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Fasting causes suppression of metabolic rate (MR) and core temperature (Tc). In contrast, food intake induces immediate elevation of MR and Tc (postalimentary hyperthermia, or thermic effect of food, TEF). These are not simply changes due to altered energy reserves, instead they are regulatory changes since, e.g., acute cold exposure can increase MR even in the state of severe fasting hypometabolism (Székely et al., 1997). The question regarding the nature of information channels for such regulatory changes has not been resolved. In the present studies MR and Tc of Wistar rats were measured (by diaferometer and thermocouples, respectively) at thermoneutrality following a 48-h food withdrawal or in connection of re-feeding. Spontaneous re-feeding for 3-h with rat-chow or saccharine-sweetened CaCO3 was followed by MR and Tc measurements. In other cases, during MR and Tc measurements, artificial re-feeding was performed: a) through a preimplanted gastric cannula either calorie-rich (FWG) or calorie-free (HD) substance was injected (water in controls), b) through a preimplanted jugular cannula either 4 ml 40% glucose or 2.5 ml 20% fat emulsion (Intralipid) (or 0.9% NaCl in controls) was infused within 2-h. All implantations were performed under intraperitoneal ketamine + xylazine (78 + 13 mg/kg) anesthesia 3-7 days before fasting, and all operated animals were given a narcotic overdose after finishing the measurements. Fasting caused suppression of MR and Tc. Spontaneous re-feeding was followed by reversal of this suppression both in chow- and CaCO3-fed rats; not the composition but the volume of ingested substance seemed to be important. Both FWG and HD injections elicited elevations in MR and Tc, although the dynamics were different for the two substances (the rise commenced earlier in case FWG was given). Neither glucose, nor Intralipid infusion modified low MR and Tc values of fasting rats. It is concluded that not caloric signals, neither oro-facial neural impulses, rather gastrointestinal signals (most likely due to stretch, nutrients, gastrointestinal hormones) may be responsible for the postalimentary rise in MR and Tc, and probably similar (or inverse) gastrointestinal signals may be detectible in the background of the fasting-induced hypometabolism and hypothermia.
Székely, M., Szelényi, Z., Kis, A., 1997. Fasting and re-feeding: alterations of resting metabolic rate and body temperature. In: Nielsen Johannsen, B., Nielsen, R. (Eds.), Thermal Physiology 1997, August Krogh Institute, Copenhagen, pp. 235-238.