V. Biourge et al., EFFECT OF WEIGHT-GAIN AND SUBSEQUENT WEIGHT-LOSS ON GLUCOSE-TOLERANCEAND INSULIN-RESPONSE IN HEALTHY CATS, Journal of veterinary internal medicine, 11(2), 1997, pp. 86-91
The effects of weight gain and subsequent weight loss on glucose toler
ance and insulin response were evaluated in 12 healthy cats. Intraveno
us glucose tolerance tests (IVGTT) were performed at entry into the st
udy, after a significant gain of body weight induced by feeding palata
ble commercial cat food ad libitum, after a significant loss of body w
eight induced by feeding a poorly palatable purified diet to discourag
e eating and promote fasting, and after recovery from fasting when bod
y weight had returned to pre-study values and cats were eating commerc
ial foods. A complete physical examination with measurement of body we
ight was performed weekly, a CBC and serum biochemistry panel were eva
luated at the time of each IVGTT, and a liver biopsy specimen obtained
2 to 4 days after each IVGTT was evaluated histologically for each ca
t. Mean serum glucose and insulin concentrations after glucose infusio
n and total amount of insulin secreted during the second 60 minutes an
d entire 120 minutes after glucose infusion were significantly (P <.05
) increased after weight gain, as compared with baseline. At the end o
f weight loss, cats had hepatic lipidosis and serum biochemical abnorm
alities consistent with feline hepatic lipidosis. There was a signific
ant (P <.05) increase in mean serum glucose concentration and t(1/2),
and a significant (P <.05) decrease in mean serum insulin concentratio
n and the glucose disappearance coefficient (K) after glucose infusion
for measurements obtained after weight loss, compared with those obta
ined after weight gain and at baseline. Insulin peak response, insulin
ogenic index, and total amount of insulin secreted during the initial
10 minutes, 20 minutes, and 60 minutes after glucose infusion were dec
reased markedly (P <.05), compared with measurements obtained after we
ight gain and at baseline. In addition, the total amount of insulin se
creted for 120 minutes after glucose infusion was decreased markedly (
P < .05) in measurements obtained after weight loss, compared with tho
se obtained after weight gain. At the end of recovery, all cats were v
oluntarily consuming food, serum biochemical abnormalities identified
after weight loss had resolved, the number and size of lipid vacuoles
in hepatocytes had decreased, and results of IVGTT were similar to tho
se obtained at baseline. These findings confirmed the reversibility of
obesity-induced insulin resistance in cats, and documented initial de
terioration in glucose tolerance and insulin response to glucose infus
ion when weight toss was caused by severe restriction of caloric intak
e.