| Backgrounds and objectives:Traditional Chinese Medicine (TCM) considers that spleen functions to control saliva. It is generally accepted that a decreased salivary alpha amylase (sAA) activity ratio before and after citric acid stimulation can be made as a reference index for the diagnosis of Pi deficiency syndrome (PDS). Previous studies indicated that PDS adults showed functional disorder of autonomic nerves, and the decreased sAA activity after citric acid stimulation was partially attributed to the inadequate N-glycosylation of salivary glycoprotein as well as sAA. Interestingly, a research group found that PDS patients showed abnormal expression pattern of couple glycosyltransferase genes which involved in N-glycans synthesis. PDS, as a major or mixed syndrome, takes a relatively high proportion in the TCM syndrome distribution for ill or sub-healthy children. However, little attempts have been made to explore the sAA activity ratio in PDS children. To our knowledge, sAA activity is mainly decided by sAA gene (AMY1) copy number, sAA protein content as well as its N-glycosylation extent, and besides, the N-glycosylated modification of sAA is mainly controlled by sympathetic nerve. The present study investigates sAA activity ratio before and after citric acid stimulation in PDS children, as well as AMY1 gene copy number, sAA protein content, N-glycosylated sAA content and non-glycosylated sAA content, aiming to provide reference evidence for the diagnosis of PDS children using sAA activity ratio before and after citric acid stimulation, and also to explore whether the decreased sAA activity ratio relates to AMY gene expression and/or the sAA N-glycosylated modifications.TCM also considers that spleen functions to control sweet taste perception. A disorder of oral sweet taste presented in some PDS patients. Recent studies indicated that sweet perception could induce cephalic phase insulin release (CPIR), which played a crucial role in blood glucose homeostasis. Moreover, sweet perception could also activate endogenous dopaminergic, serotonergic and opioidergic systems, which together involved in appetite control. It was. believed that there was close relationship between spleen and glucose and lipid metabolisms. Thus, the presnt study introduced 129. B6-Taslr3 congenic mice, of which differed in sweet taste perception, to study mice glucose homeostasis, aiming to study PDS from the view of sweet taste receptor.Methods:1. Study of salivary secretion of PDS children before and after citric acid stimulation1.1 Methodology study of saliva stimulation by citric acidNo standardized method has been established for saliva stimulation by citric acid in the study of. sAA activity ratio. We introduced adults as the participants rather than children because adults are considered to have much better compliance than children. We recruited 9 healthy adults (5 females and 4 males) on the campus of Guangzhou University of Chinese Medicine in October 2012. The average age was 25.2+1.1 years old. After salvia was collected 2 min before stimulation (BS), we used 5 different citric acid papers,0.2M/0.5 X (0.2M stands for 0.2 mmol/L citric acid and 0.5X means that the paper size is 0.5 cmX0.5 cm),0.2M/1X,0.2M/2X,0.1M/1X and 0.4M/1X, to stimulate saliva and collect the saliva during stimulation (1 min, DS) as well as after stimulation (2 min, AS). Then the sAA activity and salivary flow rate were measured. DS sAA activity ratio=DS sAA activity/BS sAA activity, and AS sAA activity ratio= AS sAA activity/BS sAA activity.1.2 Methodology study of genomic DNA extraction from saliva1.2.1 Comparison of KI method and kit methodThis is to compare KI method with standardized commercially available kit (oral swab genomic DNA extraction kit) for genomic DNA extraction from fresh saliva samples as well as those stored at room temperature for one week. It aims to verify the reliability and stability of KI method and then provides reference evidence of using this method for the genomic DNA extraction of children followed. We recruited 6 adult volunteers by ads on the campus of Guangdong Pharmaceutical University in March 2013. After saliva collection, we introduced KI method and kit method to extract genomic DNA from both fresh saliva samples and those stored at room temperature for one week. Then 1% agarose gel was used for DNA electrophoresis, and DNA yield and purity (D260/D280 and D260/D230) were determined. We then applied the extracted DNA as templates to amplify tumor protein p53 gene (TP53) and saliva specific protein gene {PRB-3) by PCR. The PCR products were then detected by 1% agarose gel electrophoresis as well.1.2.2 Verification of KI method by larger sample sizeThis is to verify the KI method by introducing more saliva samples. By ads, we recruited 47 healthy children and 52 healthy adults from Haizhu Maternal and Child Health Hospital and Guangdong Pharmaceutical University, respectively. After saliva samples were collected and stored at -80℃, the genomic DNA were extracted by KI method within one week. The measurements of DNA yield and purity as well as PCR amplification were in a fashion to that described above. Besides, in order to explore whether the salivary microbes and/or food debris in the oral cavity could interfere with PCR, the present study also amplified TP53 by fluorescence real-time PCR.1.3 Study design1.3.1 Selection of PDS children and healthy controlDiagnostic standard of PDS children. The standard was based on the draft by Pediatric Specialized Committee of China Association of Traditional Chinese and Western Medicine (1999, Xiamen). The dominant symptom items were (1) poor appetite, (2) abnormal stool, (3) sallow complexion, (4) thinness and (5) pale tongue with thin-white coating. The secondary items were (1) fatigue, (2) abdominal distension, (3) mild edema, (4) mild anemia, (5) drooling, (6) eyes kept open or abnormal sweating during sleep, and (7) weak pulse or pale fingerprint (aged< 3 years old). Children who showed at least 4 dominant items or 2 dominant items plus 2 secondary items could be diagnosed as PDS.Inclusion and exclusion criteria. Children aged 5 to 12 years old and fit with the above diagnostic standard could be included. Participants were free of psychiatric and sever somatic diseases as well as allergic constitution. Individuals using asthma medications, psychotropic substances or painkillers were excluded.Inclusion of healthy children. Children, who aged 5 to 12 years old and free of any obvious diseases as well as showed a balance of yin and yang, were included.1.3.2 Selection of thin and healthy childrenIt may be of reference significance for the study of children PDS essence to explore the molecular mechanisms of sAA activity changes in thin children. After measurement of height (cm) and weight (kg), we calculated their body mass index (BMI). The we dived all the collected children above into low-BMI (thin) and normal-BMI (healthy) children according to the BMI cut-offs by international survey of 6 large nationally representative cross-sectional studies. Besides, overweight or obese children were excluded based on the criteria established by the Working Group on Obesity in China.1.4 Saliva collection and index determination1.4.1 Saliva collectionThe saliva collection method and procedures were based on the study result from adults described above. Briefly, after a 10-min resting period, participants were instructed to seat with their eyes open and head tilted slightly forward, and to empty their mouths by swallowing all salvia. Unstimulated saliva was collected by passive drooling after saliva were accumulating in the oral cavity for 3 min. Immediately after that, we used 0.4M/1X citric acid paper to stimulate tongue tip for 1 min and then collect the stimulated saliva. During stimulation, participants were instructed to keep their tongue tips slightly upward so that citric acid might not mix into the collected saliva.1.4.2 Index determinationSalivary flow rate, pH value and total salivary protein content. Salivary flow rate (mL/min) was expressed as saliva volume (mL) to collection time expended (min). pH values were determined by pH precise paper. Total salivary protein content (mg/mL) was measured by BCA protein assay kit.sAA enzymatic activity assay. EPS-G7 method, recommended by IFCC, was applied to test sAA enzymatic activity (U/mL). sAA specific activity (U/mg)=sAA activity (U/mL)/total salivary protein content (mg/mL).sAA protein content assay. We introduced a human sAA protein sample of known quality and then by Western blot (WB) method the N-glycosylated sAA content, non-glycosylated sAA content as well as total sAA protein content were measured (mg/mL). sAA glycosylated level is the ratio of glycosylated sAA content to total sAA content.AMY1 gene copy number determination. We applied KI method, described above, to extract genomic DNA for children saliva samples. Then target gene (AMY1) and reference gene (TP53) were amplified by fluorescence real-time PCR. A reference DNA sample, which was previously determined to have 14 AMY1 diploid copies, was introduced to calculate the test DNA samples by the method of 2-ΔΔCt*14.1.5 Statistical analysisGraphPad Prism 5.0 was applied to make graphs as well as conduct statistical analysis. Measurement data was expressed as X+SD. Paired t test and independent t test were used to compare indexes within and between groups, respectively. Pearson correlation coefficient was used to analyze correlation between data sets. A P<0.05 was considered as significant.2. Study of relations between mouse sweet perception changes and its metabolism and appetite.2.1 Animal ethics, model and groupingAnimal ethics. Procedures involving animals were approved by the Institutional Animal Care and Use Committee at the Monell Chemical Senses Center prior to the experiments. All efforts were made to minimize mice suffering throughout all experiments.Animal model.129. B6-Taslr3 congenic mice from the N17F9 generation were produced and bred in-house at Monell Center (Dr. Bachmanov). The strain was produced by serial backcrossing of offspring from the 129P3/J (129) and C57BL/6ByJ (B6) intercross onto the 129 strain and selection of mice carrying a fragment of B6 chromosome 4 including the Taslr3 gene. As a result, the congenic mice have genetic background of the 129 strain and a donor chromosomal fragment containing the Taslr3 gene from the B6 strain. The size of the donor fragment does not exceed 194 kb and encompasses, besides Taslr3, several other genes that have been excluded as candidates for the Taslr3 locus. We maintained 129. B6-Taslr3 mice as a segregating congenic strain by mating congenic mice that have only one chromosome containing the B6 donor fragment (B6/129 genotype at the Taslr3 locus) with 129 inbred mice. As a result, in each backcross generation we obtained mice with two different Taslr3 genotypes, B6/129 heterozygotes and 129/129 homozygotes, as determine by TaqMan hybridization-based single nucleotide polymorphism (SNP) allelic discrimination assay. Because the B6 allele of the Taslr3 gene is dominant, B6/129 heterozygotes are phenotypically different from 129/129 homozygotes. Congenic littermates with B6/129 and 129/129 Taslr3 genotypes were used in the present study. The same mice were tested repeatedly at different ages as indicated below.Grouping.129/129 homozygotes were set as control group and B6/129 heterozygotes, which carried a foreign chromosomal fragment, was regarded as experimental group. The mice number in each group varied from 12 to 29.2.2 Maintenance and dietAll animal experiments were conducted in Dr. Bachmanov lab at Monell Center. Breeding and experiments were conducted at 23℃ with a 12:12 h light/dark cycle (light on from 7 AM to 7 PM) unless otherwise indicated. Mice were housed in groups of one to six littermates of the same sex before start of experiments (2 months old,2-mo). After experiments, male mice were housed individually while females were still kept in groups. When mice were not being tested, they had free access to pelleted Teklad Rodent Diet 8604, which contained about 70% starch-based food, and de-ionized water at all times.2.3 Experiments2.3.1 Saccharin preference testThe test can verify sweet perception difference between the two mice group. During 2-mo to 6-mo, we introduced two-bottle test to measure mice preference for 2mM and 10mM saccharin solution for 96 h (de-ionized water as a second choice). Saccharin and water intakes were expressed as per 30 g of body weight (BW, the approximate weight of an adult mouse) per day, or as a preference score (ratio of average daily solution intake to total fluid intake, in percent).2.3.2 Glucose and insulin tolerance testsSweet perception changes can lead to glucose metabolic changes. When aged 2-mo, each mouse was firstly challenged with glucose tolerance test (GTT) by intraperitoneal (IP) injection, followed with GTT by intragastric gavage (IG), and then with insulin tolerance test (ITT). The interval time was one week between tests. We did similar and repeated experiments for each mouse when they reached 6-mo.2.3.3 LabMaster analysisSweet perception changes can also lead to appetite change. LabMaster system can analyze several mice physiological and behavioral indexes including appetite. One week after 2-mo and 6-mo nuclear magnetic resonance (described below), LabMaster system was used to measure mice energy homeostasis, locomotor activity, and food and water intakes, etc. During test,O2 consumed (V02), CO2 generated (VCO2), respiratory exchange ratio (RER), energy expenditure (EE), horizontal and vertical activity, and water and food intakes were recorded every 30 min for 5 days. REE and EE could be used to evaluate mice energy homeostasis. After test, data were averaged across 24 hours.2.3.4 Body weight curve and body composition analysisGlucose metabolism, appetite and energy homeostasis can affect mice body compositions, thus it would benefit to analyze mice body weight curve as well as body compositions.Body weight curve. Mice body weights (to the nearest 0.1 g) were recorded around 10 AM at 2,3,4,5 and 6 months.Nuclear magnetic resonance (NMR). Mice were scanned right after 2-mo and 6-mo ITT, respectively, using the Bruker Minispec LF 110.Dual energy X-ray absorptiometry (DEXA). Mice were euthanized by CO2 inhalation one week after 6-mo LabMaster analysis. After death was confirmed, the body composition of each mouse was determined by dual energy X-ray absorptiometry (DEXA) using a Lunar PIXImus II densitometer.Dissection. Right after DEXA, mice adipose tissues and internal organs were excised and weighed.2.4 Statistical analysisStatistica (version 10) was introduced to conduce statistical analysis. Measurement data were expressed as mean±standard deviation(X±SD) or mean±standard error (X+SE). We used ANOVA or GLM model to analyze data and comparisons were done by post hoc (Fisher LSD test). Graphs were made either by Excel or Statistica. A P<0.05 was considered significant.Results:1. Influence of different citric acid concentration and paper size on the salivary secretion in healthy adultsUnder the same citric acid concentration (0.2M), when compared with 0.5 X, 1×and 2× stimulated significantly higher DS and AS sAA activity ratio (P<0.05), and besides,2×stimulated even more higher. The DS and AS sAA activity ratio of 1×and 2× stimulation was higher than 1, which indicated both stimuli could stimulate an increased sAA activity. Besides, the AS sAA activity ratio of both stimuli was significantly higher than its DS sAA activity ratio, respectively (P<0.05). Moreover, compared with 0.5X and 1 ×,2×stimulated higher salivary flow rate.Under the same paper size (1×),0.1M,0.2M and 0.4M could significantly increase sAA activity. Compared with 0.1M and 0.2M, the DS and AS sAA activity ratio of 0.4M were even significantly higher (P<0.05). Besides, both 0.2M and 0.4M stimulated higher AS sAA activity ratio than its DS sAA activity ratio, respectively (P<0.05). Moreover, compared with 0.1M and 0.2M,0.4M stimulated higher salivary flow rate.Study results indicated that both 0.2M/2X and 0.4M/1X stimuli could significantly stimulate salivary secretion as well as sAA activity and both AS sAA activity ratio were higher than its DS sAA activity ratio. 2. Influence of different storage conditions and extraction methods on the genomic DNA extraction from saliva2.1 Comparisons of KI method and kit method for extracting genomic DNA from fresh saliva and those stored at room temperature2.1.1 DNA yield and purityAs for DNA yield (μg), kit method extracted highest DNA content from fresh saliva (2.64±0.34), which was higher than KI method (P<0.05). However, kit method extracted lowest DNA content from saliva stored at room temperature for one week (0.51±0.11), which was lower than KI method (P<0.05). For KI method, it extracted moderate DNA content from both saliva and no difference was observed. As for DNA purity, the D260/D28o value of DNA extracted by KI method from fresh saliva and those stored at room temperature were 1.99±0.05 and 2.20±0.05, respectively. While the value of kit method for both saliva was around 1.8, which was lower than KI method (P<0.05). Besides, the D260/D230 value of KI method for both saliva was lower than that of kit method (P<0.05). Study results indicated that KI method could yield relatively stable DNA content, while the extracted DNA might also be mixed with RNA or some carbohydrates.2.1.2 DNA electrophoresisFor fresh saliva, an obvious DNA band was observed around 23kb for both KI and kit methods. However, smearing bands were also seen for kit method, which indicated DNA degradation. For saliva stored at room temperature, both methods, especially kit method, showed smearing bands, which also indicated DNA degradation. Results indicated that the extent to which DNA degraded of KI method was relatively lower for different saliva.2.1.3 DNA amplificationsResults showed that the amplifications of TP53 (192 bp) and PRB-3 (1261 bp) were all satisfactory for different DNA samples extrapted by KI and kit methods.2.2 DNA extraction by KI method from saliva stored at -80℃By using KI method, the DNA yield, purity as well as gel electrophoresis of DNA extracted from saliva stored at -80℃ showed similar results to that of from fresh saliva. Besides, the DNA samples also showed satisfactory amplification results for TP53 and PRB-3. Besides, the fluorescence real-time PCR showed that the DNA samples showed satisfactory fluorescence amplification curve for TP53and that the fluorescence melting curve had only one peak, which indicated that the microbes and food debris in saliva might not interfere with human genomic DNA amplification. Our results suggest that KI method can stably obtain adequate and high-quality DNA from saliva samples stored at different conditions when compared with commercially available kit method.3. Salivary secretion changes before and after citric acid stimulation in PDS children3.1 Sample characteristicsWe recruited 20 PDS children and 29 healthy subjects (as control) in Guangzhou Haizhu Maternal and Child Health Hospital during April to November 2013. In PDS group, there were 10 females and 10 males, of which the average age was 8+2 years old. In healthy group, there were 14 females and 15 males, of which the average age was 7±3. No difference was observed for the age and sex composition between the two group (P>0.05). All parents or guardians signed the informed consent.3.2 Within-group comparisons of salivary secretion before and after citric acid stimulation between PDS and healthy childrenFor the healthy group, the sAA activity, sAA content, N-glycosylated sAA content as well as non-glycosylated sAA content were all significantly increased after citric acid stimulation (P<0.05). Besides, the salivary flow rate and pH value were also increased (P<0.05). Results indicated that the salivary secretion of health children responded well to citric acid stimulation.For the PDS group, only salivary flow rate, pH value and sAA glycosylated level significantly increased towards stimulation (P<0.05), while other indexes for example sAA activity did not respond. Results indicated an attenuated salivary secretion of PDS children towards citric acid stimulation.3.3 Between-group comparisons of salivary secretion before and after citric acid stimulation between PDS and healthy childrenUnder citric acid stimulation, the sAA activity ratio of PDS children (1.87±1.04) was lower than that of healthy children (2.72±1.58), of which the difference reached significance (P<0.05). The result indicated that the extent to which sAA activity responded to citric acid stimulation of PDS children was obviously lower than that of healthy children, which was consistent with the reports for PDS adults.Under stimulation, the sAA glycosylated level ratio was significantly higher than that of healthy children (1.54±0.63 vs.1.20±0.45, P<0.05), which suggest that PDS children show abnormal sAA glycosylation towards citric acid stimulation.The two study groups did not differ in AMI gene copy number (PDS children: 8.57±3.21, healthy children:7.85±2.70, P<0.05), which indicated that AMI gene copy number might not contribute to the decreased sAA activity ratio. 4. Salivary secretion changes before and after citric acid stimulation in thin children4.1 Sample characteristicsFrom the collected 49 participants (described above),43 children was included in the present study, within which 21 (11 females and 10 males) and 22 (9 females and 13 males) participants were assigned to low-BMI (thin) group and normal-BMI (healthy) group, respectively. The average age of both group was the same, ie.8±2 years old. No difference was observed regarding age and sex composition between the two groups (P>0.05). 4.2 Between-group comparisons of salivary secretion before and after citric acid stimulation between thin and healthy childrenBoth groups did not differ in sAA content or sAA activity before or after citric acid stimulation (P> 0.05). However, thin children showed a significantly decreased sAA activity ratio when compared with healthy group (1.6±0.8 vs.2.3±1.0, P< 0.05). Also, its sAA content ratio was significantly lower as well (1.1±0.7 vs.2.0±1.2, P<0.05). Together, results suggest that thin children present attenuated sAA secretion response, which is consistent with the results from PDS children. Besides, no difference was observed between the two study groups regarding AMY1 gene copy number (P >0.05), which indicated that AMY1 gene copy number might not contribute to the sAA level changes in thin children.5. Influence of sweet perception changes on mice glucose metabolism and appetite5.1 Sweet perception difference between B6/129 and 129/129 miceB6/129 mice showed significantly increased intake (7.3±0.6 vs.4.6± 0.2 ml/30 g BW) and preference (91.9±1.1 vs.71.3±2.8%) for 2 mM saccharin solution compared with 129/129 (P<0.05). For higher concentration (10mM), B6/129 also showed significantly higher intake (14.1±2.2 vs.7.8±0.6 ml/30 g BW, P<0.05). These results obviously indicated that B6/129 mice, of which the chromosome contained foreign Taslr3 allele, showed pathologically higher sweet perception for saccharin than 129/129.5.2 Glucose metabolic differences between B6/129 and 129/129 mice5.2.1 Glucose tolerance testsFor IP GTT, genotype effect was detected at 6-mo (P<0.05), and post hoc comparisons showed that male B6/129 had higher blood glucose levels at 5 min, 45 min,60 min as well as 90 min than 129/129 mice (P<0.05). The results indicated that B6/129 mice had impaired IP GTT compared with 129/129.For IG GTT, male B6/129 mice showed higher blood glucose levels at 15 min, 30 min as well as 45 min than 129/129 at 2-mo (P<0.05), and male B6/129 mice also presented higher blood glucose levels at 30 min than 129/129 at 6-mo (P <0.05). The results indicated that B6/129 mice had impaired IG GTT compared with 129/129. Together with IP GTT, B6/129 mice showed impaired GTT either by IP or IG, which fit well with PDS patients who used to show impaired glucose metabolism.5.2.2 ITTMice in both groups showed a rapid decrease of blood glucose after challenged with insulin, and the blood glucose reached lowest level at 60 min and then slowed recovered. However, mice blood glucose did not return to baseline within 120 min. The present study did not detect genotype effect (P >0.05), which indicated that both mice had similar insulin sensitivity.5.3 LabMaster analysis between B6/129 and 129/129 mice5.3.1 Food and water intakesWe almost detected genotype effect on mice food intake (P=0.059), and post hoc comparisons showed that 129/129 mice had higher food intake at 21:00,08:00 as well as 11:00 than B6/129 at 2-mo (P<0.05), and moreover,129/129 also probably had higher food intake at 17:00 (P=0.082) and 18:00 (P=0.070) than B6/129 at 6-mo. The results indicated that B6/129 mice probably showed lower food intake compared with 129/129.We detected genotype effect on mice water intake (P<0.05), and post hoc comparisons showed that 129/129 mice had higher water intake at 21:00 and 12:00 than B6/129 at 2-mo (P<0.05), and moreover,129/129 also showed higher water intake at 20:00 and 23:00 at 6-mo (P<0.05). The results indicated that B6/129 mice showed lower water intake compared with 129/129. Together with food intake, our results further supported that B6/129 fit well with PDS characteristics from the view of appetite changes.5.3.2 RER and EEWe found male 129/129 mice showed higher RER at 11:00,12:00,13:00,14:00 and 15:00 than B6/129 at 2-mo (P<0.05). At 6-mo, female 129/129 also had higher RER at 00:00,03:00 and 04:00 than B6/129 (P<0.05), and moreover, male 129/129 mice showed higher RER at 14:00 and 15:00 (P<0.05). The results indicated that B6/129 mice presented significantly lower RER compared with 129/129.129/129 mice was found to had significantly higher EE than B6/129 (P< 0.05). However, the EE of 129/129 decreased over time, while B6/129 showed relatively stable EE across test session. The results indicated that B6/129 mice had significantly lower but relatively stable EE compared with 129/129. Together with RER, our results suggest a disorder of energy metabolism in B6/129 mice, which, again, further supported that B6/129 fit well with PDS characteristics from the view of energy homeostasis.5.3.3 Locomotor activityGenotype effect was detected on mice locomotor activity (P<0.05), and post hoc comparisons showed that B6/129 mice had higher activity at 22:00,00:00, 01:00 and 04:00 than 129/129 (P<0.05).5.4 Body weight curve and body composition between B6/129 and 129/129 mice5.4.1 Body weight curveWe did not found difference in mice body weight between the two study groups across the test (P>0.05).5.4.2 Body compositionNMR. We detected the interaction of genotype and age on mice fat content (P<0.05). Our results showed that B6/129 mice had higher fat content than 129/129 at 2-mo. At 6-mo, however, B6/129 mice showed lower fat content because its fat content decreased faster over time.DEXA. GLM analysis did not detect any difference between the two study group, but B6/129 fat content might be higher than 129/129.Dissection. GLM analysis showed that B6/129 mice showed higher brown fat content than 129/129 (P<0.05). Our results suggest B6/129 may have abnormal lipid metabolism, which also fit well with PDS characteristics.Conclusion:sAA activity ratio decreased towards citric acid stimulation in PDS children, which was accompanied by an abnormally increased sAA glycosylated level. However, no difference was observed regarding AMY1copy number compared with healthy group. These suggest that the sAA activity ratio after citric acid stimulation can be treated as an objective indicator for diagnosis of PDS children, and that the decreased sAA activity ratio may closely relate to its N-glycosylation modifications. We also found similar results in thin children, which suggest that PDS contribute to thinness in children and that it has scientific basis to treat thinness as a dominant symptom item in the diagnosis of PDS children.Animal experiments indicated that B6/129 mice had pathologically high sweet taste, which was similar to that described by Huangdi Neijing. B6/129 mcie showed disorders of glucose and lipid metabolisms, attenuated appetite as well as abnormal energy homeostasis, which suggest that B6/129 may serve as PDS mouse model and that "sweet perception-glucose and lipid metabolism" may serve as one possible pathogenesis for PDS. |
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