Diabetes Mellitus
History. You are presented with a IO ycar oId, intact, female poodle whose owner is upset because the dog urinates in the house. In addition, the owner has noticed that the animal now drinks larger amounts of water than in the past.
Although the owner indicates the dog has a good appetite, it appears to have lost weight over the past few months.Clinical Examination. During the examination you check the dog’s breath and detect a sweet odor. Among the organ systems you check are the eyes, and you find developing cataract formation. Because you have seen this dog many times, you check its weight and find that it has lost 2 pounds since its last admittance a year ago. You are able to run a blood glucose determination in your hospital and tell the owner that the glucose concentration is 278 mg/dL.
Comment. The findings in diabetes mellitus (DM) are all attributable to inadequate availability of insulin. Glycogen synthesis decreases in tissues, whereas glycogenolysis and gluconeogenesis increase, contributing to the high concentrations of glucose found in blood. When glucose concentrations exceed the reabsorption capacity in the tubular cells of the kidney, glucose appears in the urine. The loss of glucose in urine causes an osmotic diuresis (polyuria), and the dog compensates for this by drinking additional amounts of water. The sweetness of the breath is caused by the presence of ketone bodies. These form as the result of decreased triglyceride synthesis in adipose tissue, which stimulates lipase activity and the release of free fatty acids. These fatty acids are metabolized to ketone bodies (acetoacetate, acetone, β- hydroxybutyrate) by the liver in a situation of excess fatty acids. The end result is both a ketonemia and a ketonuria. Protein metabolism shifts toward catabolism during DM, with decreased protein synthesis and increased protein degradation by muscle cells.
This process increases the circulating concentrations of amino acids available to the liver for gluconeogenesis. The end result is nitrogen loss and a decrease in the muscle mass of the animal. The changes noted in the lenses of the eyes represent only one of a number of changes that occur in the presence of DM as a result of glycosylation of proteins, including lens proteins and hemoglobin.Treatment. Insulin administration is essential in the treatment of insulin-dependent (type I) DM. During the initial stages of treatment, considerable care must be taken to ensure that the dosage is correct. The goal of treatment is to maintain glucose concentrations between a low of 80 mg/dL and a high of 200 mg/dL, with a serum Iructosamine less than 400 μmol∕L and one or two insulin injections every 24 hours. Too much insulin has the potential for producing a hypoglycemic coma. Two other important aspects of treatment include feeding the animal a diet high in soluble fiber in conjunction with insulin administration and adequate exercise. Finally, the owner needs to be educated and prepared for the necessity of intensive involvement in the management of the disease.