Effects of resistant starch on behaviour, satiety-related hormones and metabolites in growing pigs. - PubMed - NCBI
Effects of resistant starch on behaviour, satiety-related hormones and metabolites in growing pigs.
Souza da Silva C1, Haenen D2, Koopmans SJ1, Hooiveld GJ2, Bosch G3, Bolhuis JE1, Kemp B1, Müller M2, Gerrits WJ3.
Abstract
Resistant starch (RS) has been suggested to prolong satiety in adult pigs. The present study investigated RS-induced changes in behaviour, satiety-related hormones and metabolites in catheterized growing pigs to explore possible underlying mechanisms for RS-induced satiety. In a cross-over design with two 14-day periods, 10 pigs (initial BW: 58 kg) were assigned to two treatments comprising diets containing either 35% pregelatinized starch (PS) or 34% retrograded starch (RS). Diets were isoenergetic on gross energy. Pigs were fed at 2.8× maintenance. Postprandial plasma response of satiety-related hormones and metabolites was measured at the end of each period using frequent blood sampling. Faecal and urinary energy losses were measured at the end of each period. Behaviour was scored 24 h from video recordings using scan sampling. Energy digestibility and metabolizability were ~6% lower in RS compared with PS diet (P<0.001), and metabolizable energy (ME) intake was ~3% lower in RS-fed than in PS-fed pigs (P<0.001). RS-fed pigs showed less feeder-directed (P=0.001) and drinking (P=0.10) behaviours than PS-fed pigs throughout the day. Postprandial peripheral short-chain fatty acid (SCFA) levels were higher in RS-fed than in PS-fed pigs (P<0.001). Postprandial glucose and insulin responses were lower in RS-fed than in PS-fed pigs (P<0.001). Triglyceride levels were higher in RS-fed than in PS-fed pigs (P<0.01), and non-esterified fatty acid levels did not differ between diets (P=0.90). Glucagon-like peptide-1 (GLP-1) levels were lower in RS-fed than in PS-fed pigs (P<0.001), and peptide tyrosine tyrosine (PYY) levels did not differ between diets (P=0.90). Blood serotonin levels were lower (P<0.001), whereas monoamine oxidase activity (P<0.05) and tryptophan (P<0.01) levels were higher in RS-fed than in PS-fed pigs. Despite a lower ME intake, RS seemed to prolong satiety, based on behavioural observations. Possible underlying mechanisms for RS-induced satiety include increased 24 h plasma SCFA levels, and decreased postprandial glucose and insulin responses. GLP-1 and PYY seemed not to play a role in RS-induced satiety. Low blood serotonin levels in RS-fed pigs suggested a difference in intestinal serotonin release between treatments. Increased postprandial plasma triglyceride levels corresponded with increased SCFA levels, but it is unclear whether triglycerides may have signalled satiety in RS-fed pigs.
Since my slow and extremely skeptical introduction to RP and RPF, I've been slowly convinced on the merits of many of it's, relative to mainstream, oddities. Fructose... who knew? However, I'm not convinced wrt RPF's take on RP's very general prebiotic advice, and this study in my opinion supports that notion. RS lead to decreased blood serotonin, while increasing tryptophan and MAO, suggesting definite pro-anabolic, anti-inflammatory, and pro-metabolic effects. What's you guy's take on this?
Personally I think the extremely diverse range of reactions to RS on RPF shows that individual gut flora variation probably plays a big role in this. I'm currently working on severe IBS, nocturnal MGD most likely as an autoimmune dysfunction, likely fungal overgrowth, that kinda thing. I not only tolerate peeled, cooked and cooled potatoes (RS2 from green bananas and potato starch bloats me like crazy), I thrive on them. They make me feel calmer, transform any fatigue into sleepiness for me (increased melatonin, less serotonin), improved cognitive function, social drive, and poop. Definitely not pro-serotonin.
Animal Pharm: Cooked/Crystallized RS3 Trumps Raw RS2: They are Vastly Different for Our Guts
Since RS2 makes me feel awful, and RS3 amazing, I hypothesize that I have an overgrowth of sorts in my proximal colon, and the faster fermentation time is actually deleterious in this case. A case where overly reductionist thinking could do real harm.
Although I can't find the study ATM, I recall reading that recently, researchers pinpointed the exact mechanism by which SCFA production improved glucose homeostasis. They found that the intestinal cells actually were creating glucose with the SCFAs, shutting down gluconeogenesis in the liver, as it was now already being done. Metformin in a pill, without all the other unwanted effects (unless you get bloated of course). I dunno, the glucose stabilization thing sounds very peaty to me. Nothin' says safety like stable blood glucose.
Curious on anyone's opinion on this paper or your experience with RS.
Effects of resistant starch on behaviour, satiety-related hormones and metabolites in growing pigs.
Souza da Silva C1, Haenen D2, Koopmans SJ1, Hooiveld GJ2, Bosch G3, Bolhuis JE1, Kemp B1, Müller M2, Gerrits WJ3.
Abstract
Resistant starch (RS) has been suggested to prolong satiety in adult pigs. The present study investigated RS-induced changes in behaviour, satiety-related hormones and metabolites in catheterized growing pigs to explore possible underlying mechanisms for RS-induced satiety. In a cross-over design with two 14-day periods, 10 pigs (initial BW: 58 kg) were assigned to two treatments comprising diets containing either 35% pregelatinized starch (PS) or 34% retrograded starch (RS). Diets were isoenergetic on gross energy. Pigs were fed at 2.8× maintenance. Postprandial plasma response of satiety-related hormones and metabolites was measured at the end of each period using frequent blood sampling. Faecal and urinary energy losses were measured at the end of each period. Behaviour was scored 24 h from video recordings using scan sampling. Energy digestibility and metabolizability were ~6% lower in RS compared with PS diet (P<0.001), and metabolizable energy (ME) intake was ~3% lower in RS-fed than in PS-fed pigs (P<0.001). RS-fed pigs showed less feeder-directed (P=0.001) and drinking (P=0.10) behaviours than PS-fed pigs throughout the day. Postprandial peripheral short-chain fatty acid (SCFA) levels were higher in RS-fed than in PS-fed pigs (P<0.001). Postprandial glucose and insulin responses were lower in RS-fed than in PS-fed pigs (P<0.001). Triglyceride levels were higher in RS-fed than in PS-fed pigs (P<0.01), and non-esterified fatty acid levels did not differ between diets (P=0.90). Glucagon-like peptide-1 (GLP-1) levels were lower in RS-fed than in PS-fed pigs (P<0.001), and peptide tyrosine tyrosine (PYY) levels did not differ between diets (P=0.90). Blood serotonin levels were lower (P<0.001), whereas monoamine oxidase activity (P<0.05) and tryptophan (P<0.01) levels were higher in RS-fed than in PS-fed pigs. Despite a lower ME intake, RS seemed to prolong satiety, based on behavioural observations. Possible underlying mechanisms for RS-induced satiety include increased 24 h plasma SCFA levels, and decreased postprandial glucose and insulin responses. GLP-1 and PYY seemed not to play a role in RS-induced satiety. Low blood serotonin levels in RS-fed pigs suggested a difference in intestinal serotonin release between treatments. Increased postprandial plasma triglyceride levels corresponded with increased SCFA levels, but it is unclear whether triglycerides may have signalled satiety in RS-fed pigs.
Since my slow and extremely skeptical introduction to RP and RPF, I've been slowly convinced on the merits of many of it's, relative to mainstream, oddities. Fructose... who knew? However, I'm not convinced wrt RPF's take on RP's very general prebiotic advice, and this study in my opinion supports that notion. RS lead to decreased blood serotonin, while increasing tryptophan and MAO, suggesting definite pro-anabolic, anti-inflammatory, and pro-metabolic effects. What's you guy's take on this?
Personally I think the extremely diverse range of reactions to RS on RPF shows that individual gut flora variation probably plays a big role in this. I'm currently working on severe IBS, nocturnal MGD most likely as an autoimmune dysfunction, likely fungal overgrowth, that kinda thing. I not only tolerate peeled, cooked and cooled potatoes (RS2 from green bananas and potato starch bloats me like crazy), I thrive on them. They make me feel calmer, transform any fatigue into sleepiness for me (increased melatonin, less serotonin), improved cognitive function, social drive, and poop. Definitely not pro-serotonin.
Animal Pharm: Cooked/Crystallized RS3 Trumps Raw RS2: They are Vastly Different for Our Guts
Since RS2 makes me feel awful, and RS3 amazing, I hypothesize that I have an overgrowth of sorts in my proximal colon, and the faster fermentation time is actually deleterious in this case. A case where overly reductionist thinking could do real harm.
Although I can't find the study ATM, I recall reading that recently, researchers pinpointed the exact mechanism by which SCFA production improved glucose homeostasis. They found that the intestinal cells actually were creating glucose with the SCFAs, shutting down gluconeogenesis in the liver, as it was now already being done. Metformin in a pill, without all the other unwanted effects (unless you get bloated of course). I dunno, the glucose stabilization thing sounds very peaty to me. Nothin' says safety like stable blood glucose.
Curious on anyone's opinion on this paper or your experience with RS.
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