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Diet and canine pancreatitis

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Diet and canine pancreatitis* *Based on article in Dutch (1) Main points Acute pancreatitis is believed to result from premature, excessive activation of digestive enzymes, causing acinar-cell injury and local inflammatory reactions. Diagnosis of acute pancreatitis in the dog involves the outcomes of physical examination, clinical chemistry and imaging. The condition may resolve spontaneously, or merge into chronic or recurrent pancreatitis. Acute pancreatitis may also lead to pancreatic necrosis, inflammation of surrounding tissues and systemic complications with fatal course. Subclinical, chronic pancreatitis may bring about diabetes mellitus and exocrine, pancreatic insufficiency. Recovering and recovered patients are quite often prescribed a low-fat, dietetic food. There are no published clinical studies on the efficacy of fat restriction with regard to recurrence of canine pancreatitis. The principle is that fat restriction limits secretion of cholecystokinin, thus preventing hyperstimulation of the pancreas. Dry and wet veterinary foods with pancreatitis as therapeutic indication contain 15-30 energy% fat (Note 1). The range for regular dry dog foods is 20-45 energy%. Clearly, some pancreatic diets are higher in fat than low-fat, regular dry foods. Three dog experiments indicate that ≥ 60% dietary energy as fat entails a risk of pancreatitis development. Feeding healthy dogs a high-fat, protein-deficient diet produced macroscopic and microscopic abnormalities of the pancreas, pointing to pancreatitis. Three out of 9 dogs with epilepsy unfolded pancreatitis after consumption of a fat-rich diet. In dogs with experimentally induced pancreatitis, preceding high intake of fat intensified the severity of clinical responses and pancreatic lesions. Hypothetical, underlying reasons for fat-induced pancreatitis are pancreatic hyperstimulation, increased fragility of acinar membranes, and excessive, eicosanoid-mediated inflammation. There are no epidemiological studies on diet and canine pancreatitis. Case-control studies have identified obesity as a risk factor of canine pancreatitis. As mentioned above, three studies indicate that diets high in fat can provoke or exacerbate pancreatitis, but dose response, safe upper limit and the role of fat type are unknown. Moreover, the nature of fat-induced pancreatitis may differ from that of acute pancreatitis seen in practice. Nevertheless, it is prudent to avoid high-fat diets, in any case diets with more than 60 energy% fat, so as to decrease the risk of (recurrent) pancreatitis. Some commercial, complete dog foods contain more than 60 energy% fat. The ranges of fat content in various dog foods roughly are as follows: dry foods, 20-45 energy%, canned foods, 35-65%; deep-frozen foods, 50-70%; freeze-dried foods, 35-75%. In an attempt to prevent pancreatitis, foods with more than 60 energy% should not be fed as sole source of nutrition. Low-fat food may decrease the risk of (recurrent) pancreatitis and has the additional benefit of allowing somewhat easier control and attainment of ideal body weight, which appears to be a protective factor.
Dier-en-Arts 2016; Nr 4: 102-105.
Anton C. Beynen
Diet and canine pancreatitis*
*Based on article in Dutch (1)
Main points
Acute pancreatitis is believed to result from premature, excessive activation of digestive enzymes,
causing acinar-cell injury and local inflammatory reactions. Diagnosis of acute pancreatitis in the dog
involves the outcomes of physical examination, clinical chemistry and imaging. The condition may
resolve spontaneously, or merge into chronic or recurrent pancreatitis. Acute pancreatitis may also
lead to pancreatic necrosis, inflammation of surrounding tissues and systemic complications with
fatal course. Subclinical, chronic pancreatitis may bring about diabetes mellitus and exocrine,
pancreatic insufficiency.
Recovering and recovered patients are quite often prescribed a low-fat, dietetic food. There are no
published clinical studies on the efficacy of fat restriction with regard to recurrence of canine
pancreatitis. The principle is that fat restriction limits secretion of cholecystokinin, thus preventing
hyperstimulation of the pancreas. Dry and wet veterinary foods with pancreatitis as therapeutic
indication contain 15-30 energy% fat (Note 1). The range for regular dry dog foods is 20-45 energy%.
Clearly, some pancreatic diets are higher in fat than low-fat, regular dry foods.
Three dog experiments indicate that ≥ 60% dietary energy as fat entails a risk of pancreatitis
development. Feeding healthy dogs a high-fat, protein-deficient diet produced macroscopic and
microscopic abnormalities of the pancreas, pointing to pancreatitis. Three out of 9 dogs with
epilepsy unfolded pancreatitis after consumption of a fat-rich diet. In dogs with experimentally
induced pancreatitis, preceding high intake of fat intensified the severity of clinical responses and
pancreatic lesions. Hypothetical, underlying reasons for fat-induced pancreatitis are pancreatic
hyperstimulation, increased fragility of acinar membranes, and excessive, eicosanoid-mediated
inflammation.
There are no epidemiological studies on diet and canine pancreatitis. Case-control studies have
identified obesity as a risk factor of canine pancreatitis. As mentioned above, three studies indicate
that diets high in fat can provoke or exacerbate pancreatitis, but dose response, safe upper limit and
the role of fat type are unknown. Moreover, the nature of fat-induced pancreatitis may differ from
that of acute pancreatitis seen in practice. Nevertheless, it is prudent to avoid high-fat diets, in any
case diets with more than 60 energy% fat, so as to decrease the risk of (recurrent) pancreatitis.
Some commercial, complete dog foods contain more than 60 energy% fat. The ranges of fat content
in various dog foods roughly are as follows: dry foods, 20-45 energy%, canned foods, 35-65%; deep-
frozen foods, 50-70%; freeze-dried foods, 35-75%. In an attempt to prevent pancreatitis, foods with
more than 60 energy% should not be fed as sole source of nutrition. Low-fat food may decrease the
risk of (recurrent) pancreatitis and has the additional benefit of allowing somewhat easier control
and attainment of ideal body weight, which appears to be a protective factor.
High fat intake by healthy dogs
In 1948, Lindsay et al. (2) published an uncontrolled study, indicating that a very-high-fat, protein-
deficient diet caused pancreatitis in dogs. The diet consisted of low-fat meat, lard, sucrose, B
vitamins, vitamins A and D, bone ash, salts and cellulose. The percentage distribution of dietary
energy between proteins, fats and carbohydrates was 5:79:16. The energy% of protein corresponds
with 2.9 g/MJ, which is 39% below the minimum requirement of adult dogs (3). The amount of food
offered was superfluous. After 35 days, all 13 dogs had fatty liver. In 11 dogs, pancreatic lesions
were macroscopically visible. Microscopically, interstitial and peripancreatic fat necrosis and fibrosis
were observed. Clinical symptoms are not described. Four and 9 dogs, respectively, had lost and
gained weight.
Epileptic dogs
In a clinical trial (4), dogs with epilepsy received a control diet for three to six months; the
percentage energy composition of the diet was 23:31:46 (protein: fat: carbohydrate). After the
baseline monitoring period, dogs with five or more seizures either remained on the control diet or
were switched to a fat-rich diet with energy composition of 18:79:3. Two of the 31 dogs on the
control diet and three out of the 9 on the high-fat diet developed pancreatitis. The outcome alerts to
high susceptibility of pancreatitis in epileptic dogs and intensification by high fat intake. One case-
control study has identified epilepsy as a risk factor of pancreatitis (5), but another study did not (6).
Dog model of pancreatitis
Haig (7) has investigated the influence of food composition on the severity of experimentally
induced pancreatitis. Dogs consumed one of five diets (n = 6/dietary group), including a commercial
wet food as reference. Four diets comprised refined ingredients (casein, plant oil or lard, starch),
salts and vitamins. The semipurified control diet had an energy composition of 26:21:53. The other
diets were either high in protein (87:6:7), high in fat (21:62:17) or high in carbohydrates (8:7:85). The
dogs fed the reference, high-protein or high-fat diet became heavier, but details as to food intake
and weight change are not given.
After each dog had been fed its diet for six weeks, pancreatitis was induced. The major pancreatic
duct was cannulated, and a mixture of ox bile and trypsin was infused into the pancreas. Water was
allowed ad libitum after the operation and the diet was provided again beginning 24 hours after
operation. The dogs were examined clinically for two days, followed by euthanasia and autopsy. The
severity of pancreatitis was evaluated on the basis of various findings: clinical presentation
(recovering or not), gross pathology (edema, bleeding, necrosis) and microscopic examination
(pancreatic and peripancreatic fat necrosis). All six dogs fed on the high-fat diet showed severe
abnormalities. None or one out of the six dogs in each of the other four dietary groups had serious
signs of pancreatitis.
Possible mechanism
As to the etiology of dietary-fat-induced pancreatitis, the most common hypothesis is that excessive
fat feeding causes hyperstimulation of the pancreas and ensuing, intracellular activation of digestive
enzymes. Those events may also hold for fat-amplified pancreatitis. Using the four semipurified diets
described above, the effect of macronutrients on secretion of digestive enzymes was determined
(8). The diets were fed for a period of 7 weeks. During the last three weeks, pure pancreatic juice
was obtained by inserting a cannula into the major pancreatic duct and directing the juice into vials.
Juice flow was stimulated by continuously injecting secretin and pancreozymin. The high-fat diet,
which aggravated the induced pancreatitis (7), did not differently influence the secretion of digestive
enzymes. That outcome does not support the hyperstimulation hypothesis, but does not refute it
either as the release of active enzymes within pancreatic cells was not measured.
In another study (9), Haig fed the four diets to healthy dogs for 6 weeks. The high-fat diet gave
greatest weight gain. While the dogs were under anesthesia, biopsies were taken from the processus
unicatus, lobus quadratus and right cortex renalis. Then, the pancreatic, hepatic and renal cells were
isolated, incubated under different conditions, and their survival quantified. Acinar cells from the
dogs fed the high-fat diet, compared with acinar cells from the other donor dogs, were less sturdy:
they were three times as sensitive to the physical and chemical stress of saline, 7 times as sensitive
to ox bile and 40 times as sensitive to ox bile and trypsin combined. The destructive effect mediated
by the high-fat diet was specific to the pancreatic acinar cells. There was no diet effect on the stress-
determined survival of the liver and kidney cells.
Haig’s study (9) suggests that copious fat intake diminishes the stability of acinar cells, thereby
somehow increasing the risk of pancreatitis. Another idea is based on studies with human patients
with acute pancreatitis, isolated acinar cells, obese mice and rats (10, 11). High intake of unsaturated
fats leads to fat accumulation in pancreatic acinar cells, which is believed to cause excessive, lipolytic
release of pro-inflammatory polyunsaturated fatty acids, thus increasing the risk of pancreatitis.
Early nutrition in acute pancreatitis
To provide “pancreatic rest” in dogs with acute pancreatitis, food is often withheld until clinical signs
resolve. There is evidence that feeding within 48 hours of hospitalization for canine acute
pancreatitis, decreases the time to return to voluntary intake (12). The sick dogs were non-assisted
fed or assisted fed via a nasoesophageal tube. It also appears that enteral nutrition is superior to
parenteral nutrition. In dogs with taurocholate-trypsin-induced pancreatitis, intra-jejunal versus
parenteral nutrition had benefits (13-16). A small-scale study in dogs with spontaneous acute
pancreatitis, found that esophageal versus parenteral feeding reduced vomiting and abdominal pain
(17).
Note 1
Diet composition can be quantified and qualified in terms of its energy sources: by the percentages
of metabolizable energy from proteins, fats and carbohydrates. That information allows direct
comparisons of different diets with regard to their macronutrient compositions. Clearly, an increase
in the proportion of one macronutrient necessarily involves a decrease in the proportion of one or
both other macronutrients. High-fat diets may be relatively low in carbohydrates and/or protein. It
should be noted that for adult dogs the minimum protein requirement is 4.78 g/MJ (3) or 8.1
energy%. Feeding carbohydrate-free diets to dogs is feasible, but protein content in the diet should
be higher than the proposed requirement (3), in order to support gluconeogenesis (cf. 18).
A macronutrient under study must be substituted for an iso-energetic amount of another
macronutrient in the base diet. If not, the nutrient:energy ratios are altered, causing different
intakes of nutrients at unchanged energy consumption (cf. 19, 20), and thus extra variables. The
necessary macronutrient exchange implies that the observed effect is always the net effect of
addition of one and omission of another macronutrient.
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... In the dog, a high-fat (> 60 energy% fat) diet may cause pancreatitis, but the dose-response relationship is unknown (13). There are no prospective, dietary studies in dogs with pancreatitis, but it is likely that fat restriction contributes to control of the condition and prevention of (recurrent) pancreatitis. ...
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