Gluconeogenesis in Weanling Rats with Hypothalamic Obesity[*]

Abstract

The plasma concentration of urea before and after nephrectomy, the in vivo incorporation of bicarbonate and alanine into liver glycogen and plasma glucose, and the in vitro incorporation of alanine into liver glucose were measured in weanling rats with and without obesity induced by ventromedial hypothalamic (VMN) lesions. Basal urea levels were higher in obese rats and rose more rapidly than normal after nephrectomy. Bicarbonate incorporation into liver glycogen and plasma glucose was greater in fed obese than in fed control rats. Fasting increased incorporation into liver glycogen in both groups, but the incorporation into plasma glucose was increased by fasting much more in control than obese rats. Obese rats incorporated more alanine than normal into liver glycogen and plasma glucose in vivo, but in vitro there was no observable difference in alanine conversion to glucose by the liver slice. These results indicate that gluconeogenesis is increased in vivo in the weanling rat with hypothalamic obesity. The precise signal by which the production of VMN lesions initiates this sequence of events remains unknown.

Key words

Ventromedial Hypothalamic Lesion - Gluconeogenesis

1 Supported by Veterans Administration funds and by a grant from the National Institute of General Medical Science (#15768)

1 Supported by Veterans Administration funds and by a grant from the National Institute of General Medical Science (#15768)