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Sugar in dog foods

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Abstract

Sugar in dog foods Sugar loosely refers to carbohydrates, but in everyday language it is table or granulated sugar, with sucrose as common chemical name. Sucrose is made up of two simple sugars, glucose and fructose. It is extracted and refined from sugar cane or beet. Added sugar in the diet is generally considered bad: it is seen as a taste enhancer containing a lot of calories, with no essential nutrients. Unsurprisingly, many owners reject sugary dog foods as being the presumed cause of overweight, tooth decay and other disorders. Various petfood manufacturers have responded by advertising " no added sugar " on their websites. At times, the catchphrase turns up on a dog food label. Added sucrose is declared in the ingredient list as sugar or sucrose, but there may also be beet pulp and/or molasses as sucrose-rich ingredients. The sucrose content of dog food is not disclosed, but the manufacturer may be contacted. Dental caries in the dog population is rare and unrelated to dietary sucrose (1, 2). There is no specific role for sucrose in the widespread canine obesity due to caloric excess; the amount of calories rather than source is crucial. Adding sucrose to dog food makes it more appetizing. It is easy to anticipate that palatable food promotes obesity in dogs, but there is no research-based evidence. Whichever food is dished up, it is always prudent to adjust portion size to dog weight. The dog digests dietary sucrose efficiently and utilizes the glucose and fructose components. Puppies were maintained with good growth on experimental diets very high in sucrose. A similar diet fed to bitches during pregnancy, parturition and lactation supported general health and satisfactory reproduction. It is reasonable to conclude that the assessed, maximum amount of sucrose in dry, extruded kibbles does not harm dogs. Palatability Adult dogs given free access to dry food, a pan with distilled water and another one with 10% sucrose (w/v), showed a strong preference for the sweetened water (3). A study in puppies found that the preference threshold for sucrose was about 0.003%, with maximum liking reached at 3% (4). In two-choice tests, dogs clearly ate more sucrose-supplemented than unsupplemented diet. The preference results were similar for a dry, vegetarian-protein formula mixed with sucrose at 1% or 20% of the total diet (5). Indirect comparison indicates that sucrose added to a semimoist (4) or semipurified food (6) increased palatability. Utilization Adult dogs fed a carbohydrate-free, meat-based diet had low sucrase activity in small intestinal mucosa, but a diet made with meat meal and 41% sucrose (g/100 g dry matter, throughout this text) substantially increased the activity within 14 days (7). In two dogs given that sucrose diet for 5 days, apparent ileal sucrose digestibility was almost 100% (8).
Creature Companion 2017; August: 34, 36.
Anton C. Beynen
Sugar in dog foods
Sugar loosely refers to carbohydrates, but in everyday language it is table or granulated sugar,
with sucrose as common chemical name. Sucrose is made up of two simple sugars, glucose and
fructose. It is extracted and refined from sugar cane or beet. Added sugar in the diet is generally
considered bad: it is seen as a taste enhancer containing a lot of calories, with no essential
nutrients.
Unsurprisingly, many owners reject sugary dog foods as being the presumed cause of overweight,
tooth decay and other disorders. Various petfood manufacturers have responded by advertising
“no added sugar” on their websites. At times, the catchphrase turns up on a dog food label. Added
sucrose is declared in the ingredient list as sugar or sucrose, but there may also be beet pulp
and/or molasses as sucrose-rich ingredients. The sucrose content of dog food is not disclosed, but
the manufacturer may be contacted.
Dental caries in the dog population is rare and unrelated to dietary sucrose (1, 2). There is no
specific role for sucrose in the wide-spread canine obesity due to caloric excess; the amount of
calories rather than source is crucial. Adding sucrose to dog food makes it more appetizing. It is
easy to anticipate that palatable food promotes obesity in dogs, but there is no research-based
evidence. Whichever food is dished up, it is always prudent to adjust portion size to dog weight.
The dog digests dietary sucrose efficiently and utilizes the glucose and fructose components.
Puppies were maintained with good growth on experimental diets very high in sucrose. A similar
diet fed to bitches during pregnancy, parturition and lactation supported general health and
satisfactory reproduction. It is reasonable to conclude that the assessed, maximum amount of
sucrose in dry, extruded kibbles does not harm dogs.
Palatability
Adult dogs given free access to dry food, a pan with distilled water and another one with 10%
sucrose (w/v), showed a strong preference for the sweetened water (3). A study in puppies found
that the preference threshold for sucrose was about 0.003%, with maximum liking reached at 3% (4).
In two-choice tests, dogs clearly ate more sucrose-supplemented than unsupplemented diet. The
preference results were similar for a dry, vegetarian-protein formula mixed with sucrose at 1% or
20% of the total diet (5). Indirect comparison indicates that sucrose added to a semimoist (4) or
semipurified food (6) increased palatability.
Utilization
Adult dogs fed a carbohydrate-free, meat-based diet had low sucrase activity in small intestinal
mucosa, but a diet made with meat meal and 41% sucrose (g/100 g dry matter, throughout this text)
substantially increased the activity within 14 days (7). In two dogs given that sucrose diet for 5 days,
apparent ileal sucrose digestibility was almost 100% (8).
After 10 days on a semipurified diet with 62% sucrose as only digestible carbohydrate, adult dogs
(n=4) showed a considerable postprandial blood glucose response and excreted sucrose and fructose
in urine (9). Urinary loss of total sugar equaled 0.3 % of sucrose intake, corroborating another study
(10). Apparently, intactly absorbed sucrose and fructose traces ended up in urine.
Safety
There are no long-term, controlled, dose-response studies that addressed the safety of sucrose
consumption by dogs. Some insight can be obtained from earlier nutrient-requirement studies
employing semipurified, high-sucrose diets.
Different research groups (11-14) reported that nutritionally optimized, semipurified diets
containing 49 to 69% sucrose, fed for 6 to 27 weeks, supported good health and satisfactory body-
weight gain in weanling dogs. Bitches fed semipurified diets with 69% sucrose showed no evidence
of unthriftiness, had normal hair coats and good consistency of stools (15). Their pups had expected
body weights at birth and weaning, while mortality was in the upper normal range.
Fructose
Fasted dogs fed diets containing about 66% fructose instead of glucose had lost part of their capacity
to dispose of blood glucose after glucose ingestion (16) or after intravenous administration of
glucose together with insulin (17, 18). Dietary fructose, displacing 66% glucose or 18% starch, raised
fasting blood insulin concentrations, but left glucose unchanged (17, 19). Fasting triglyceride levels
were increased by 66% fructose in the diet (17), but not by 18% fructose (19) or 24-50% sucrose (20,
21).
Replacement of 18% dietary starch by fructose, albeit not as only variable, reduced hepatic glucose
uptake and glycogensynthase activity in dogs (19). Thus, hepatic metabolism shifted from
glycogenesis to lipogenesis, for which is fructose is both activator (22) and excellent substrate (23).
High intakes of fructose in place of starch may induce insulin resistance. However, the dose-
response relationship is unknown, while fructose quantity equals almost twice that of sucrose. Dogs
develop obesity-associated insulin resistance, but not type-2 diabetes (24). Nevertheless, chronic
adverse effects of insulin resistance cannot be excluded.
Practical implications
The main sucrose sources in dog food are refined sucrose, beet pulp (8-25% sucrose), beet/cane
molasses (about 60%) and bakery byproducts (about 20%). Considering regular formulations,
extruded dog foods hold considerably less than 10% sucrose. An unspecified dry food had 2%
sucrose according to sophisticated analysis (25). Certain semimoist foods, in the form of rings, slices
or rolls, contain added sugar. A frozen food features all three sucrose-rich ingredients. It is unknown
whether the foods’ sucrose contents affect insulin sensitivity.
Literature
1. Hale FA. Dental caries in the dog. J Vet Dent 1998; 15: 79-83.
2. Lewis TM. Resistance of dogs to dental caries: a two-year study. J Dental Res 1965; 44: 1354-1357.
3. Grace J, Russek M. The influence of previous experience on the taste behavior of dogs toward
sucrose and saccharin. Physiol Behav 1969; 4: 553-558.
4. Ferrell F. Preference for sugars and nonnutritive sweeteners in young beagles. Neurosci Biobehav
Rev 1984; 8: 199-203.
5. Houpt KA, Coren B, Hintz HF, Hilderbrant JE. Effect of sex and reproductive status on sucrose
preference, food intake, and body weight of dogs. J Am Vet Med Assoc 1979; 174: 1083-1085.
6. Tôrres CL, Hickenbottom SJ, Rogers QR. Palatability affects the percentage of metabolizable
energy as protein selected by adult beagles. J Nutr 2003; 133: 3516-3522.
7. Kienzle E. Enzymaktivität in Pancreas, Darmwand und Chymus des Hundes in Abhängigkeit von
Alter und Futterart. J Anim Physiol Anim Nutr 1988; 60: 276-288.
8. Mühlum A. Untersuchungen über die praecaecale und postileale Verdaulichkeit verschiedener
Kohlenhydrate beim Hund. Dissertation, Tierärtzliche Hochschule Hannover, 1987.
9. Bennet MJ, Coon E. Mellituria and postprandial blood sugar curves in dogs after the ingestion of
various carbohydrates with the diet. J Nutr 1966: 88: 163-168.
10. Schünemann C, Mühlum A, Meyer H. Precaecal and post ileal digestibility of various
carbohydrates in dogs. Nutrition, malnutrition and dietetics in the dog and cat (Edney ATB,ed),
British Veterinary Association, 1987, pp 23-26.
11. Schaefer AE, McKibbin JM, Elvehjem CA. Studies on the vitamin B complex in the nutrition of the
dog. J Nutr 1942; 23: 491-500.
12. Singal SA, Sydenstricker VP, Littlejohn JM. The rôle of tryptophan in the nutrition of dogs on
nicotinic acid-deficient diets. J Biol Chem 1948; 176: 1051-1062.
13. Mabee DM, Morgan AF. Evaluation by dog growth of egg yolk protein and six other partially
purified proteins, some after heat treatment. J Nutr 1951; 43: 261-279.
14. Gessert CF, Phillips PH. Protein in the nutrition of the dog. J Nutr 1956; 58: 415-421.
15. Ontko JA, Phillips PH. Reproduction and lactation studies with bitches fed semipurified diets. J
Nutr 1958; 65: 2211-2218.
16. Hill R, Chaikoff IL. Loss and repair of glucose-disposal mechanism in dog fed fructose as sole
dietary carbohydrate. Proc Soc Exp Biol Med 1956; 91: 265-267.
17. Martinez FJ, Rizza RA, Romero JC. High-fructose feeding elicits insulin resistance, hyperinsulinism,
and hypertension in normal mongrel dogs. Hypertension 1994; 23: 456-463.
18. Pamies-Andreu E, Fiksen-Olsen M, Rizza RA, Romero JC. High-fructose feeding elicits insulin
resistance without hypertension in normal mongrel dogs. Am J Hypertens 1995; 8: 732-738.
19. Coate KC, Kraft G, Courtney Moore M, Smith MS, Ramnanan C, Irimia JM, Roach PJ, Farmer B,
Neal DW, Williams P, Cherrington AD. Hepatic glucose uptake and disposition during short-term high
fat vs. high-fructose feeding. Am J Physiol Endocrinol Metab 2014; E151-E160.
20. Grande F, Prigge WF. Serum lipid changes produced by dogs subsitituting coconut oil for either
sucrose or protein in the diet. J Nutr 1974; 104: 613-618.
21. Schultz AL, Grande F. Effects of starch and sucrose on the serum lipids of dogs before and after
thyroidectomy. J Nutr 1968; 94: 71-73.
22. Carmona A, Freedland RA. Comparison among the lipogenic potential of various substrates in rat
hepatocytes: the differential effects of fructose-containing diets on hepatic lipogenesis. J Nutr 1989;
119: 1304-1310.
23. Clark DG, Rognstad R, Katz J. Lipogenesis in rat hepatocytes. J Biol Chem 1974; 249: 2028-2036.
24. Rand JS, Fleeman LM, Farrow HA, Appleton DJ, Lederer R. Canine and feline diabetes mellitus:
nature or nuture? J Nutr 2004; 134: 2072S-2080S.
25. Ellingson DJ, Anderson P, Berg DP. Analytical method for sugar profile in pet food and animal
feeds by high-performance anion-exchange chromatography with pulsed amperometric detection. J
AOAC Int 2016; 99: 342-352.
... Glycerol is a colorless, odorless, viscous liquid with 60% sweetness potency, compared with table sugar. Adding sucrose to dog food makes it more appetizing (11). ...
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