Gastric distension by a meal or experimental means will decrease subsequent meal intake in dogs.

Satiety is a complex process that involves both neuronal and hormonal signals to the brain. Through this complicated system, our bodies relay to our brain long-term signals (i.e., how often to eat) and short-term signals (i.e., when to stop eating a meal). Examples include stretch receptors in the stomach, which signals to the brain that we are full. Hormonal signals include those that tell our brains we are hungry versus full. Ghrelin is a hormonal signal that increases before meals and decreases following consumption of a meal in many species. Hormonal signals that tell us we are full include glucagon-like peptide-1 (GLP-1), leptin, peptide YY (PYY) and choleocytekinin (CCK).

Current literature regarding satiety has mostly focused on humans and human models, but there has been some evaluation of different nutrients on satiety in dogs. The literature in dogs has focused on changing the diet macronutrient profile (protein, fat, fiber concentrations) or evaluation of the macronutrients themselves. This research may be used to help pets lose weight, decrease negative behaviors associated with putting your pet on a weight loss diet or, preferably, to prevent weight gain.

Dr. Kelly Swanson’s group evaluated the changes in hormone concentrations after a dose of one macronutrient (chicken=protein, maltodextrin=carbohydrate, lard=fat, water=control) in adult dogs (Lubbs et al., 2010). While the authors noted no difference in post-prandial ghrelin concentrations, the GLP-1 concentrations tended to be elevated in dogs fed lard. It was also noted in this work that satiety hormones are highly variable throughout the day, and therefore, more sensitive tests for these hormones may be needed.

Classifying entire macronutrient groups as having the same affect on satiety may not be the most accurate method. Different types of ingredients, which provide a predominate macronutrient (i.e., beef versus chicken), may affect satiety differently. We recently evaluated different protein sources, beef, chicken, pork, salmon and pollock (Vester Boler, 2010). While we were able to influence satiety hormones and plasma AA in the dog after a protein pre-meal, we were unable to influence food intake. Numerically, dogs consumed the least amount of food after consumption of a salmon or chicken pre-meal. This corresponded with many responses noted with decreased glucose and ghrelin and increased insulin, GLP-1 and several plasma amino acids. This may indicate that each protein source should be evaluated individually.

Another way to affect satiety is by stimulating stretch receptors in the stomach. Gastric distension by a meal or experimental means will decrease subsequent meal intake in dogs (Pappas et al, 1989). This idea of “gut fill” is one mechanism by which feeding a high-fiber diet is expected to be satiating. The animal must consume a greater amount of food to meet their caloric need. Dietary fiber, however, may provide more benefits than “gut fill” alone, as fibers that are able to be fermented in the large bowel may also affect satiety hormones.

Dr. Guido Bosch evaluated test diets containing 8.5% cellulose (non-fermentable) or 8.5% beet pulp + 2% inulin (fermentable) (Bosch et al., 2009). The authors assessed voluntary food intake by feeding the same diet 6 hours after the morning meal of the test diet. Voluntary food intake tended to be lower in dogs fed the fermentable fiber diet. Neither diet in this experiment affected the gut hormones tested (glucose, insulin, PYY, GLP-1 or ghrelin) as was expected. It may be that the affect of fermentable fiber on satiety is not directly regulated through the hormones measured in this study.

A combination of high-protein, high-fiber diets (HPHF) may provide the most benefit to controlling satiety and weight gain/loss. Voluntary food intake of a commercially prepared HPHF diet was lower compared to a high-protein or high-fiber diet alone (Weber et al., 2007). The two high-fiber diets, however, contained different types of fiber sources, which complicate the results. The high-fiber diet contained mostly non-fermentable fiber, while the HPHF diet contained a mixture of non-fermentable and fermentable fiber sources. This is important as an increased satiety response may be due to fermentable fiber and not necessarily the combination of HPHF.

Unfortunately, very little data regarding satiety in cats has been published. Many of the satiety hormonesare reported to respond similar to humans and other species, including ghrelin (Ida et al., 2007), leptin (Vester et al., 2009), and CCK (Backus et al., 1995). Their response, of both hormones and food intake to different macronutrients, however, is not yet reported in the literature.

A further complicating matter is that steroid hormones play a large role in the influence of satiety hormones. Cats and dogs that are spayed or neutered are at an increased risk for becoming obese, and it has been well documented that many animals will reduce energy expenditure and increase food intake following the surgery (Belsito et al., 2009; Lund et al., 2006). Removing estrogen also decreases leptin sensitivity (Meli et al, 2004) and increases fat deposition in rodent models (Hamosh and Hamosh, 1975). Administering estradiol to cats after spaying decreases food intake (Cave et al., 2007), which indicates loss of estrogen, leads to changes in satiety signals in cats as well.

This is an obvious area of research that needs to be explored further considering the large numbers of dogs and cats that are spayed or neutered.

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