Obesity: Health and mobility risks (Sponsored by Iams)

Obesity: Health and mobility risks (Sponsored by Iams)

Jan 01, 2011

Obesity is the most common nutritional disorder in dogs. A 1986 study estimated the prevalence of canine obesity to be 24%,1 and a similar 2005 study estimated the incidence of obesity to be 41%.2 About 50% of dogs in the United States between the ages of 5 and 10 years are overweight or obese.3

Along with this increase in pet obesity comes an increase in obesity-associated health problems. Health problems caused or complicated by obesity include:

  • Decreased life expectancy
  • Reduced quality of life
  • Chronic inflammation
  • Joint/musculoskeletal problems and osteoarthritis
  • Pulmonary and cardiovascular disease
  • Exercise and heat intolerance
  • Compromised immune function
  • Pancreatitis
  • Increased morbidity and mortality during and after anesthesia (many anesthetics are fat soluble, so recovery may take longer).

White adipose tissue: A major endocrine organ

For many years, white adipose tissue (WAT) was considered metabolically inert. Its primary role in disease was attributed to the effects of increased weight bearing causing stress on joints and increased cardiac workload. However, our understanding of WAT's physiologic role changed in 1994 with the discovery of a hormone, leptin, which is produced predominantly by WAT.4 Since that discovery, numerous other protein signals and factors, called adipokines, have been shown to be secreted by WAT. As a result, WAT is no longer viewed simply as a vehicle for storage and release of fatty acids. Instead, WAT is recognized as a major endocrine organ and signaling tissue, which interacts extensively with other organs in overall physiologic and metabolic control. Two of these important adipokines secreted by adipose tissue are leptin and adiponectin.


The hormone leptin plays a key role in regulating energy balance. Leptin is constitutively secreted by adipocytes, and its transcriptional regulation depends on energy flux within adipocytes. Leptin stimulates energy expenditure (thermogenesis) to help balance the effects of excessive caloric intake. In addition, leptin's release from adipose tissue is a key trigger for the hypothalamus that results in decreased appetite and reduced food intake in normally responsive, nonobese individuals.5

In people and rodents, plasma leptin concentrations are highly correlated with body mass index, and most obese individuals have high levels of plasma leptin. This increase in leptin associated with obesity is partly due to an increase in the amount of leptin-secreting adipose tissue.6 Furthermore, as the leptin level increases, it induces leptin resistance in target cells and interferes with the normal feedback in the hypothalamus that downregulates food intake. As a result, leptin becomes ineffective at controlling food intake, a condition known as leptin resistance. A similar obesity-associated increase in plasma leptin occurs in dogs, and the greater the degree of obesity, the higher the plasma leptin levels.7-9 In a study by Ishioka and colleagues,7 dogs with a body condition score (BCS) of 3/5 had mean plasma leptin levels of 3.0 ± 0.4 ng/ml; dogs with a BCS of 4/5 had mean plasma leptin levels of 8.6 ± 0.7 ng/ml; and dogs with BCS of 5/5 had mean plasma leptin levels of 12.8 ± 0.8 ng/ml. Therefore, plasma leptin is a good index of adiposity in dogs, as it is in people and rodents.

Leptin also alters cytokine production by immune cells, and transcription of leptin is increased by proinflammatory cytokines, such as tumor necrosis factoralpha (TNF-α), interleukin-1β (IL-1β), and interleukin-6 (IL-6).10 As a result, leptin appears to be proinflammatory and may contribute to oxidative injury.