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Dietary resistant starch dose-dependently reduces adiposity in obesity-prone and obesity-resistant male rats
Animal studies show that diets containing resistant starch (RS) at levels not achievable in the human diet result in lower body weight and/or adiposity in rodents. We aimed to determine whether RS dose-dependently reduces adiposity in obesity-prone (OP) and obesity-resistant (OR) rats. Male Sprague-...
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Published in: | Nutrition & metabolism 2012-10, Vol.9 (1), p.93-93 |
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description | Animal studies show that diets containing resistant starch (RS) at levels not achievable in the human diet result in lower body weight and/or adiposity in rodents. We aimed to determine whether RS dose-dependently reduces adiposity in obesity-prone (OP) and obesity-resistant (OR) rats.
Male Sprague-Dawley rats (n=120) were fed a moderate-fat, high-energy diet for 4 wk. Rats that gained the most weight (40%) were classified as obesity-prone (OP) and obesity-resistant (OR) rats were the 40% that gained the least weight. OP and OR rats were randomly allocated to one of six groups (n=8 for each phenotype). One group was killed for baseline measurements, the other five groups were allocated to AIN-93 based diets that contained 0, 4, 8, 12 and 16% RS (as high amylose maize starch) for 4 wk. These diets were matched for total carbohydrate content. At 0, 4 and 7 wk from the start of the study insulin sensitivity was calculated by homeostasis model assessment of insulin resistance (HOMA-IR) and adiposity was determined by dual-energy X-ray absorptiometry (DXA). At 8 wk, rats were euthanized and fat pad weights, intestinal digesta short chain fatty acid (SCFA) pools and plasma gut hormone levels were determined.
Obesity prone rats gained less weight with 4, 12 and 16% RS compared to 0% RS, but the effect in OR animals was significant only at 16% RS. Irrespective of phenotype, diets containing ≥8% RS reduced adiposity compared to 0% RS. Energy intake decreased by 9.8 kJ/d for every 4% increase in RS. All diets containing RS increased total SCFA pools in the caecum and lowered plasma GIP concentrations compared to the 0% RS, whereas plasma GLP-1 and PYY were increased when the diet contained at least 8% RS. Insulin sensitivity was not affected by RS.
RS in amounts that could be potentially consumed by humans were effective in reducing adiposity and weight gain in OP and OR rats, due in part to a reduction in energy intake, and changes in gut hormones and large bowel carbohydrate fermentation. |
doi_str_mv | 10.1186/1743-7075-9-93 |
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Male Sprague-Dawley rats (n=120) were fed a moderate-fat, high-energy diet for 4 wk. Rats that gained the most weight (40%) were classified as obesity-prone (OP) and obesity-resistant (OR) rats were the 40% that gained the least weight. OP and OR rats were randomly allocated to one of six groups (n=8 for each phenotype). One group was killed for baseline measurements, the other five groups were allocated to AIN-93 based diets that contained 0, 4, 8, 12 and 16% RS (as high amylose maize starch) for 4 wk. These diets were matched for total carbohydrate content. At 0, 4 and 7 wk from the start of the study insulin sensitivity was calculated by homeostasis model assessment of insulin resistance (HOMA-IR) and adiposity was determined by dual-energy X-ray absorptiometry (DXA). At 8 wk, rats were euthanized and fat pad weights, intestinal digesta short chain fatty acid (SCFA) pools and plasma gut hormone levels were determined.
Obesity prone rats gained less weight with 4, 12 and 16% RS compared to 0% RS, but the effect in OR animals was significant only at 16% RS. Irrespective of phenotype, diets containing ≥8% RS reduced adiposity compared to 0% RS. Energy intake decreased by 9.8 kJ/d for every 4% increase in RS. All diets containing RS increased total SCFA pools in the caecum and lowered plasma GIP concentrations compared to the 0% RS, whereas plasma GLP-1 and PYY were increased when the diet contained at least 8% RS. Insulin sensitivity was not affected by RS.
RS in amounts that could be potentially consumed by humans were effective in reducing adiposity and weight gain in OP and OR rats, due in part to a reduction in energy intake, and changes in gut hormones and large bowel carbohydrate fermentation.</description><identifier>ISSN: 1743-7075</identifier><identifier>EISSN: 1743-7075</identifier><identifier>DOI: 10.1186/1743-7075-9-93</identifier><identifier>PMID: 23098187</identifier><language>eng</language><publisher>England: BioMed Central Ltd</publisher><subject>Adiposity ; Body weight ; Diabetes ; Diet ; Fatty acids ; Incretin ; Insulin ; Insulin resistance ; Insulin sensitivity ; Obesity ; Physiological aspects ; Prevention ; Resistant starch ; Rodents ; Short chain fatty acid ; Starch ; Type 2 diabetes</subject><ispartof>Nutrition & metabolism, 2012-10, Vol.9 (1), p.93-93</ispartof><rights>COPYRIGHT 2012 BioMed Central Ltd.</rights><rights>2012 Belobrajdic et al.; licensee BioMed Central Ltd. This is an Open Access article distributed under the terms of the Creative Commons Attribution License ( http://creativecommons.org/licenses/by/2.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.</rights><rights>Copyright ©2012 Belobrajdic et al.; licensee BioMed Central Ltd. 2012 Belobrajdic et al.; licensee BioMed Central Ltd.</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-b643t-47fbdd9b1030c406f2c3a77452299a10c579c9140a54e58f132693519b7583743</citedby><cites>FETCH-LOGICAL-b643t-47fbdd9b1030c406f2c3a77452299a10c579c9140a54e58f132693519b7583743</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC3541085/pdf/$$EPDF$$P50$$Gpubmedcentral$$Hfree_for_read</linktopdf><linktohtml>$$Uhttps://www.proquest.com/docview/1267735448?pq-origsite=primo$$EHTML$$P50$$Gproquest$$Hfree_for_read</linktohtml><link.rule.ids>230,314,727,780,784,885,25753,27924,27925,37012,37013,44590,53791,53793</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/23098187$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Belobrajdic, Damien P</creatorcontrib><creatorcontrib>King, Roger A</creatorcontrib><creatorcontrib>Christophersen, Claus T</creatorcontrib><creatorcontrib>Bird, Anthony R</creatorcontrib><title>Dietary resistant starch dose-dependently reduces adiposity in obesity-prone and obesity-resistant male rats</title><title>Nutrition & metabolism</title><addtitle>Nutr Metab (Lond)</addtitle><description>Animal studies show that diets containing resistant starch (RS) at levels not achievable in the human diet result in lower body weight and/or adiposity in rodents. We aimed to determine whether RS dose-dependently reduces adiposity in obesity-prone (OP) and obesity-resistant (OR) rats.
Male Sprague-Dawley rats (n=120) were fed a moderate-fat, high-energy diet for 4 wk. Rats that gained the most weight (40%) were classified as obesity-prone (OP) and obesity-resistant (OR) rats were the 40% that gained the least weight. OP and OR rats were randomly allocated to one of six groups (n=8 for each phenotype). One group was killed for baseline measurements, the other five groups were allocated to AIN-93 based diets that contained 0, 4, 8, 12 and 16% RS (as high amylose maize starch) for 4 wk. These diets were matched for total carbohydrate content. At 0, 4 and 7 wk from the start of the study insulin sensitivity was calculated by homeostasis model assessment of insulin resistance (HOMA-IR) and adiposity was determined by dual-energy X-ray absorptiometry (DXA). At 8 wk, rats were euthanized and fat pad weights, intestinal digesta short chain fatty acid (SCFA) pools and plasma gut hormone levels were determined.
Obesity prone rats gained less weight with 4, 12 and 16% RS compared to 0% RS, but the effect in OR animals was significant only at 16% RS. Irrespective of phenotype, diets containing ≥8% RS reduced adiposity compared to 0% RS. Energy intake decreased by 9.8 kJ/d for every 4% increase in RS. All diets containing RS increased total SCFA pools in the caecum and lowered plasma GIP concentrations compared to the 0% RS, whereas plasma GLP-1 and PYY were increased when the diet contained at least 8% RS. Insulin sensitivity was not affected by RS.
RS in amounts that could be potentially consumed by humans were effective in reducing adiposity and weight gain in OP and OR rats, due in part to a reduction in energy intake, and changes in gut hormones and large bowel carbohydrate fermentation.</description><subject>Adiposity</subject><subject>Body weight</subject><subject>Diabetes</subject><subject>Diet</subject><subject>Fatty acids</subject><subject>Incretin</subject><subject>Insulin</subject><subject>Insulin resistance</subject><subject>Insulin sensitivity</subject><subject>Obesity</subject><subject>Physiological aspects</subject><subject>Prevention</subject><subject>Resistant starch</subject><subject>Rodents</subject><subject>Short chain fatty acid</subject><subject>Starch</subject><subject>Type 2 diabetes</subject><issn>1743-7075</issn><issn>1743-7075</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2012</creationdate><recordtype>article</recordtype><sourceid>PIMPY</sourceid><sourceid>DOA</sourceid><recordid>eNp1kl2P1CAUhhujcdfRWy9NE2_0oisUKHBjMlm_JtnExI9rQuF0lklbRqAb999LnXV2q2tIgBxeHjjnPUXxHKMzjEXzBnNKKo44q2QlyYPi9Bh4eGd_UjyJcYcQIVSix8VJTZAUWPDTon_nIOlwXQaILiY9pjLPwVyW1keoLOxhtDCmflbYyUAstXV7H126Lt1Y-hbmbbUPfoRSj_YYuQUOuocy6BSfFo863Ud4drOuiu8f3n87_1RdfP64OV9fVG1DSaoo71prZYsRQYaipqsN0ZxTVtdSaowM49JITJFmFJjoMKkbSRiWLWeC5JxXxebAtV7v1D64IWeovHbqd8CHrdIhOdODMm2rCbVNhxmiorbC1J2lDKiUttUMZ9bbA2s_tQNYk2sRdL-ALk9Gd6m2_koRRjESLAPWB0Dr_H8AyxPjBzU7p2bnlFSSZMarm08E_2OCmNTgooG-1yP4KSpcc0KEoGjO_eVf0p2fwpjLnVUN5_lbVNyqttkb5cbO56fNDFVrRihBCOduWRVn96jysDA4kw3vXI4vLrxeXMiaBD_TVk8xqs3XL_fCTfAxBuiOJcFIzb39bxFe3HXiKP_TzOQXjLvzMg</recordid><startdate>20121025</startdate><enddate>20121025</enddate><creator>Belobrajdic, Damien P</creator><creator>King, Roger A</creator><creator>Christophersen, Claus T</creator><creator>Bird, Anthony R</creator><general>BioMed Central Ltd</general><general>BioMed Central</general><general>BMC</general><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>ISR</scope><scope>3V.</scope><scope>7QP</scope><scope>7RV</scope><scope>7TS</scope><scope>7X7</scope><scope>7XB</scope><scope>88E</scope><scope>8FI</scope><scope>8FJ</scope><scope>8FK</scope><scope>8G5</scope><scope>ABUWG</scope><scope>AFKRA</scope><scope>AZQEC</scope><scope>BENPR</scope><scope>CCPQU</scope><scope>DWQXO</scope><scope>FYUFA</scope><scope>GHDGH</scope><scope>GNUQQ</scope><scope>GUQSH</scope><scope>K9.</scope><scope>KB0</scope><scope>M0S</scope><scope>M1P</scope><scope>M2O</scope><scope>MBDVC</scope><scope>NAPCQ</scope><scope>PIMPY</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>PRINS</scope><scope>Q9U</scope><scope>7X8</scope><scope>5PM</scope><scope>DOA</scope></search><sort><creationdate>20121025</creationdate><title>Dietary resistant starch dose-dependently reduces adiposity in obesity-prone and obesity-resistant male rats</title><author>Belobrajdic, Damien P ; King, Roger A ; Christophersen, Claus T ; Bird, Anthony R</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-b643t-47fbdd9b1030c406f2c3a77452299a10c579c9140a54e58f132693519b7583743</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2012</creationdate><topic>Adiposity</topic><topic>Body weight</topic><topic>Diabetes</topic><topic>Diet</topic><topic>Fatty acids</topic><topic>Incretin</topic><topic>Insulin</topic><topic>Insulin resistance</topic><topic>Insulin sensitivity</topic><topic>Obesity</topic><topic>Physiological aspects</topic><topic>Prevention</topic><topic>Resistant starch</topic><topic>Rodents</topic><topic>Short chain fatty acid</topic><topic>Starch</topic><topic>Type 2 diabetes</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Belobrajdic, Damien P</creatorcontrib><creatorcontrib>King, Roger A</creatorcontrib><creatorcontrib>Christophersen, Claus T</creatorcontrib><creatorcontrib>Bird, Anthony R</creatorcontrib><collection>PubMed</collection><collection>CrossRef</collection><collection>Gale In Context: Science</collection><collection>ProQuest Central (Corporate)</collection><collection>Calcium & Calcified Tissue Abstracts</collection><collection>Nursing & Allied Health Database (ProQuest)</collection><collection>Physical Education Index</collection><collection>ProQuest Health & Medical Collection</collection><collection>ProQuest Central (purchase pre-March 2016)</collection><collection>Medical Database (Alumni Edition)</collection><collection>Hospital Premium Collection</collection><collection>Hospital Premium Collection (Alumni Edition)</collection><collection>ProQuest Central (Alumni) (purchase pre-March 2016)</collection><collection>Research Library (Alumni Edition)</collection><collection>ProQuest Central (Alumni)</collection><collection>ProQuest Central</collection><collection>ProQuest Central Essentials</collection><collection>ProQuest Central</collection><collection>ProQuest One Community College</collection><collection>ProQuest Central Korea</collection><collection>Health Research Premium Collection</collection><collection>Health Research Premium Collection (Alumni)</collection><collection>ProQuest Central Student</collection><collection>Research Library Prep</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><collection>Nursing & Allied Health Database (Alumni Edition)</collection><collection>Health & Medical Collection (Alumni Edition)</collection><collection>Medical Database</collection><collection>Research Library</collection><collection>Research Library (Corporate)</collection><collection>Nursing & Allied Health Premium</collection><collection>Publicly Available Content Database</collection><collection>ProQuest One Academic Eastern Edition (DO NOT USE)</collection><collection>ProQuest One Academic</collection><collection>ProQuest One Academic UKI Edition</collection><collection>ProQuest Central China</collection><collection>ProQuest Central Basic</collection><collection>MEDLINE - Academic</collection><collection>PubMed Central (Full Participant titles)</collection><collection>Directory of Open Access Journals (Open Access)</collection><jtitle>Nutrition & metabolism</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Belobrajdic, Damien P</au><au>King, Roger A</au><au>Christophersen, Claus T</au><au>Bird, Anthony R</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Dietary resistant starch dose-dependently reduces adiposity in obesity-prone and obesity-resistant male rats</atitle><jtitle>Nutrition & metabolism</jtitle><addtitle>Nutr Metab (Lond)</addtitle><date>2012-10-25</date><risdate>2012</risdate><volume>9</volume><issue>1</issue><spage>93</spage><epage>93</epage><pages>93-93</pages><issn>1743-7075</issn><eissn>1743-7075</eissn><abstract>Animal studies show that diets containing resistant starch (RS) at levels not achievable in the human diet result in lower body weight and/or adiposity in rodents. We aimed to determine whether RS dose-dependently reduces adiposity in obesity-prone (OP) and obesity-resistant (OR) rats.
Male Sprague-Dawley rats (n=120) were fed a moderate-fat, high-energy diet for 4 wk. Rats that gained the most weight (40%) were classified as obesity-prone (OP) and obesity-resistant (OR) rats were the 40% that gained the least weight. OP and OR rats were randomly allocated to one of six groups (n=8 for each phenotype). One group was killed for baseline measurements, the other five groups were allocated to AIN-93 based diets that contained 0, 4, 8, 12 and 16% RS (as high amylose maize starch) for 4 wk. These diets were matched for total carbohydrate content. At 0, 4 and 7 wk from the start of the study insulin sensitivity was calculated by homeostasis model assessment of insulin resistance (HOMA-IR) and adiposity was determined by dual-energy X-ray absorptiometry (DXA). At 8 wk, rats were euthanized and fat pad weights, intestinal digesta short chain fatty acid (SCFA) pools and plasma gut hormone levels were determined.
Obesity prone rats gained less weight with 4, 12 and 16% RS compared to 0% RS, but the effect in OR animals was significant only at 16% RS. Irrespective of phenotype, diets containing ≥8% RS reduced adiposity compared to 0% RS. Energy intake decreased by 9.8 kJ/d for every 4% increase in RS. All diets containing RS increased total SCFA pools in the caecum and lowered plasma GIP concentrations compared to the 0% RS, whereas plasma GLP-1 and PYY were increased when the diet contained at least 8% RS. Insulin sensitivity was not affected by RS.
RS in amounts that could be potentially consumed by humans were effective in reducing adiposity and weight gain in OP and OR rats, due in part to a reduction in energy intake, and changes in gut hormones and large bowel carbohydrate fermentation.</abstract><cop>England</cop><pub>BioMed Central Ltd</pub><pmid>23098187</pmid><doi>10.1186/1743-7075-9-93</doi><tpages>1</tpages><oa>free_for_read</oa></addata></record> |
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subjects | Adiposity Body weight Diabetes Diet Fatty acids Incretin Insulin Insulin resistance Insulin sensitivity Obesity Physiological aspects Prevention Resistant starch Rodents Short chain fatty acid Starch Type 2 diabetes |
title | Dietary resistant starch dose-dependently reduces adiposity in obesity-prone and obesity-resistant male rats |
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