OBjECTIVE:To compare the correlations between salivary alpha-amylase(sAA) activity and amylase,alpha 1(salivary) gene(AMY1) copy number or its gene expression between splenic asthenia and healthy children,and investig...OBjECTIVE:To compare the correlations between salivary alpha-amylase(sAA) activity and amylase,alpha 1(salivary) gene(AMY1) copy number or its gene expression between splenic asthenia and healthy children,and investigate the reasons of attenuated sAA activity ratio before and after citric acid stimulation in splenic asthenia children.METHODS:Saliva samples from 20 splenic asthenia children and 29 healthy children were collected before and after citric acid stimulation.AMY1 copy number,sAA activity,and total sAA and glycosylated sAA contents were determined,and their correlations were analyzed.RESULTS:Although splenic asthenia and healthy children had no differences in AMY1 copy number,splenic asthenia children had positive correlations between AMY1 copy number and sAA activity before or after citric acid stimulation.Splenic asthenia children had a higher sAA glycosylated proportion ratio and glycosylated sAA content ratio,while their total sAA content ratio and sAA activity ratio were lower compared with healthy children.The glycosylated sAA content ratio was higher than the total sAA content ratio in both groups.Splenic asthenia and healthy children had positive correlations between total sAA or glycosylated sAA content and sAA activity.However,the role played by glycosylated sAA content in sAA activity in healthy children increased after citric acid stimulation,while it decreased in splenic asthenia children.CONCLUSION:Genetic factors like AMY1 copy number variations,and more importantly,sAA glycosylation abnormalities leading to attenuated sAA activity after citric acid stimulation,which were the main reasons of the attenuated sAA activity ratio in splenic asthenia children compared with healthy children.展开更多
For the last decade, low serum amylase(hypoamylasemia) has been reported in certain common cardiometabolic conditions such as obesity, diabetes(regardless of type), and metabolic syndrome, all of which appear to have ...For the last decade, low serum amylase(hypoamylasemia) has been reported in certain common cardiometabolic conditions such as obesity, diabetes(regardless of type), and metabolic syndrome, all of which appear to have a common etiology of insufficient insulin action due to insulin resistance and/or diminished insulin secretion. Some clinical studies have shown that salivary amylase may be preferentially decreased in obese individuals, whereas others have revealed that pancreatic amylase may be preferentially decreased in diabetic subjects with insulin dependence. Despite this accumulated evidence, the clinical relevance of serum, salivary, and pancreatic amylase and the underlying mechanisms have not been fully elucidated. In recent years, copy number variations(CNVs) in the salivary amylase gene(AMY1), which range more broadly than the pancreatic amylase gene(AMY2A and AMY2B), have been shown to be well correlated with salivary and serum amylase levels. In addition, low CNV of AMY1, indicating low salivary amylase, was associated with insulin resistance, obesity, low taste perception/satiety, and postprandial hyperglycemia through impaired insulin secretion at early cephalic phase. In most populations, insulin-dependent diabetes is less prevalent(minor contribution) compared with insulin-independent diabetes, and obesity is highly prevalent compared with low body weight. Therefore, obesity as a condition that elicits cardiometabolic diseases relating to insulin resistance(major contribution) may be a common determinant for low serum amylase in a general population. In this review, the novel interpretation of low serum, salivary, and pancreas amylase is discussed in terms of major contributions of obesity, diabetes, and metabolic syndrome.展开更多
基金National Natural Science Foundation of China(the Mechanism Study of Salivary Alpha Amylase Activity Change in Pi-Deficiency Syndrome Patients Based on the AMY1 Copy Number Variations,N-Glycosylated Protein Level andβ-Adrenergic Receptor Activation,No.81102703)Science and Technology Planning Project of Guangdong Province(miRNA as Material Basis for the New Hypothesis"Pi-Metabolism Relevance,"and Study on the Molecular Mechanisms of Treating Metabolic Disorders Through Pi,No.2013A032500005)and Administration of Traditional Chinese Medicine of Guangdong Province in China(Study on the Relevance Between the Pi-Deficiency Syndrome and Gene Differential Expression Profile of Immunity and Metabolism in Type 2 Diabetic Mellitus,No.20123001)
文摘OBjECTIVE:To compare the correlations between salivary alpha-amylase(sAA) activity and amylase,alpha 1(salivary) gene(AMY1) copy number or its gene expression between splenic asthenia and healthy children,and investigate the reasons of attenuated sAA activity ratio before and after citric acid stimulation in splenic asthenia children.METHODS:Saliva samples from 20 splenic asthenia children and 29 healthy children were collected before and after citric acid stimulation.AMY1 copy number,sAA activity,and total sAA and glycosylated sAA contents were determined,and their correlations were analyzed.RESULTS:Although splenic asthenia and healthy children had no differences in AMY1 copy number,splenic asthenia children had positive correlations between AMY1 copy number and sAA activity before or after citric acid stimulation.Splenic asthenia children had a higher sAA glycosylated proportion ratio and glycosylated sAA content ratio,while their total sAA content ratio and sAA activity ratio were lower compared with healthy children.The glycosylated sAA content ratio was higher than the total sAA content ratio in both groups.Splenic asthenia and healthy children had positive correlations between total sAA or glycosylated sAA content and sAA activity.However,the role played by glycosylated sAA content in sAA activity in healthy children increased after citric acid stimulation,while it decreased in splenic asthenia children.CONCLUSION:Genetic factors like AMY1 copy number variations,and more importantly,sAA glycosylation abnormalities leading to attenuated sAA activity after citric acid stimulation,which were the main reasons of the attenuated sAA activity ratio in splenic asthenia children compared with healthy children.
文摘For the last decade, low serum amylase(hypoamylasemia) has been reported in certain common cardiometabolic conditions such as obesity, diabetes(regardless of type), and metabolic syndrome, all of which appear to have a common etiology of insufficient insulin action due to insulin resistance and/or diminished insulin secretion. Some clinical studies have shown that salivary amylase may be preferentially decreased in obese individuals, whereas others have revealed that pancreatic amylase may be preferentially decreased in diabetic subjects with insulin dependence. Despite this accumulated evidence, the clinical relevance of serum, salivary, and pancreatic amylase and the underlying mechanisms have not been fully elucidated. In recent years, copy number variations(CNVs) in the salivary amylase gene(AMY1), which range more broadly than the pancreatic amylase gene(AMY2A and AMY2B), have been shown to be well correlated with salivary and serum amylase levels. In addition, low CNV of AMY1, indicating low salivary amylase, was associated with insulin resistance, obesity, low taste perception/satiety, and postprandial hyperglycemia through impaired insulin secretion at early cephalic phase. In most populations, insulin-dependent diabetes is less prevalent(minor contribution) compared with insulin-independent diabetes, and obesity is highly prevalent compared with low body weight. Therefore, obesity as a condition that elicits cardiometabolic diseases relating to insulin resistance(major contribution) may be a common determinant for low serum amylase in a general population. In this review, the novel interpretation of low serum, salivary, and pancreas amylase is discussed in terms of major contributions of obesity, diabetes, and metabolic syndrome.