus xxxxx” category, which I can’t say I’m always comfortable with.
Conscientious vets and nurses all over the country are concerned about the fat content of pet foods, wanting to minimise the risk of a flare in acute signs – and rightly so given the impact that true pancreatitis has on the pet’s health.
A good rule of thumb is to look at fat sensitivity critically, particularly as we know how valuable this macronutrient can be to most dogs and cats. In dogs, fat can consistently be between 80-95% digestible 2 and may assist greatly in the recovery process, packing approximately 2.5 times the caloric value than its carbohydrate counterpart.3
However, where PLI doesn’t confirm diagnosis and a fasting hypertriglyceridaemia isn’t found on bloods, likelihood is that the individual in question may have simply taken on a high-fat meal which overwhelms the gastrointestinal system’s digestive capacity, leading to sometimes foul osmotic diarrhoea.
In these circumstances, allowing the individual to recover from the upset with a highly digestible, low residue diet alongside supportive therapy is often enough to facilitate a return to normal, healthy function.
With this in mind, our case, presented on a busy Saturday morning surgery is “Lottie”, a six-year-old entire (ex-breeding bitch) Labrador Retriever. She has come to us as a PU/PD case which the head nurse who booked in the appointment has pegged as a UTI case, putting the cephalosporin vial within your easy reach.
Lottie is a little on the heavy side (BSC 6/9) but has recently lost weight, according to her conscientious owner who weighs her every other week. She’s gone off her food (a commercial diet which is rationed carefully now that she’s not breeding) and her stool quality seems to be shifting “more toward the liquid than solid-style”.
As you talk through the history, your examination and the problem, you realise that this case may not be the open-and-shut book that you hoped for. You pop your head out of the consulting room, pleased to see the strain of the full waiting room at least slightly relieved by a smiling colleague taking in their second puppy vaccination.
Let’s fast forward through our increasingly close relationship with Lottie and her owner to two weeks later, when they both visit the surgery for the fourth time.
It turns out that urine analysis revealed a bacterial cystitis, promptly treated with an ongoing course of antibiotics. Alongside these results, the laboratory has flagged glycosuria on UA and it seems that our increased urination and reflex drinking probably originated first from the diabetes mellitus (confirmed by a fasting hyperglycaemia), also diagnosed last week. You embark upon stabilisation with insulin and the long journey of diabetes management.
Not unlike many canine diabetic cases, bloods also showed a hyperlipidaemia, with amylase and lipase above reference ranges too.
Now that you’re getting to know the owner quite well, further meticulous questioning has revealed that in fact, Lottie’s stools have never really been as normal as you’d expect. Rarely are they completely “pick-upable” on walks in the park and sometimes they’re downright offensive.
Your mind now boggles at the thought of a pancreatic work-up (cPLI, etc.) but first you review the food that was mentioned in your initial consult to find that while ration volumes were being controlled, the formula was in fact one that Lottie enjoyed while in breeding condition, for dogs at “performance” level.
You note that the fat content is higher than the maintenance products you sell in-house which makes you think that a full nutritional assessment is in order too. There’s no drought of science supporting the nutritional management of cases of both diabetes and hyperlipidaemia/pancreatitis and this should really be taken into account.
Lottie is a case of compounding pathologies and dietary interests. Many may ask what came first, pancreatitis or diabetes?
Excessive pancreatic damage is said to be responsible for the development of diabetes in 28% of cases 1 and it makes sense that a late-stage fibrotic pancreas should lead to deficits in both digestive (exocrine) and glycaemic control (endocrine) functions.
On the other hand, diabetes leads to alterations in lipid metabolism. Increased serum triglycerides and cholesterol are found in the insulin-deficient animal. Here, clearance of chylomicrons (large lipoproteins in the blood) is impaired due to insufficient activation of lipoprotein lipase in vascular endothelial cells by insulin.2
In plain English, this means free fatty acids become more available in the blood-stream and a resultant lipaemic sample may be seen even in a fasted blood test.
Regardless of aetiology, glucose regulation by means of insulin therapy should assist the resolution of Lottie’s hyperlipidaemic state.
Foods formulated for the diabetic dog boast many features, some of which have a strong evidence base, others variable.
Low carbohydrate levels are a common starting point, related closely to the nutritional objectives shared in human and feline diabetic diets. Rationale now supports consistency in carbohydrate feeding and suggests rice should be avoided in preference for more complex sources such as barley and sorghum.1
Fat restriction makes sense given the derailment of lipid metabolism with insulin deficiency. We should keep in mind the recommendation to bring fat level below 20% on a metabolisable energy basis in chronic pancreatitis cases.7
What is most key is digestibility and Lottie’s responsiveness to different levels of fat. Simply providing her with a higher quality diet with a lesser total fat intake than her previous diet is likely to be of benefit.
Current thinking is that bringing fat levels below 30% metabolisable energy will lead to improved lipid profiles.1 Monitor weight in your patients, however, particularly if they’re in poor body condition.
All considered and, in Lottie’s case, we can be thankful that diabetic diets are usually low-to-moderate in fat, provide carbohydrate levels and composition which aims to moderate insulin requirements and as a result, derive much of their energy content from protein sources.
These diet features mean that with conscientious feeding alongside medical stabilisation (did anyone say neutering?), Lottie’s future looks brighter than it did before she entered the clinic that fateful Saturday.
I’d reach for a diabetic diet first in Lottie’s case, allowing us to address glucose homoeostasis alongside the predisposition to fat sensitivity.
If her gastrointestinal tract fails to respond with well-formed motions, we always have the option of GI low fat ahead of us.
References and additional reading
- Fleeman, L. and Rand, J. (2006) Diabetes mellitus: nutritional strategies. In: Pibot, P., Biourge, V. and Elliott, D. eds. Encyclopedia of Canine Clinical Nutrition, Paris: Aniwa, pp192-221.
- Hand, M., Thatcher, C., Remillard, R. and Roudebush, P. (eds) (2000) Small Animal Clinical Nutrition, Kansas: Mark Morris Institute.
- Grandjean, D. (2006) Everything you need to know about the role played by nutrients in the health of dogs and cats. Aimargues: Royal Canin.
- Scheneck, P. (2006) Canine hyperlipidaemia: causes and nutritional management. In: Pibot, P., Biourge, V. and Elliott, D. eds. Encyclopedia of Canine Clinical Nutrition, Paris: Aniwa, pp222-250.
- Simpson, K. (2006) The role of nutrition in the pathogenesis and the management of exocrine pancreatic disorders. In: Pibot, P., Biourge, V. and Elliott, D. eds. Encyclopedia of Canine Clinical Nutrition, Paris: Aniwa, pp162- 191.
- Watson, D. (2005) How I approach polydipsia and polyuria. Veterinary Focus 15 (3): 27-31.
- Wiberg, M. E., Nurmi, A. and Westermarck, E. (1999) Serum trypsinlike immunoreactivity measurement for the diagnosis of subclinical exocrine pancreatic insufficiency. J Vet Intern Med 13: 426-432.
