In Vitro [U-¹⁴C]Glucose Utilization by Tissues of Weanling Rats with Lateral Hypothalamic Area Lesions One Month after Lesion Production

The role of the lateral hypothalamic area (LHA) in intermediary metabolism was investigated by quantitation of [U-¹⁴C]glucose oxidation to ¹⁴CO₂ and ¹⁴C incorporation into the glycogen and lipid fraction of the liver, epididymal fat pad, and diaphragm. Weanling male Sprague-Dawley rats received bilateral electrolytic lesions in the LHA (LHAL rats). Sham-operated rats were either fed ad libitum (CON-ADLIB) or pair-gained to the LHAL rats (CON-PG). The experiment was terminated 1 month after lesion production. LHAL rats were significantly (SIG) lighter and shorter and ate less than CON-ADLIB; LHAL rats were also SIG shorter than CON-PG, pointing to a food intake-independent lesion effect. Both LHAL and CON-PG rats had SIG less percent carcass fat than CON-ADLIB, but there was no SIG difference between LHAL and CON-PG rats. Also, LHAL rats had a SIG higher percentage of carcass protein than both CON-ADLIB and CON-PG. Furthermore, LHAL rats incorporated SIG less glucose into liver glycogen than CON-ADLIB but SIG more into CON-PG, whereas CON-PG rats incorporated SIG less into liver glycogen than CON-ADLIB, again suggesting a food intake-independent effect. There was no difference among the groups in glucose oxidation and incorporation into lipids and glycogen in both diaphragm and epididymal fat pads and liver total lipid. However, livers of CON-PG metabolized SIG more [U-¹⁴C] glucose to CO₂ than did livers of CON-ADLIB, suggesting a food intake-dependent effect. There was no difference between LHAL and CON-PG rats in this parameter. These data indicate that the majority of the changes in weanling rats 1 month after LHAL must be due to the greatly reduced food intake precipitated by the lesions rather than some specific food intake-independent “metabolic” lesion effect.