From fat to fit—Avoiding six common mistakes while helping pets combat obesity (Sponsored by Nestlé Purina)
Part of the 2011 Nestlé Purina Veterinary Symposium publication
Mar 28, 2011
CUSTOM VETERINARY MEDIA
We veterinarians are all aware that weight problems affect 30% to 40% of our patients. The effects of obesity are far-reaching, predisposing our patients to insulin resistance, type II diabetes, orthopedic disease, and possibly even cancer.1-3 We all know that a pet is not in ideal health if it is not at its ideal weight, but many of us have also discovered how difficult it can be to motivate clients to help their pets lose weight. In this article, I will describe six common mistakes veterinarians make when implementing weight-management programs and explain how best to avoid them.
Mistake #1 — Not backing your recommendations with hard science
To drive home the importance of weight loss to my clients, I now discuss the ramifications of obesity and chronic inflammation on the pet's body. Although this does not motivate every client to be more interested in his dog's or cat's body condition, it may persuade those owners who are on the fence to try a weight-loss program.The pathophysiology of obesity is becoming much clearer. Fat is now recognized as an endocrine organ, since adipose tissue releases local and systemic cytokines (known as adipokines) that are thought to regulate systemic inflammation and food intake.1 A handful of measurable mediators of chronic inflammation and adipokines have been defined in dogs and cats.1 The picture of obesity and chronic inflammation in pets is similar to the evolving human story. When fat from obese animals is examined histologically, apoptotic/necrotic adipocytes are surrounded by inflammatory macrophages. This results in a chronic inflammatory response. This process may stimulate further release of inflammatory mediators from surrounding adipocytes, creating a chronic inflammatory stimulus back and forth between macrophages and adipocytes.
There are 40 to 50 identified adipokines released from fat cells. The ones of clinical importance in dogs and cats are adiponectin, leptin, monocyte chemotactic protein-1, and resistin. Adiponectin is the most abundant adipokine in the bloodstream in all species, but it does not circulate as a single monomer only. It circulates and has its best insulin-propagating activity as large polymers of six to 18 bonded monomers. In this form, it is called high-molecular-weight (HMW) adiponectin.4 HMW adiponectin is released from adipocytes in lean people and its secretion is severely diminished in obese people, with post-gastric-bypass surgery patients showing increases in serum HMW adiponectin.5 This is important because adiponectin improves insulin signaling; therefore, when obese animals stop secreting it, insulin resistance can ensue.
Table 1 shows results from a recent study examining adipokine concentrations before and after a weight-loss program in dogs. The results show that all of the aforementioned adipokines except for adiponectin decrease after about 25% weight loss in a group of dogs, similar to other reports.8,9 This decrease in inflammatory adipokines corresponds with a drop in the systemic marker of inflammation, the acute phase protein called C-reactive protein (CRP). In obese people, the increased inflammation is associated with an increased risk of heart disease and type II diabetes.10 The chronic health ramifications of this slightly elevated inflammatory response in dogs and cats still need to be investigated.
Although there is much left to be studied, we do know that obesity has a multitude of systemic effects and predisposes pets to many problems. We can do a better job of communicating to clients what is definitively known about the short- and long-term health risks of obesity in pets.