Jacquie S. Rand, BVSc (Hons), DVSc (DACVIM); Gregory Martin
CAUSES OF FELINE OBESITY
Regulation of food intake and body weight involves a complex balance between long-term control of fat mass involving insulin, adrenal steroids and leptin signals to the CNS and short-term, meal-related signals. Cats will normally limit their food intake to their energy requirements. However, in some instances cats appear unable to regulate energy balance. Our research has demonstrated that despite elevated circulating leptin levels in obese cats associated with increased fat mass, they continue to overeat and gain weight. This paradox of increased leptin concentrations in obesity has been observed in other species and is hypothesized to be a consequence of 'leptin resistance'.
A number of risk factors have been identified for obesity. Physical inactivity, extended sleeping periods and indoor confinement are associated with an increased incidence of obesity. Neutering results in weight gain, predominantly as fat mass in both genders. With neutering, reductions in roaming and in general physical activity occur along with increased food intake and the efficiency of energy utilization. Neutered male cats are more likely than females to gain excessive weight. The incidence of feline obesity increases with age peaking between the ages of six and eight years. Many pure bred cats such as Siamese or Abyssinians are leaner than most mixed breed cats, suggesting a genetic influence on body weight may exist in cats, as it does in humans. Chronic administration of corticosteroids and progestins, particularly megestrol acetate, induce polyphagia resulting in weight gain. The human-animal-relationship of owners of overweight cats is characterized by a higher intensity of the bond between owner and cat, and by increased humanization compared with the relationship in owners of normal weight cats.
CONSEQUENCES OF FELINE OBESITY
Obesity in companion animals has been shown to predispose to, or cause a number of medical conditions including glucose intolerance and diabetes mellitus as well as surgical and anaesthetic complications, reproductive compromise, non-allergic skin conditions, lameness, feline lower urinary disease, hepatic lipidosis and immuno-incompetence.
We investigated the effect of weight gain on glucose tolerance, insulin sensitivity, hematological and biochemical parameters and leptin concentrations in 16 healthy research cats. Previous studies in rodents, dogs, and humans have linked obesity with increased susceptibility to infection, altered immunity and impaired host defense mechanisms. In our study in cats, we found significant reductions in total white cell numbers as well as neutrophils, eosinophils and lymphocytes after weight gain. In addition, obese cats had a significantly lower red cell count, packed cell volume and mean platelet volume (MPV) compared with when they were lean. These small but significant reductions in both red and white blood cell lines, combined with a lowered MPV, are suggestive of mild generalized bone marrow suppression. Hypertriglyceridaemia was also present in our cats after becoming obese.
Cats in our study developed hyperinsulinaemia and reduced insulin sensitivity with weight gain. In fact, the insulin sensitivity index (SI) as measured by Bergman's Minimal model, was 53% lower in cats after weight gain, indicating that obese cats were significantly less sensitive to insulin compared to when they were of normal-weight. Cats with the highest basal insulin concentrations after weight gain were also the most insulin resistant. Glucose effectiveness (SG), was also significantly decreased in obese cats indicating that glucose utilization, independent of insulin, was reduced. Other characteristic metabolic features of obesity evident in the obese cats included basal hyperinsulinaemia and an exaggerated insulin response to glucose during the glucose tolerance test. Seven cats were identified as developing impaired glucose tolerance with weight gain. Before gaining weight, these cats tended to have higher insulin concentrations, and lower insulin sensitivity and glucose effectiveness than cats that maintained normal glucose tolerance with weight gain. Our results suggest that some cats may have an underlying predisposition to develop glucose intolerance, and if these cats become obese and inactive, they may be more at risk of developing overt type 2 diabetes mellitus.
In the same study, we documented a threefold increase in plasma leptin concentrations in cats as a result of weight gain. We also demonstrated the existence of a strong relationship between leptin and insulin resistance in both lean and obese cats similar to that reported in humans, however it is still unclear as to whether leptin is causally involved in this relationship.
Unlike their ancestors, modern domestic cats no longer hunt for food, have become relatively inactive and tend to overeat resulting in an increased incidence of overweight and obese cats. These changes parallel those that have occurred in the urbanization of many of the world's indigenous populations that have high levels of diabetes. In addition, cats are predominantly fed commercial diets, many of which contain significant levels of highly digestible cereal which cats as obligate carnivores, did not evolve to eat. These factors increase the demand for insulin production from the pancreatic beta cells and lend credence to the hypothesis of 'beta-cell exhaustion' as an important element in the pathogenesis of feline type 2 diabetes mellitus.
In both cats and humans, amyloid deposition in the pancreatic islets is the most consistent histological finding. Amyloid is formed from amylin (IAPP), a hormone which is co-secreted with insulin. In diabetic cats, a large amount of amyloid is deposited in the islets, replacing the cells and leading to a reduction in overall beta cell mass.
ASSESSMENT AND MANAGEMENT OF FELINE OBESITY
A safe and effective weight reducing regime involves restricting caloric intake to 60%-75% of estimated caloric requirements for ideal body weight (approximately 60 kcal/kg of ideal body weight per day), with the aim to maintain weight loss at approximately 1.0 to 1.5% per week. Regular weight checks, initially fortnightly then monthly, with appropriate adjustments of intake should be made. There is considerable individual variation in caloric requirements between cats, and food intake needs to be individually adjusted to ensure appropriate weight loss. Additionally, methods to increase energy output such as backyard activity enclosures, laser pointers and food cubes should be instituted. A recent study found that active playing for 10 minutes daily was as effective as calorie restriction in achieving weight loss in obese cats. Several dietary manipulations have been investigated including the addition of chromium or carnitine, vitamin A supplementation, and altering macronutrient sources.
In cats, dietary chromium supplementation has been shown to aid in the preservation of lean body mass at the expense of fat during weight loss. In addition, our research has shown that dietary chromium supplementation in the form of chromium tripicolinate results in small, but significant dose-dependent improvements in glucose tolerance in normal-weight cats. Thus, the addition of chromium to feline diets may aid in the treatment of obese cats by improving both glucose metabolism and body composition.
Carnitine, a co-factor of fatty acid metabolism, has been shown to promote the maintenance of lean body mass during weight reduction. In obese cats, carnitine supplementation during a weight loss program increased the rate of fatty acid oxidation and accelerated the rate of weight loss, possibly via increasing energy utilization.
In rats, dietary vitamin A supplementation increased mitochondrial uncoupling protein (UCP) expression and reduced adiposity. Studies have shown that cats supplemented with vitamin A resist weight gain following a high-fat diet. Vitamin A has been shown to normalize the elevated leptin levels that occur in obese cats. Because obese cats with the highest leptin concentrations are also the most insulin resistant, there maybe a physiological link between leptin and insulin resistance in obesity. Therefore, if Vitamin A supplementation reduces leptin concentrations it may also improve insulin sensitivity.
Traditionally, a high fiber diet has been promoted for weight management in dogs and cats, although there is little scientific evidence to substantiate its effectiveness. Additionally, unwanted side effects such as increased fecal bulk and frequency of defecation may contribute to the lack of compliance of such diets in clinical practice. The inclusion of dietary fermentable fiber however, may be beneficial in the management of obesity. Fermentation of fiber by intestinal bacteria produces short chain fatty acids (SCFA) which in turn, stimulate the release of proglucagon from the intestinal lining cells. Proglucagon is further broken down to glucagon-like peptide-1 (GLP-1), which increases insulin secretion from the pancreatic islets.
The provision of meals containing adequate amounts of amino acids, particularly essential amino acids, is necessary for the anabolic effect of insulin on muscle protein synthesis. In a study of nine diabetic cats, a high protein, low carbohydrate diet has been shown to induce satiety as well as reduce the dose of insulin required. In another study in normal cats, compared to a high protein and low carbohydrate diet, a low protein and high carbohydrate diet produced hyperinsulinaemia and decreased NEFA mobilization which may in the long term, lead to weight gain, obesity and beta-cell 'exhaustion' in cats fed ad libitum.
The proportion of calories ingested as carbohydrate is one of the main determinants of post-prandial glucose and insulin concentrations. Diets with moderate to low carbohydrate content (<25% of calories) are the most appropriate for preventing diabetes in predisposed cats and for managing diabetes. Dietary carbohydrate source is also a consideration when developing diets for both healthy cats as well as for obese, glucose intolerant cats. Certain carbohydrate sources such as sorghum and barley have been shown to lower the post-prandial glucose and/or insulin responses in dogs and cats when compared with rice. The inclusion of these types of starches in feline diets may improve glucose control in cats, reduce insulin and possibly amylin secretion, thereby minimizing pancreatic amyloid deposition and beta-cell 'exhaustion'. Therefore, diets with restricted carbohydrate content and formulated using low-glycemic increase carbohydrates are likely important for the prevention or management of obesity-induced glucose intolerance and diabetes.
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