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The article presents a study on incorporating exercise by using an underwater treadmill and active client education into a weight management program for obese dogs. In the study, eight obese client-owned dogs participated in a three monthly weight management program. Monthly blood tests were taken to ensure that the dogs remained healthy during the course of the trial.

This study aimed to investigate the contributions of two factors potentially impairing glucagon response to insulin-induced hypoglycemia (IIH) in insulin-deficient diabetes: 1 ) loss of paracrine disinhibition by intra-islet insulin and 2 ) defects in the activation of the autonomic inputs to the islet. Plasma glucagon responses during hyperinsulinemic-hypoglycemic clamps ([Formula: see text]40 mg/dL) were assessed in dogs with spontaneous diabetes ( n = 13) and in healthy nondiabetic dogs ( n = 6). Plasma C-peptide responses to intravenous glucagon were measured to assess endogenous insulin secretion. Plasma pancreatic polypeptide, epinephrine, and norepinephrine were measured as indices of parasympathetic and sympathoadrenal autonomic responses to IIH. In 8 of the 13 diabetic dogs, glucagon did not increase during IIH (diabetic nonresponder [DMN]; ∆ = -6 ± 12 pg/mL). In five other diabetic dogs (diabetic responder [DMR]), glucagon responses (∆ = +26 ± 12) were within the range of nondiabetic control dogs (∆ = +27 ± 16 pg/mL). C-peptide responses to intravenous glucagon were absent in diabetic dogs. Activation of all three autonomic responses were impaired in DMN dogs but remained intact in DMR dogs. Each of the three autonomic responses to IIH was positively correlated with glucagon responses across the three groups. The study conclusions are as follows: 1 ) Impairment of glucagon responses in DMN dogs is not due to generalized impairment of α-cell function. 2 ) Loss of tonic inhibition of glucagon secretion by insulin is not sufficient to produce loss of the glucagon response; impairment of autonomic activation is also required. 3 ) In dogs with major β-cell function loss, activation of the autonomic inputs is sufficient to mediate an intact glucagon response to IIH. NEW & NOTEWORTHY In dogs with naturally occurring, insulin-dependent (C-peptide negative) diabetes mellitus, impairment of glucagon responses is not due to generalized impairment of α-cell function. Loss of tonic inhibition of glucagon secretion by insulin is not sufficient, by itself, to produce loss of the glucagon response. Rather, impaired activation of the parasympathetic and sympathoadrenal autonomic inputs to the pancreas is also required. Activation of the autonomic inputs to the pancreas is sufficient to mediate an intact glucagon response to insulin-induced hypoglycemia in dogs with naturally occurring diabetes mellitus. These results have important implications that include leading to a greater understanding and insight into the pathophysiology, prevention, and treatment of hypoglycemia during insulin treatment of diabetes in companion dogs and in human patients.

Physical activity improves outcome of weight loss in obese humans, but limited information exists for dogs. Eight obese dogs (body condition score 5/5), of various breeds and genders, undertook a 3-month weight-loss program which included exercise using lead walks and underwater treadmill exercise. The median number of treadmill exercise sessions per dog was 13 (range: 5 to 17). Median distance walked per session was 0.97 km (range: 0.05 to 2.7 km) (0.6 miles; range: 0.03 to 1.70 miles) and this increased sequentially over the course of the study (P < 0.001). Mean [± standard deviation (s)] percentage of starting weight loss over the 3 mo was 18.9 ± 5.44%, equivalent to a rate of weight loss of 1.5 ± 0.43% per week. Thoracic and abdominal girth also declined significantly during the program (P < 0.0001 for both). This study demonstrates the potential benefit of including an organized exercise regimen, utilizing an underwater treadmill, in conventional canine weight management programs.