Abstract
Obesity and diabetes mellitus are common diseases in humans, dogs and cats and their prevalence is increasing. Obesity has been clearly identified as a risk factor for type 2 diabetes in humans and cats but recent data are missing in dogs, although there is evidence that the unprecedented rise in canine obesity in the last decade has led to a rise in canine diabetes of similar magnitude. The insulin resistance of obesity has often been portrayed as major culprit in the loss of glucose control; however, insulin resistance alone is not a good indicator of progression to diabetes in people or pets. A loss of beta cell function is necessary to provide the link to impaired fasting and post-prandial plasma glucose. Increased endogenous glucose output by the liver is also a prerequisite for the increase in fasting blood glucose when non-diabetic obese humans and pets develop diabetes. This may be due to decreased hepatic insulin sensitivity, decreased insulin concentrations, or a combination of both. While inflammation is a major link between obesity and diabetes in humans, there is little evidence that a similar phenomenon exists in cats. In dogs, more studies are needed to examine this important issue.
Highlights
Obesity is the most common nutritional disorder in dogs and cats and has been shown to be a risk factor for the development of type 2 diabetes in cats and humans
The obese diabetic dogs were characterized by high glucose and high fasting insulin concentrations but were unable to mount an appropriate insulin response when challenged with high glucose concentrations. It was suggested in a recent study of a small number of obese non-diabetic dogs which had normal fasting plasma glucose (FPG) and normal glucose tolerance that obese dogs do not develop a type of diabetes similar to type 2 seen in humans because they increase insulin output, including first phase, in response to obesity, whereas people do not [5]
Using the gold-standard method to evaluate insulin sensitivity, the euglycemic hyperinsulinemic clamp, we found that in cats obesity leads to a decrease in glucose effectiveness and an increase in insulin resistance, similar to what has been shown in people and dogs [16,17]
Summary
Obesity is the most common nutritional disorder in dogs and cats and has been shown to be a risk factor for the development of type 2 diabetes in cats and humans. It was suggested in a recent study of a small number of obese non-diabetic dogs which had normal fasting plasma glucose (FPG) and normal glucose tolerance that obese dogs do not develop a type of diabetes similar to type 2 seen in humans because they increase insulin output, including first phase, in response to obesity, whereas people do not [5] Such statement about a difference between dog and human insulin secretion is not supported by evidence from human clinical studies. Phase and total insulin concentrations increased until 100% increase in fat mass was reached (Figure 1), when a blunting of early insulin secretion and altered glucose clearance was seen, indicating that under extreme conditions (high degree of resistance and high glucose dose), the response of the beta cell to glucose becomes abnormal These results are similar to those described in people by Matsumoto and coworkers, who compared glucose tolerance, insulin secretion, and insulin sensitivity in a large number of non-obese and obese Japanese subjects [22]. A loss of beta cell function is necessary to provide the link to impaired fasting and post-prandial plasma glucose
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