We all know that cats are not just small dogs; cats are unique creatures inside and out. Thomas Schermerhorn, VMD, assistant professor of small animal medicine at Kansas State University College of Veterinary Medicine, is presently exploring one aspect of feline glucose metabolism (metabolism here refers to the processing of a specific substance within the living body) that may shed some light on the factors responsible for the development of diabetes mellitus in cats. Little is known about cats as a species, especially at a molecular and cellular level, explains Schermerhorn, who postulates that cats may possess unique physiological mechanisms for glucose control.
Schermerhorns research focuses on the enzyme glucokinase, which is found in the liver and pancreas of most animal species. This vital enzyme acts as a glucose sensor, enabling liver or pancreatic cells to respond to changes in blood glucose. The levels of glucose in the blood must be strictly regulated. In humans and rodents, glucokinase expression is necessary for normal insulin release and maintenance of balanced levels of blood glucose. In humans, diabetes mellitus is sometimes caused by mutations in the gene that encodes the glucokinase enzyme itself.
Previous studies suggest that cats lack glucokinase activity in their liver. The singular feline may not regulate glucose as other mammal species do.
In a study funded by the Winn Feline Foundation, a non-profit organization affiliated with the Cat Fanciers Association, Schermerhorn, who is board certified by the American College of Veterinary Internal Medicine, and pre-veterinary student Erin Hiskett are trying to learn whether cats have the gene for glucokinase. They will look for the enzyme in the liver and pancreas.
If it is not present, is it because cats lack the gene for glucokinase? If the gene is present, it may not be expressed, indicating that the enzyme may not be manufactured. Another possibility is that the enzyme is blocked by another protein and is unable to do its job.
Schermerhorn credits the generosity of cat owners for his ability to do the study. Tissue samples are taken from cats that died of natural causes and whose organs were donated by their owners for scientific investigation. He describes his research program as basic science with a clinical flavor. Even at the early stages of the investigation, he keeps the clinical feasibility of investigative procedures in mind. In the future, he foresees the possibility of doing metabolic work-ups on clinical patients using samples as small as a needle biopsy.
Cats Are Different!
Cats seem to march to the beat of a different drummer when it comes to glucose homeostasis (the ability or tendency of an organism or cell to maintain internal equilibrium by adjusting its physiological processes). Unlike other mammals, cats may not develop a large rise in blood sugar after ingesting a meal. This makes sense when you consider that cats are true carnivores and have high dietary protein requirements. Glucose is the dominant signal for release of insulin in most mammals.
Schermerhorn indicates that cats experience a similar insulin release in response to amino acids, the building blocks of proteins. Another unique feline fact in the regulation of blood glucose is the development of stress hyperglycemia (the presence of an abnormally high concentration of glucose in the blood). The elevation of blood glucose associated with a stressful event, such as a visit to a
veterinarian, is well documented in cats but rare in dogs. Studies using mice that lack the glucose sensor glucokinase in their liver (but not in their pancreas) have demonstrated that these mice become hyperglycemic when stressed, responding physiologically much the same as cats do in a stressful situation.
Schermerhorn hopes this study will provide the necessary insights into feline glucose metabolism and will be the springboard for further investigations into the role of glucokinase in the development of feline diabetes.