Salivary amylase is a gene present in humans. It is not yet known why a salivary amylase deficiency increases froguel amylase salivaire. Comme la concentration en amylase salivaire n’est pas significativement différente parmi les 4 groupes, les auteurs concluent que la présence d’hydrates de. The parotid iso-α-amylases were isoelectric at pH , , and and mixed A. Carlier, M. BonteIsoelement des isoenzymes de l’amylase salivaire par.

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Salivary cortisol was measured as a reference of stress amyalse. They identified a region in chromosome 1 that is unique because it contains a gene, salivary amylase AMY1present in a single form in humans.

Thus, individuals with low salivary amylase have abnormally high glycemia when they eat starch. Saliva samples were obtained before stress induction and 15, 30, and 60 min afterwards.

Only the salivary form seems to be associated with obesity. Nature Genetics, March 30, For 10, years, since agriculture began, the number of AMY1 copies has increased, evidence of natural selection and human evolution: Paris, 27 March Saliva: One billion people worldwide are overweight.

For that purpose, after the design of the assay, an analytical and a clinical validation were carried out. Instead of having only two copies of this gene one from the father, one from the mother the number of AMY1 copies varies in humans from one to Eichler, Francois Pattou, Timothy D.


The objective of this study was to develop a time-resolved immunofluorometric assay TR-IFMA for quantification of salivary alpha-amylase in sheep. The assay also demonstrated a high level of accuracy, as determined by linearity under dilution.

Validation of an assay for quantification of alpha-amylase in saliva of sheep.

The researchers showed that people with the smallest number of salivary amylase copies and therefore salivairee amylase levels in the blood are ten times more at risk of becoming obese. They open important perspectives for more effective obesity prevention and treatment that salivaaire into account food digestion and degradation in the intestines.

The analytical validation of the assay showed intra- and inter-assay coefficients of variation CVs of 6. For clinical validation, a model of acute stress testing was conducted to determine whether expected significant changes in alpha-amylase were picked up in the newly developed assay.

These entirely novel findings point to a genetic predisposition to obesity via complex carbohydrate digestion and its effects on the intestinal bacterial flora.

Yet its number of copies can vary from one to 20, depending on the individual. Skip to content skip to menu.

French and British researchers went further by studying obesity-discordant Swedish siblings, analyzing their genome and the genes in adipose tissue, which are expressed differently in obese subjects and in those with normal weight.

The second is that poor starch digestion could change the intestinal flora, thereby contributing indirectly to obesity or even diabetes. The first is that chewing and partially digesting food in the mouth could have a hormonal effect inducing satiety, which would be reduced in the case of AMY1 deficiency.



Researchers have noticed that people with the smallest number of AMY1 copies and therefore little amylase enzyme in their blood are ten times more at risk of becoming obese. Low copy number of the salivary amylase gene predisposes to obesity. It is not yet known why a salivary amylase deficiency increases obesity: The assay developed in this study could be used to measure salivary alpha-amylase in the saliva of sheep and this enzyme could be a possible noninvasive biomarker of stress in sheep.

In that model, 11 sheep were immobilized and confronted with a sheepdog to induce stress. There are two forms of amylase: That is what initial metabolomic studies conducted in patients with high or low salivary amylase suggest 3. salivaife

Saliva : a new trail in obesity genetics – CNRS Web site – CNRS

Carlsson, Andrew Walley, Evan Amylqse. Traduit par Docteur Serge Messier. This work, published on March 30, in Nature Genetics, reveals for the first time a genetic link between complex carbohydrate digestion and obesity.