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170shown to be significantly higher when high-starch foods such as corn, rice, and potatoes (but not apples)are first chewed and then swallowed, rather than swallowed directly. In addition, it has been suggestedthat oral digestion of starch is critically important for energy absorption during episodes of diarrhea.Diarrheal diseases can have a significant effect on fitness; for example, such diseases caused 15% ofworldwide deaths among children younger than 5 years as recently as 2001.”Wenn wir mit Perry et al. eine so weitreichende Bedeutung von higher salivaryamylase protein levels annehmen, dann stehen hinter einem Verlust dieser levels inhigh-starch populations zahlreiche menschliche Dramen – die salivary amylaseprotein levels hätten dann über Tod und Leben vieler Menschen entschieden. EinUrteil zu dieser Frage möchte ich mir an dieser Stelle nicht erlauben. Die Autorenfahren fort:"Lastly, salivary amylase persists in the stomach and intestines after swallowing, thereby augmenting theenzymatic activity of pancreatic amylase in the small intestine. Higher AMY1 copy number and aconcomitant increase in salivary amylase protein level are therefore likely to improve the efficiency withwhich high-starch foods are digested in the mouth, stomach, and intestines, and may also buffer againstthe potential fitness-reducing effects of intestinal disease.”Solche positiven Funktionen sind nicht unwahrscheinlich. Da aber die low-starchpopulations mit ihrem Verlust an AMY1-Kopien auch davon betroffen sind("augmenting the enzymatic activity of pancreatic amylase in the small intestine"geht mit dem Verlust der hohem Kopienzahl ja verloren), fragt man sich vielleicht,warum die höhere AMY1-Kopienzahl überhaupt in irgendeiner Population verlorengehen konnte.Perry et al. (2007) berichten sodann zu ihren Studien an Schimpansen undBonobos das Folgende:"To understand better the evolutionary context of human AMY1 copy number variation, we analyzedpatterns of AMY1 copy number variation in chimpanzees (Pan troglodytes) and bonobos (Pan paniscus). Incontrast to the extensive copy number variation we observed in humans, each of 15 wild-born westernchimpanzees (P. t. verus) showed evidence of only 2 diploid AMY1 copies (Fig. 3c and SupplementaryFig. 4 online), which is consistent with previous findings. Although we observed evidence of a gain inAMY1 copy number in bonobos relative to chimpanzees (Supplementary Fig. 4 online), our sequencebasedanalyses suggest that each of these AMY1 copies has a disrupted coding sequence and may benonfunctional (Supplementary Fig. 5 online). Therefore, the average human has ca. 3 times more AMY1copies than chimpanzees, and bonobos may not have salivary amylase at all. "Die Aussage ("may not have salivary amylase at all") zu den Bonobos istinzwischen widerlegt. Behringer et al. stellen 2012, p. 476, unter anderem fest:"Here, we present the first data on intra- and inter-individual variation of sAA [salivary alpha-Amylase]activity in captive bonobos and compare the results with information from other ape species and humans.Our results indicate that sAA activity in the bonobo samples was significantly lower than in thehuman samples but within the range of other great ape species. In addition, sAA activity wassignificantly higher in samples collected at times when subjects had been exposed to stressors (judged bychanges in behavioral patterns and cortisol levels) than in samples collected at other times. Our resultsindicate that bonobos possess functioning sAA and, as in other species, sAA activity is influenced byautonomic nervous system activity." 300300 Behringer V, Deschner T, Möstl E, Selzer D, Hohmann G. (2012): Stress affects salivary alpha-Amylase activity in bonobos. Physiol Behav105: 476-482. http://www.ncbi.nlm.nih.gov/pubmed/21945369 und das geamte Paper:http://www.eva.mpg.de/primat/staff/verena_behringer/pdf/behringer_et_al.2012.pdf (p. 481: "Compared to chimpanzees, bonobos have a largernumber of AMY1 copies and appear to be polymorphic, at least in Exon 3 [3]. If, as has been suggested, amylase activity increases with copynumber [2], bonobo saliva should have higher sAA activity. However, molecular modifications in coding regions of the AMY1 gene (a frameshift on AMY1 Exon 7 and a stop codon on AMY1 Exon 3) suggest that bonobos may be unable to produce functioning sAA [3]. Our resultsshow that sAA activity in bonobos is comparable to other great ape species and humans and, thus, it might be possible that other genes became