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Diet and canine pancreatitis

  • July 2019
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Anton Beynen
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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.
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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.
Literature
1. Beynen A.C. Voeding en pancreatitis bij de hond. Dier-en-Arts 2016; Nr 4: 102-105.
2. Lindsay S, Entenman C, Chaikoff IL. Pancreatitis accompanying hepatic disease in dogs fed a high
fat, low protein diet. Arch Pathol 1948; 45: 635-638.
3. National Research Council. Nutrient requirements of dogs and cats. National Academy of Sciences,
Washington DC, 2006.
4. Patterson EE, Munana KR, Kirk CA, Lowry SR, Armstrong PJ. Results of a ketogenic food trial for
dogs with idiopathic epilepsy. J Vet Intern Med 2005; 19: 421.
5. Hess RS, Kass PH, Shofer FS, Van Winkle TJ, Washabau RJ. Evaluation of risk factors for fatal acute
pancreatitis in dogs. J Am Vet Med Assoc 1999; 214: 46-51.
6. Cook AK, Breitschwerdt EB, Levine JF, Bunch SE, Linn LO. Risk factors associated with acute
pancreatitis in dogs: 101 cases (1985-1990). J Am Vet Med Assoc 1993; 203: 673-679.
7. Haig THB. Experimental pancreatitis intensified by a high fat diet. Surg Gynecol Obstet 1970; 131:
914-918.
8. Haig THB. Pancreatic digestive enzymes: influence of a diet that augments pancreatitis. J Surg Res
1970; 10: 601-607.
9. Haig THB. Nutritional alteration of pancreatic acinar cell stability. Ann Surg 1970; 172: 852-860.
10. Navina S, Acharya C, DeLany JP, Orlichenko LS, Baty CJ, Shiva SS, Durgampudi C, Karlsson JM, Lee
K, Bae KT, Furlan A, Behari J, Liu S, McHale T, Nichols L, Papachristou GI, Yadav D, Singh VP.
Lipotoxicity causes multisystem organ failure and exacerbates acute pancreatitis in obesity. Sci
Transl Med 2011; 107: 107ra110
11. Matsuda A, Makino N, Tozawa T, Shirahata N, Honda T, Ikeda Y, Sato H, Ito M, Kakizaki Y,
Akamatsu M, Ueno Y, Kawata S. Pancreatic fat accumulation, fibrosis, and acinar cell injury in the
Zucker diabetic fatty rat fed a chronic high-fat diet. Pancreas 2014; 43: 735Y743
12. Harris JP, Parnell NK, Griffith EH, Saker KE. Retrospective evaluation of the impact of early enteral
nutrition on clinical outcomes in dogs with acute pancreatitis: 34 cases (2010-2013). J Vet Emerg Crit
Care 2017; 27: 425-433.
13. Qin H-L, Su Z-D, Gao Q, Lin Q-T. Early intrajejunal nutrition: bacterial translocation and gut barrier
function of severe acute pancreatitis in dogs. Hepatobilliary Pancreatic Dis Int 2002; 1: 150-154.
14. Qin H-L, Su Z-D, Hu L-G, Ding Z-X, Lin Q-T. Effect of early intrajejunal nutrition on pancreatic
pathological features and gut barrier function in dogs with acute pancreatitis. Clin Nutr 2002; 21:
469-473.
15. Qin H-L, Su Z-D, Hu L-G, Ding Z-X, Lin Q-T. Parenteral versus early intrajejunal nutrition: Effect on
pancreatitic natural course, entero-hormones release and its efficacy on dogs with acute
pancreatitis. World J Gastroenterol 2003; 9: 2270-2273.
16. Qin H-L, Su Z-D, Hu L-G, Ding Z-X, Lin Q-T. Effect of parenteral and early intrajejunal nutrition on
pancreatic digestive enzyme synthesis, storage and discharge in dog models of acute pancreatitis.
World J Gastroenterol 2007; 21: 1123-1128.
17. Mansfield CS, James FE, Steiner JM, Suchodolski JS, Robertson ID, Hosgood G. A pilot study to
assess tolerability of early enteral nutrition via esophagostomy tube feeding in dogs with severe
acute pancreatitis. J Vet Intern Med 2011; 25: 419-425.
18. Beynen AC. All-meat diets for dogs. Creature Companion 2015; June: 52-53.
DOI: 10.13140/RG.2.2.22137.47208
19. Beynen AC, Coates ME. Nutrition and experimental results. In: Principles of Laboratory Animal
Science (Van Zutphen LFM, Baumans V, Beynen AC, eds), Elsevier B.V., Amsterdam, 2001, pp 111-
127.
20. Beynen AC. Pet food label: analysis panel. Creature Companion 2014; May: 62-63.
DOI: 10.13140/RG.2.2.34720.38405
... 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. ...
Beynen AC, 2022. Diet and feline triaditis
Article
Full-text available
  • Apr 2022
Diet and feline triaditis* *Based on article in Dutch (1) Main points Triaditis is a condition whereby inflammations of the pancreas, hepatobiliary system and small intestine occur simultaneously. Roughly 30 to 50% of the cats with pancreatitis or cholangitis/hepatitis also has triaditis (2, 3). The clinical symptoms are diverse, but anorexia, vomiting, diarrhea and weight loss are commonly perceivable. A definitive diagnosis of triaditis requires histopathological examination of all three organs involved. There is no published, clinical research with regard to the efficacy of dietary therapy in feline triaditis. For treatment in the long term, the dietetic food should support all three affected organs as good as possible. The hereby proposed composition of such a therapeutic food is necessarily based on theoretical considerations only. The dietetic food should be nutritionally complete and anti-inflammatory. Inhibition of the inflammations in the three affected organs is based on hypoallergenic protein sources and high contents of eicosapentaenoic acid (EPA) and gamma-linolenic acid (GLA). In addition, hepatic urea synthesis and copper excretion are relieved by relatively low dietary levels of protein and copper. A relatively low fat content is a prudent measure in controlling pancreatitis. Pathogenesis In cats, when compared with dogs, the common bile duct and pancreatic duct have a common entry to the duodenum. That could imply that pancreatitis easily leads to cholangitis/hepatitis or vice versa. However, there is no evidence that triaditis results from organ interactions or rather by separate processes. Within hypothetical models, both acute pancreatitis and intestinal inflammation could initiate the development of triaditis (2, 3). Acute triaditis Immediate, enteral, nutritional support is indicated in acute triaditis accompanied by, amongst others, persistent emesis, anorexia, hypotension and/or pyrexia (2). As soon as the patient can eat by her/himself, a suitable dietetic food should be started. In warmed and wet form, intake of the food can possibly be stimulated. Food intake may be further supported and initiated by force feeding if it is not associated with fierce resistance of the patient. Dietetic foods Within the European Union, triaditis is not legally permitted as particular nutritional purpose of a commercial dietetic food for cats (4). A manufacturer of therapeutic foods, which is also present at the European market, offers in the United Kingdom three veterinary diets that meet "nutritional solutions" for cats with triaditis (5). The diet as required by the triaditis patient is described as a hypoallergenic (if needed), highly digestible diet without energy restriction.
... Diets very high in fat, or containing more than 60 energy% fat, entail a risk of pancreatitis in dogs (28). That risk should be weighed when very-high-fat diets are considered/used in an attempt to prevent canine cancer. ...
Beynen AC, 2020. Diet and canine cancer
Article
Full-text available
  • Sep 2020
Diet and canine cancer In over 350,000 insured, Swedish dogs, cancer was the major cause of death, accounting for 18% of the bereavements (1). In the Swiss Canine Cancer Registry (2), the most frequent tumor diagnosis was adenoma/adenocarcinoma, or benign/cancerous tumors of covering, epithelial tissues. The most affected body parts were the mammary gland in female dogs and the gastrointestinal tract in males. Between dog breeds, there were considerable differences in the predilection sites of various cancers (2). Diet composition likely affects both the development of canine cancer and its disease course, but there is only fragmentary information from published research. A controlled study to compare diets with regard to prevention of canine cancer is virtually undoable (cf. 3). Two case-control studies (4, 5) compared the diets of female dogs with or without breast cancer. Such studies can identify associations between diet and cancer, but not causal relationships. One cohort study (6) linked the multiple-variable diets of dogs with breast cancer to their survival times. In a clinical trial, dogs with lymph-node cancer were fed diets that differed as to one composite variable (7). The two case-control studies had opposite outcomes concerning the pre-diagnosis diets of dogs with breast cancer: the affected dogs had either consumed somewhat less or more fat. However, both studies found that dogs with breast cancer had juvenile overweight more often than the control dogs. The cohort study shows that a high-protein, high-carbohydrate, low-fat diet was associated with a 1.5-years increase in survival time in dogs with breast cancer. In the clinical trial, dietary fish oil plus the amino acid arginine, when compared with soybean oil alone, elongated survival time by 3 months in dogs with lymphoma. There are too little research data for evidence-based dietary guidelines to prevent or manage canine cancer. The two case-control studies had contradictory outcomes. Reproducibility of the cohort and clinical study is unknown. Taken together, it may be concluded that commercially available diets for the treatment and management of canine cancer lack a solid and broad scientific foundation. The same applies to recipes of home-made diets for dogs with cancer. In the two case-control studies, dogs with breast cancer were more often reported by their owners to have been "obese" or "not thin" as puppies. Perhaps, prevention of overweight may not only increase life span of dogs (3), but also reduce breast-cancer risk in female dogs even though the disease is associated with aging (8). For the time being, longevity promotion in individual dogs means portion-controlled feeding of a complete diet with body condition as compass (3, Note 1).
Petfood label: analysis panel
Research
Full-text available
  • Apr 2014
Petfood label: analysis panel The petfood label displays an analysis panel with the food's nutrient composition, but the value is limited. Moreover, specific expertise is required to evaluate the analysis panel. Owners may follow the principle that the best judge of a commercial petfood is the animal itself. Information regarding the nutrient composition of a commercial petfood is found in the analysis panel on the label. Here, manufacturers declare the concentrations of up to about 10 nutrients, including protein and fat, expressed as percentages in the product. In addition, the added amounts of a few vitamins and trace elements may be presented. There are more than 40 essential nutrients. It is evident that petfood cannot be properly evaluated on the basis of the label only. Complete petfood cannot be approved unconditionally on the basis of the analysis panel, but it can be disqualified. The exercise requires calculation of nutrient:energy ratios in the food and evaluation of these ratios in the light of the recommended nutrient allowances. For meaningful comparisons of the nutrient profiles of different petfoods, the values in the analysis panels also have to be converted into nutrient:energy ratios. Few pet owners are comfortable with the necessary mathematics and with interpreting the results. Nutrient percentage Substance of the analysis panel is determined by law in many countries. Guaranteed analysis panels show minimum and maximum percentages and thus mostly are not reflecting the exact amounts of the nutrients in the food. Typical analysis panels display conforming percentages. Food in a particular package may deviate from the typical composition. Foods with the same label are manufactured over time in different production batches using similar, but not necessarily identical ingredients. Basic percentages in the analysis panel concern crude protein, crude fat, crude fiber and crude ash. The adjective crude refers to the analytical procedures that yield outcomes with little nutritional relevance. For instance, the protein and fat measurements tell nothing about the amino acid and fatty acid patterns. The crude fiber fraction is poorly characterized. Nutrient availability The amounts of nutrients in foods as determined by chemical analysis are not fully available to the animal. Between foods, nutrient availability can differ. Commercial dog foods with comparable declared and analysed composition may differ as to digestibility (1). Puppies were fed on one of four dry foods with identical guaranteed analysis panel (2). Digestibility of crude protein was measured as the percentage of ingested protein not recovered in feces. Between the four foods, protein digestibility ranged between 69 and 80%. Weight gain of the puppies also differed among the dietary groups. Even though two foods have identical or similar analysis panels, the animal's response can differ substantially.
All-meat diets for dogs
Research
Full-text available
  • Jul 2015
All-meat diets for dogs All-meat dog diets can vary widely as to ingredient and nutrient composition, but they all lack fiber and digestible carbohydrates. When the diet is free of liver and not supplemented, it is deficient in vitamins A and D. Diets only containing boneless animal parts fall short in calcium. Diets rich in thyroid gland tissue cause poisoning with thyroid hormone. It is said that a true all-meat diet for dogs is nutritionally adequate only if it adheres to the prey-model concept. Accordingly, the diet should consist of whole (production) animals or mirror them in the form of a mixture of their body parts. Turning the prey-model concept into practice is virtually impossible. Moreover, nutritional adequacy of whole prey is not proven by long-term feeding experiments or extensive nutrient analyses. It is worth mentioning that whole broiler chicken, as sole source of nourishment, may induce skeletal disease in growing dogs of large breeds through its high calcium content, while the high level of protein may enhance the development of chronic kidney disease in senior dogs (1). Digestible carbohydrates furnish glucose, but they are not essential nutrients. When carbohydrate intake is zero, glucose will be formed from non-carbohydrate precursors which include certain amino acids derived from proteins. This implies that an all-meat diet should contain more protein than carbohydrate-containing foods. An all-meat diet rich in fat and therefore not superfluous in protein could lead to protein deficiency, especially in puppies and breeding bitches. On the other hand, low-fat, all-meat diets may be so excessive in protein that they elicit diarrhea. All-meat diets All-meat diets may be defined as diets consisting of one or more animal tissues. According to the prey-model concept, the complete nutrient profile dogs need is attained when the diet is modeled on ratio of the parts found in intact animals. Over time, rations must not contain muscle meat only, but also head, skin, bone, organs and entrails. Older publications (2) say that arctic dogs thrive on rations containing fresh meat in the form of white whale, walrus, seal and bear. Dried fish, especially cod and halibut, has also been used. However, it is unknown whether the dogs ate these animal feedstuffs exclusively. Moreover, it is uncertain whether the classical arctic dog rations supported a long and healthy life. Dogs foods marketed as complete, raw frozen or raw freeze-dried, and also some canned foods, get close to all-meat nutrition, but they contain a little plant ingredients. There are people who believe that meat is the only thing a dog should ever be fed. Strictly meat diets take different forms. Variable diet components may be fed raw, cooked or dried and be purchased in fresh, frozen, dry or canned form. Using true all-meat rations only, it is difficult to formulate a week menu that meets the dog's nutrient requirements eked out over the concerning period. Thus, all-meat diets entail risks of imbalances.
Pancreatic Fat Accumulation, Fibrosis, and Acinar Cell Injury in the Zucker Diabetic Fatty Rat Fed a Chronic High-Fat Diet
Article
Full-text available
  • Apr 2014
The histological alteration of the exocrine pancreas in obesity has not been clarified. In the present study, we investigated biochemical and histological changes in the exocrine pancreas of obese model rats. Zucker lean rats were fed a standard diet, and Zucker diabetic fatty (ZDF) rats were divided into 2 groups fed a standard diet and a high-fat diet, respectively. These experimental groups were fed each of the diets from 6 weeks until 12, 18, 24 weeks of age. We performed blood biochemical assays and histological analysis of the pancreas. In the ZDF rats fed a high-fat diet, the ratio of accumulated pancreatic fat area relative to exocrine gland area was increased significantly at 18 weeks of age in comparison with the other 2 groups (P < 0.05), and lipid droplets were observed in acinar cells. Subsequently, at 24 weeks of age in this group, pancreatic fibrosis and the serum exocrine pancreatic enzyme levels were increased significantly relative to the other 2 groups (P < 0.01). In ZDF rats fed a chronic high-fat diet, fat accumulates in pancreatic acinar cells, and this fatty change seems to be related to subsequent pancreatic fibrosis and acinar cell injury.This is an open-access article distributed under the terms of the Creative Commons Attribution-NonCommercial-NoDerivatives 3.0 License, where it is permissible to download and share the work provided it is properly cited. The work cannot be changed in any way or used commercially. http://creativecommons.org/licenses/by-nc-nd/3.0.
Lipotoxicity Causes Multisystem Organ Failure and Exacerbates Acute Pancreatitis in Obesity
Article
Full-text available
Obesity increases the risk of adverse outcomes during acute critical illnesses such as burns, severe trauma, and acute pancreatitis. Although individuals with more body fat and higher serum cytokines and lipase are more likely to experience problems, the roles that these characteristics play are not clear. We used severe acute pancreatitis as a representative disease to investigate the effects of obesity on local organ function and systemic processes. In obese humans, we found that an increase in the volume of intrapancreatic adipocytes was associated with more extensive pancreatic necrosis during acute pancreatitis and that acute pancreatitis was associated with multisystem organ failure in obese individuals. In vitro studies of pancreatic acinar cells showed that unsaturated fatty acids were proinflammatory, releasing intracellular calcium, inhibiting mitochondrial complexes I and V, and causing necrosis. Saturated fatty acids had no such effects. Inhibition of lipolysis in obese (ob/ob) mice with induced pancreatitis prevented a rise in serum unsaturated fatty acids and prevented renal injury, lung injury, systemic inflammation, hypocalcemia, reduced pancreatic necrosis, and mortality. Thus, therapeutic approaches that target unsaturated fatty acid-mediated lipotoxicity may reduce adverse outcomes in obese patients with critical illnesses such as severe acute pancreatitis.
Retrospective evaluation of the impact of early enteral nutrition on clinical outcomes in dogs with pancreatitis: 34 cases (2010-2013)
Article
Objective: To evaluate the effect of early enteral nutritional therapy on time to return to voluntary intake, maximum food consumption, incidence of gastrointestinal intolerance (GI), and total hospitalization time for dogs with acute pancreatitis. Design and setting: Retrospective analysis of dogs with pancreatitis at a veterinary teaching hospital between 2010 and 2013. Animals: Thirty-four client-owned dogs diagnosed with acute or acute-on-chronic pancreatitis. Procedures and interventions: Medical records of dogs evaluated for inappetence, anorexia, and GI for which a diagnosis of pancreatitis was recorded were reviewed. The time to initiation of food offerings since hospitalization were recorded in addition to signalment, historical medical conditions, chief complaint, physical examination findings, diagnostic results, treatments provided, timing of food offering (within 48 h of hospitalization, early feeding group (EFG) versus delayed feeding group (DFG), diet therapy (low fat versus high fat), caloric intake (% resting energy requirement), incidence of GI (%), and length of hospitalization (LOH) (days). A Clinical Severity Index Score (CSIS) was determined for each patient. Measurements and main results: Dogs in the EFG demonstrated a decreased time to return of voluntary intake (2.1 days, EFG versus 2.7 days, DFG; P = 0.05) and time (days) to maximum intake (3, EFG versus 3.4 DFG) as compared to the DFG dogs. The DFG exhibited more GI versus EFG irrespective of CSIS grouping (60% versus 26%, P = 0.04). A CSIS ≥ 7 was associated with prolonged LOH (P = 0.004); however, time to initiation of feeding and diet selection did not impact LOH (P = 0.8). Conclusions and clinical relevance: Results of the study suggested that feeding within 48 hours of hospitalization for canine pancreatitis has a positive impact on return to voluntary intake and decreases the frequency of GI in these patients, independent of CSIS. The traditional protocol of withholding food during hospitalization may not be necessary nor yield the most benefit for patient recovery; subsequently early enteral refeeding should be considered.
Nutrition and experimental results
Article
  • Jan 2001
Results of ketogenic food trial for dogs with idiopathic epilepsy
Article
  • Jan 2005
Pancreatitis accompanying hepatic disease in dogs fed a high fat, low protein diet
Article
  • Jan 1948
A Pilot Study to Assess Tolerability of Early Enteral Nutrition via Esophagostomy Tube Feeding in Dogs with Severe Acute Pancreatitis
Article
The putative role of the gut in amplification of systemic inflammation in acute pancreatitis is gaining credence, and intraluminal nutrition has been shown to decrease inflammation in experimental models of pancreatitis. Prepyloric feeding often is used in people with acute pancreatitis, but has not been evaluated in dogs. Early intervention with enteral nutrition (EN) delivered proximal to the pylorus will be well tolerated in dogs with acute pancreatitis and provide justification for further larger trials. Ten dogs with severe acute pancreatitis in an open-label, prospective pilot study. Dogs were treated with plasma transfusion and standard care, and then consecutively assigned to receive either EN via esophagostomy tube feeding or parenteral nutrition (PN). Outcome was used to determine optimal study size for future studies, and complications were compared between the 2 groups. A significantly greater number of vomiting or regurgitating episodes occurred in dogs receiving PN. The dogs receiving EN did not demonstrate any noticeable postprandial pain. There were more catheter-related complications in the PN group. There was no difference in outcome between the 2 treatments, and 43 dogs for each treatment would be required in future studies to determine a difference in outcome. Early EN delivered proximal to the pylorus is well tolerated in dogs with severe pancreatitis and resulted in fewer complications than PN. Prospective trials in a larger cohort are justified to fully establish the potential benefit of early EN, preferably compared with minimal enteral nutrition.
Experimental pancreatitis intensified by a high fat diet
Article
  • Dec 1970