ABSTRACT
Expression of uncoupling protein-1 (UCP1) is increased by cold acclimation and overfeeding, and reduced in fasting and genetic obesity. It is known that the mitochondrial UCP1 in the brown adipose tissue (BAT) is an important key molecule for non-shivering thermogenesis. On the other hand, ethanol (EtOH) alters thermoregulation in humans and laboratory animals. However, the relationship between EtOH intake and UCP1 expression is not yet clear. Accordingly, the present study employed the technique of real-time quantitative polymerase-chain reaction (PCR) to investigate the effects of EtOH (0.5 or 2.0 g/kg) on the expression of UCP1 mRNA in the mouse BAT. Control mice were injected with the same volume of physiological saline intraperitoneally (IP). IP injection of EtOH (0.5 g/kg) caused a decrease and an increase of the expression of BAT UCP1 mRNA at 1 and 4 hours, respectively. Treatment with EtOH (2.0 g/kg) caused an increases of the expression of BAT UCP1 mRNA at both 2 and 4 hours. BAT UCP1 mRNA levels in both groups increased at 4 hours after EtOH administration. The levels of UCP1 mRNA returned to the control levels by 8 hours after EtOH administration. The expression of BAT UCP1 mRNA was upregulated following EtOH administration, although a lower dose of EtOH initially reduced the expression of UCP1 mRNA in BAT. These findings suggest that EtOH-induced UCP1 mRNA expression in BAT reflects an alteration of the set point of thermogenesis.
Subject(s)
Adipose Tissue, Brown , Carrier Proteins/genetics , Ethanol/pharmacology , Gene Expression Regulation/drug effects , Membrane Proteins/genetics , RNA, Messenger/metabolism , Adipose Tissue, Brown/drug effects , Adipose Tissue, Brown/physiology , Animals , Carrier Proteins/metabolism , Ethanol/administration & dosage , Humans , Ion Channels , Male , Membrane Proteins/metabolism , Mice , Mitochondrial Proteins , Thermogenesis/physiology , Time Factors , Uncoupling Protein 1ABSTRACT
Differences of alcohol drinking behavior, brain dopamine (DA) and serotonin (5-HT) levels and releases in the striatum were investigated in stroke-prone spontaneously hypertensive rats (SHRSP) and age-matched stroke-resistant spontaneously hypertensive rats (SHRSR). Voluntary alcohol (EtOH) consumption in SHRSP rats increased at 1 and 2 hours in the 4 hour time access. In the DA level, SHRSP showed decreases in the caudate-putamen (C/P) and dorsal raphe nucleus (DRN) compared with in SHRSR. 5-HT levels in the C/P, ventral tegmental area-subtantia nigra (V/S) and DRN of the SHRSP were decreased compared with that in SHRSR. The basal extracellular levels of 5-HT release in the C/P were increased in SHRSP as compared with those in SHRSR. K(+)- or EtOH-induced DA and 5-HT releases in the C/P of the SHRSP were a lower magnitude than those in SHRSR. Increased basal extracellular 5-HT releases showing low levels of 5-HT in the C/P of SHRSP mean an abnormality of serotonergic neuronal functions in a normal physiological condition. Higher voluntary alcohol drinking behavior, so called lower susceptibility to EtOH, in the SHRSP may be associated with the degenerated rewarding system including the DRN. These results suggest that the hypertensive state causes the dysfunction in the striatum of the brain rewarding system and induces the risk for increasing alcohol consumption to compensate for the alteration of serotonergic neurons.
Subject(s)
Alcoholism/genetics , Brain/drug effects , Ethanol/pharmacology , Genetic Predisposition to Disease , Hypertension/genetics , Rats, Inbred SHR/genetics , Alcohol Drinking/genetics , Alcohol Drinking/metabolism , Alcoholism/metabolism , Animals , Brain/metabolism , Dopamine/metabolism , Ethanol/administration & dosage , Food Preferences/drug effects , Hypertension/metabolism , Rats , Rats, Inbred WKY , Serotonin/metabolism , Stroke/complications , Stroke/geneticsABSTRACT
We investigated whether age of drinking onset and/or the housing condition in experimental animals affected alcohol drinking behavior to extrapolate the experimental findings to alcohol drinking patterns of aged people. At the time of the experiments, all 1-, 4-, 10- and the 16-month-old rats were divided into two groups, isolated and aggregated groups, and then maintained in the same housing conditions for six months. The amounts of voluntary alcohol consumption (g/kg/day) of all rats were investigated by two-bottle methods at 7, 10, 16 and 22 months old. No significant difference in alcohol drinking behavior was shown in the 7- and 10-month-old rats. A decrease in voluntary alcohol consumption was shown in the 16-month-old rats of the aggregated groups. In the 22-month old rats, a significant suppression of voluntary alcohol consumption was found in the aggregated groups compared with the isolated group. The results demonstrate that an important determinant of EtOH intake is related to environmental factors. It was suggested that alcohol drinking behavior strongly depends on the housing conditions and the age of onset of alcohol drinking.