***TASK*** the task is to summarize an input biomedical literature in six sentences 
    ***INPUT*** the input is a biomedical literature 
    ***OUTPUT*** the output is the summary of an input biomedical literature in six sentences 
    ***DOCUMENTATION*** 
    ***EXAMPLES*** 
    Input: The sweet taste of nonnutritive sweeteners has been reported to increase hunger and food intake through the mechanism of cephalic-phase insulin release ( CPIR ) . We investigated the effect of oral sensation of sweetness on CPIR and other indexes associated with glucose metabolism using nutritive and nonnutritive sweetened tablets as stimuli . At lunchtime , 12 normal-weight men sucked for 5 min a sucrose , an aspartame-polydextrose , or an unsweetened polydextrose tablet ( 3 g ) with no added flavor . The three stimuli were administered in a counterbalanced order , each on a separate day at 1-wk intervals . Blood was drawn continuously for 45 min before and 25 min after the beginning of sucking and sample s were collected at 1-min intervals . Spontaneous oscillations in glucose , insulin , and glucagon concentrations were assessed as were increments ( slopes ) of fatty acid concentrations during the baseline period . The nature of the baseline ( oscillations : glucose , insulin , and glucagon ; and slopes : fatty acids ) was taken into account in the analyses of postexposure events . No CPIR and no significant effect on plasma glucagon or fatty acid concentrations were observed after the three stimuli . However , there was a significant decrease in plasma glucose and insulin after all three stimuli . Only the consumption of the sucrose tablet was followed by a postabsorptive increase in plasma glucose and insulin concentrations starting 17 and 19 min , respectively , after the beginning of sucking . In conclusion , this study suggested that oral stimulation provided by sweet nonflavored tablets is not sufficient for inducing CPIR In humans little is known as to whether taste solutions applied to the tongue elicit cephalic phase insulin release ( CPIR ) . The aim of this study was to re-examine if any effect of different taste solutions on CPIR occurs . Under fasting conditions healthy human subjects sipped , and washed out their mouths with eight taste solutions ( sucrose , saccharin , acetic acid , sodium chloride , quinine hydrochloride , distilled water , starch , and sodium glutamate ) for 45 s and spat them out again . The taste stimuli were not swallowed ; they were applied in a r and omized order , each on a separate day . Blood collection for determination of plasma glucose and plasma insulin concentrations was performed 3 min before and 3 , 5 , 7 and 10 min after taste stimulation . Ratings of quality , intensity and hedonic characteristics were also obtained . A significant increase of plasma insulin concentration was apparent after stimulation with sucrose and saccharin . In conclusion , the current data suggest that the sweeteners sucrose and saccharin activate a CPIR even when applied to the oral cavity only To determine whether sweet-tasting solutions are effective elicitors of cephalic phase insulin release ( CPIR ) in humans , two studies were conducted using nutritive and nonnutritive sweeteners as stimuli . Normal weight men sipped and spit four different solutions : water , aspartame , saccharin , and sucrose . A fifth condition involved a modified sham-feed with apple pie . The five stimuli were administered in counterbalanced order , each on a separate day . In study 1 , subjects tasted the stimuli for 1 min ( n = 15 ) and in study 2 ( n = 16 ) , they tasted the stimuli for 3 min . Arterialized venous blood was drawn to establish a baseline and then at 1 min poststimulus , followed by every 2 min for 15 min and then every 5 min for 15 min . In both study 1 and study 2 , no significant increases in plasma insulin were observed after subjects tasted the sweetened solutions . In contrast , significant increases in plasma insulin occurred after the modified sham-feed with both the 1 min and 3 min exposure . These results suggest that nutritive and nonnutritive sweeteners in solution are not adequate stimuli for the elicitation of CPIR 
    Output:
    
However , the available evidence indicates that the LCS-treated yogurts did not actually taste sweet to rats in the published studies .
This indicates that caloric intake alone can not explain the elevated weight gain .
Third , there is evidence that LCSs and yogurt can each alter the gut microbiota of rodents .
Given recent work indicating that changes in gut microbiota can modulate body weight , it is possible that the combination of LCS and yogurt alters the gut microbiota in ways that promote weight gain .
While this hypothesis remains speculative , it is consistent with the observed rodent data .