Site of action of putative lipostatic factor: food intake and peripheral pentose shunt activity.

Obesity due to overfeeding in one parabiotic rat results in mild hypophagia and specific loss of fat from its partner. Studies were conducted to determine whether the changes in body composition were reversible and whether the nonsignificant reduction in food intake was a primary response to a humoral lipostatic factor. Tube feeding partners of overfed rats 0.5 g more food per day than eaten voluntarily prevented loss of fat, although hepatic and adipose glucose-6-phosphate dehydrogenase activities were depressed. Glucose flux through the pentose phosphate pathway was inhibited in both adipose and hepatic tissue from thin partners of obese rats, although fatty acid synthesis was depressed only in adipose tissue. Response to insulin by adipocytes from ad libitum partners of obese rats appeared to be blunted, but insulin sensitivity was normal. When overfeeding stopped, both partners returned to control body composition, suggesting that the changes observed in parabiotic partners of obese rats were physiological responses to a putative circulating lipostatic factor rather than a nonspecific consequence of parabiosis.