Biomedical subjects

Xiao Qiu Xiao

Publications and source records attributed to Xiao Qiu Xiao.

4 recordsLinked to original sources

PubMed2005

Deoxyribonucleic acid microarray analysis of gene expression pattern in the arcuate nucleus/ventromedial nucleus of hypothalamus during lactation.

Lactation is characterized by extreme hyperphagia and negative energy balance resulting from a large energy drain due to milk production and by a suppression of cyclic ovarian function. Increases in neuropeptide Y and agouti-related protein and a decrease in proopiomelanocortin expression in the arcuate nucleus of hypothalamus (ARH) may contribute to the hyperphagia to maintain energy balance and to the suppression of LH secretion associated with lactation. However, little is known about the full extent of neuroendocrine changes in the ARH that may contribute to the various adaptations occurring during lactation. To address this issue, we used Affymetrix microarray to acquire a reliable profile of the lactation-induced transcriptional changes in micropunches containing the ARH and a portion of the ventromedial nucleus of the hypothalamus. Using high stringency criteria, 12 genes were identified as being differentially regulated during lactation, and an additional 10 genes and three transcribed sequences were identified using moderate stringency criteria. Changes in neuropeptide Y, enkephalin, tyrosine hydroxylase, and dynorphin, genes previously shown to be differentially regulated during lactation, provide validation for the microarray analysis. New genes identified as being differentially expressed include those related to neurotransmission, growth factors, signal transduction, and structure remodeling. These data identify new genes in ARH/ventromedial nucleus of the hypothalamus that may play an important role in the adaptations of lactation related to hyperphagia, milk production, and the suppression of cyclic reproductive function and may contribute to elucidating a framework for integrating changes in energy intake with the regulation of reproductive function during lactation.

Animals↗

PubMed2004

Metabolic adaptations in skeletal muscle during lactation: complementary deoxyribonucleic acid microarray and real-time polymerase chain reaction analysis of gene expression.

Lactation and fasting are two physiological models characterized by negative energy balance. Our previous studies demonstrated that uncoupling protein (UCP) 3 expression in skeletal muscle was down-regulated during lactation and up-regulated during fasting. The present studies used cDNA microarray and real-time PCR to perform a systems and comparative analysis in gene expression in skeletal muscle under conditions of negative energy balance. Gastrocnemius skeletal muscle RNA pools were generated from the following groups of rats: cycling diestrous females, cycling females with 48 h of fasting, lactation, and lactation + leptin. Of those known genes studied, 35 genes were up-regulated and 49 were down-regulated during lactation. Leptin treatment during lactation reversed the differential regulation of about 80% of these genes, demonstrating the importance of the leptin suppression to the changes in skeletal muscle metabolism. GenMAPP analysis revealed a coordinated regulation at key steps in glycolysis/gluconeogenesis, the tricarboxylic acid cycle, and lipid metabolism, indicating an increased rate of lactate production through glycolysis and reduced fatty acid degradation in skeletal muscle during lactation. Particular interest was paid to those genes that changed in a similar manner to UCP3 mRNA. Many of these genes that were decreased during lactation and increased during fasting are involved in fatty acid degradation and transport, including acyl-coenzyme A dehydrogenase for medium chain fatty acid, carnitine palmitoyltransferase 1, and fatty acid translocase. The current studies provide a basis for investigating the mechanisms underlying metabolic adaptations during lactation and fasting and highlight the importance of UCP3 in lipid metabolism.

Adaptation, Physiological↗

PubMed2003

Inhibition of uncoupling protein expression during lactation: role of leptin.

Uncoupling proteins (UCPs) are mitochondrial proteins that play a role in regulation of energy expenditure by uncoupling respiration from ATP synthesis. Lactation is a physiological condition characterized by negative energy balance due to the loss of energy sources to the production of milk. The objective of the current study was to investigate whether UCP mRNA and protein expressions were altered during lactation compared with those after 48 h of fasting. Lactation significantly reduced serum leptin levels, and removal of pups for 48 h increased serum leptin to higher levels than those observed in control rats. Compared with control rats, mRNA expression of UCP1 and UCP3 in brown adipose tissue (BAT) was dramatically reduced during lactation and fasting. The reduction in mRNAs was reflected by a lowered UCP1 protein level, and to some extent, UCP3 protein. Treatment of lactating rats with exogenous leptin (3 mg/kg) or removal of pups for 48 h completely reversed the down-regulation of UCP1 and UCP3 mRNA expression in BAT, and pup removal led to a recovery of protein expression. In contrast to BAT, UCP3 expression in skeletal muscle was increased in fasted rats and decreased during lactation. Similar changes were observed in serum free fatty acid levels. These changes are consistent with the idea that the utilization of free fatty acids as a fuel source is spared during lactation. As in BAT, leptin treatment and removal of pups were able to restore changes in mRNA expression of UCP3 in skeletal muscle during lactation. The present results suggest that the inhibition of leptin secretion during lactation is involved in the down-regulation of UCP expression in BAT and skeletal muscle, which, in turn, is responsible for the decrease in metabolic fuel oxidation and thermogenesis.

Adipose Tissue, Brown↗

PubMed2002

Huperzine A attenuates amyloid beta-peptide fragment 25-35-induced apoptosis in rat cortical neurons via inhibiting reactive oxygen species formation and caspase-3 activation.

Huperzine A, a novel Lycopodium alkaloid originally discovered in the Chinese herb Qian Ceng Ta (Huperzia serrata), is a reversible, potent, and selective acetylcholinesterase (AChE) inhibitor and has been extensively used for the treatment of Alzheimer's disease (AD) in China. The present studies were designed to investigate effects of huperzine A on amyloid beta-peptide fragment 25-35 (Abeta25-35)-induced neuronal apoptosis and potential mechanisms in primary cultured rat cortical neurons. After exposure of the cells to Abeta25-35 (20 microM), apoptotic cell death was observed as evidenced by a significant decrease in cell viability, alteration of neuronal morphology, and DNA fragmentation. Pretreatment of the cells with huperzine A (0.01-10 microM) prior to Abeta25-35 exposure significantly elevated the cell survival and reduced Abeta25-35-induced nuclei fragmentation. Reactive oxygen species (ROS)-based fluorescence, caspase-3-like fluorogenic cleavage, and Western blot analysis demonstrated that huperzine A reduced Abeta25-35-induced ROS formation in a dose-dependent manner, and 1 microM of huperzine A attenuated Abeta25-35-induced caspase-3 activity at 6, 12, 24, and 48 hr posttreatment. Our results provide the first direct evidence that huperzine A protects neurons against Abeta25-35-induced apoptosis via the inhibition of ROS formation and caspase-3 activity.

Alkaloids↗