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Obesity as an endocrine disease (Proceedings)

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Aug 01, 2011

Obesity is at epidemic proportions in the United States and worldwide. Despite major public health initiatives spanning several decades, human obesity has reached prevalence rates nearing 40% in some states. Obesity in dogs and cats has followed this trend. Obesity is loosely defined as body weight 20% above the ideal, or as accumulation of body fat to the extent that it affects the animal's health.

Risk factors for obesity

There are several risk factors for obesity in dogs. These include breed (e.g., Labrador Retriever, Cairn Terrier, Cavalier King Charles Spaniel, Scottish Terrier, Cocker Spaniel); neutering; and several owner behavioral and socioeconomic factors. Owner factors include over-humanizing pets, owner obesity, time spent observing pet eating, and lower income. Interestingly, the type of food a dog is fed is not associated with obesity. A recent study showed that cats gained 40% of their body weight by being fed free-choice food for 3 months after spaying. To maintain pre-spay body weight, food intake had to be reduced by 30%. Similar studies have demonstrated increased obesity in neutered dogs as well. The simple reason for obesity is that energy intake exceeds energy expenditure. This can occur when a dog has excessive caloric intake (food and treats) or reduced energy expenditure (e.g., reduced activity, illness or injury resulting in less exercise).

Some medical conditions (endocrinopathies, such as hypercortisolism and hypothyroidism) and drugs (steroids and anticonvulsants) are associated with obesity. Medical conditions should be considered carefully in the clinical approach to an obese animal. Hypothyroidism is diagnosed commonly in dogs and is often suspected as a prime differential in obese dogs. This disease, however, is widely overdiagnosed, and owners are often frustrated when their dogs fail to lose weight despite thyroid hormone supplementation. Hypercortisolism (Cushing's syndrome), on the other hand, may be underdiagnosed. Glucocorticosteroid hormones, endogenous or exogenous, are known to cause increased body fat in many species, and it is important to consider this syndrome as a differential in obese dogs. While genetic factors are also probably involved in the predisposition of some breeds to obesity (e.g., Labrador retrievers have a higher incidence of obesity than is seen in other breeds of like size), the role of inheritance in canine obesity needs more study.

"[There is a] popular belief, particularly among lean individuals, that regulation of body weight is largely a matter of willpower. It is hard to imagine such a view of the regulation of any similarly important aspect of physiology, for example blood pressure, persisting for so long." -A.M. Wren and S.R. Bloom, Imperial College London, Gastroenterology 2007;132:2116-2130

Endocrinology of adipose tissue and obesity

Based on the current understanding of fat endocrinology, it is reasonable to consider obesity a true medical disorder rather than simply a lifestyle/willpower issue. Fat is an endocrine organ that secretes a variety of hormones and cytokines.3 These are collectively termed "adipokines." Leptin and adiponectin are the best characterized fat-derived hormones. Leptin is important in regulation of energy balance and satiety. Leptin concentrations in the circulation increase in obesity, but this is because of leptin resistance, so the beneficial effects of leptin are lost. Adiponectin is a hormone with several functions, but the most important is probably in conferring insulin sensitivity. As body fat increases, adiponectin concentrations drop, contributing to the insulin resistance of obesity. The effects of adiponectin and leptin have been documented in dogs. Other hormones secreted by fat cells include resistin and vistatin, which are involved in insulin resistance, and apelin, which may contribute to hypertension in obesity. These hormones have not been well-studied in dogs and cats. Vistatin affects insulin secretion.

In addition to hormones, inflammatory cytokines are secreted by adipose tissue. Abnormally increased concentrations of adipose-derived tumor necrosis factor-alpha, for example, provides an illustration of obesity as a systemic inflammatory condition.

Other proinflammatory adipokines are present in obesity as well.

Gut-derived hormones, which are critical for appetite control and glucose homeostasis, are also abnormal during obesity.7 In particular, ghrelin, a powerful orexigenic hormone secreted by the gastrointestinal tract, remains elevated longer post-prandially in obese human patients, although studies of this effect have not been reported in dogs or cats. As a result of ghrelin dysregulation, obese patients need less food but are more hungry, illustrating the vicious cycle of obesity and loss of appetite control.

In addition to the abnormal endocrine functions of adipose tissue itself, other endocrine systems are affected by obesity. Increased serum thyroid hormone concentrations, believed to reflect thyroid hormone resistance, have been documented in canine obesity, as have increases in circulating concentrations of prolactin, insulin, and insulin-like growth factor 1. Obese dogs secrete more cortisol in response to ACTH stimulation than do lean dogs, further illustrating the multisystemic nature of the medical disorder of obesity.