The effects of food reward on circadian system function were investigated in the hypothalamic nuclei, prefrontal cortex and liver. Food rewards of small hedonic and caloric value were provided for 16 days 3 h after light phase onset to male Wistar rats. The daily pattern of locomotor activity was monitored. Gene expression profiling performed in the dorsomedial hypothalamus (DMH) and liver at the time of reward delivery indicated transcriptional factors egr1 and npas2 as possible mediators of food reward effects. Candidate genes were measured in the suprachiasmatic nuclei (SCN), DMH, arcuate nucleus (ARC), prefrontal cortex (PFC) and liver along with per2 expression. A daily pattern in glycemia and per2 expression in the SCN was emphasized by food reward. The expression of egr1 was rhythmic in the SCN, DMH, PFC and liver and food reward weakened or diminished this rhythm. The expression of npas2 was rhythmic in all tissues except for the PFC where food reward induced rhythm in npas2 expression. Food reward induced npas2 and egr1 expression in the DMH at the time of reward delivery. We suppose that the DMH and PFC participate in the adjustment of the circadian system to utilize food reward-induced input via egr1 and npas2 expression.

A b s t r a c tThe authors studied a group of healthy men of an average age 24.4±2.1 yrs (x ± SEM) before the oral intake of ethanol and 1 and 2 hours after its ingestion. The volunteers, n= 10, of an average weight 79.1 kg ± 2.7 kg (± SEM) consumed within one minute 0.42 g ethanol/kg of individual body weight diluted in water (ratio 1:3). Concentrations of alcohol in venous blood were determined using Widmark method. One hour after the peroral intake the ethanol concentration reached 0.39±0.02 g/kg, 2 hours after peroral intake it was 0.33±0.03 g/kg.Parameters of acid-base balance (ABB) from venous blood samples were monitored in probands. Compared with baseline values, the pH of blood did not change significantly. The values of pCO 2 in blood were significantly decreased, even the values of actual HCO 3 -and standard HCO 3 -. The decrease of base excess continued 2 hours after intake of ethanol. There were significant variations in ABB (paired t -test), however in tolerable range. The values of glycaemia, AST, ALT, GGT, and AMS before ethanol intake and 1 and 2 hours after intake of ethanol were in the reference range and they did not change significantly.The authors find important to document even "small" intake of alcohol which may be the cause of ABB shift to a pathological range. The doctors should always keep this in mind when doing the diagnostic statement. The changes of ABB due to alcohol consumption must be expected, especially if they are associated with other pathological conditions affecting the ABB.