SOMATIC PARAMETERS, ORGAN GROWTH, AND PLASMA SUBSTRATES IN WEANLING RATS WITH LATERAL HYPOTHALAMIC-LESIONS ONE MONTH POSTOPERATIVELY

Somatic and some metabolic aspects of the syndrome that follows bilate ral destruction of the lateral hypothalamic area (LHA) have been studi ed primarily in mature rats. Fewer data are available for the weanling rat. Weanling Sprague-Dawley rats received small (10 mC) bilateral el ectrolytic lesions (LHAL). Sham-operated controls were pair-gained to LHAL rats (CON-PG) or fed ad lib (CON-ADLIB). All rats were killed 1 m onth after LHAL Both LHAL and CON-PG weighed less, had less carcass fa t, and were shorter than CON-ADLIB. Also, LHAL were somewhat, but sign ificantly (SIGN), shorter than CON-PG. Rats with LHAL has less carcass protein than CON-ADLIB in percent but not in absolute terms. Liver, e pididymal fat pads, diaphragm, kidneys adrenals, testes, spleen, and h eart grew SIGN smaller in LHAL vs. CON-ADLIB, but in no instance was t here a SIGN difference between LHAL and CON-PG. In body weight percent age, some of these differences (liver, kidneys, heart) were not SIGN. Both LHAL and CON-PG had larger adrenals than CON-ADLIB and both LHAL and CON-PG had SIGN less protein in their livers, epididymal fat pads, and diaphragm than CON-ADLIB. In organ weight percentage, however, LH AL rats had more protein in their livers and fat pads than CON-ADLIB a nd LHAL rats had less protein in fat pads than CON-PG in absolute but not in percent organ weight terms. Plasma glucose was similar in all g roups, but LHAL had SIGN lower triglycerides and total cholesterol tha n CON-ADLIB. Compared to CON-PG, LHAL had SIGN lower total cholesterol but SIGN higher high-density lipoprotein (HDL) cholesterol and albumi n than CON-ADLIB. It is concluded that some of the changes observed ar e evidently due to the hypocaloric food intake of LHAL rats, whereas s everal parameters [linear growth, spleen size, fat pad protein (absolu te), total cholesterol, and total protein] are presumably due to a ''t rue'' lesion effect. This could come about by interference by the lesi ons with control systems of intermediary metabolism as have been sugge sted by stimulation studies.