[ { "key": "BXNNKQ3T", "version": 39, "library": { "type": "group", "id": 139325, "name": "Carbohydrate Metabolism", "links": { "alternate": { "href": "https://www.zotero.org/groups/carbohydrate_metabolism", "type": "text/html" } } }, "links": { "self": { "href": "https://api.zotero.org/groups/139325/items/BXNNKQ3T", "type": "application/json" }, "alternate": { "href": "https://www.zotero.org/groups/carbohydrate_metabolism/items/BXNNKQ3T", "type": "text/html" }, "up": { "href": "https://api.zotero.org/groups/139325/items/JJ478N5D", "type": "application/json" } }, "meta": { "createdByUser": { "id": 181756, "username": "rwesley007", "name": "", "links": { "alternate": { "href": "https://www.zotero.org/rwesley007", "type": "text/html" } } }, "numChildren": 0 }, "data": { "key": "BXNNKQ3T", "version": 39, "parentItem": "JJ478N5D", "itemType": "attachment", "linkMode": "imported_file", "title": "Pawlak et al_2004_Effects of dietary glycaemic index on adiposity, glucose homoeostasis, and.pdf", "accessDate": "", "url": "", "note": "", "contentType": "application/pdf", "charset": "", "filename": "Pawlak et al_2004_Effects of dietary glycaemic index on adiposity, glucose homoeostasis, and.pdf", "md5": "23f2fbeec6f887f6c2928bdbab18b741", "mtime": 1400356652101, "tags": [], "relations": {}, "dateAdded": "2014-05-17T19:54:14Z", "dateModified": "2014-05-17T19:54:34Z" } }, { "key": "JJ478N5D", "version": 40, "library": { "type": "group", "id": 139325, "name": "Carbohydrate Metabolism", "links": { "alternate": { "href": "https://www.zotero.org/groups/carbohydrate_metabolism", "type": "text/html" } } }, "links": { "self": { "href": "https://api.zotero.org/groups/139325/items/JJ478N5D", "type": "application/json" }, "alternate": { "href": "https://www.zotero.org/groups/carbohydrate_metabolism/items/JJ478N5D", "type": "text/html" } }, "meta": { "createdByUser": { "id": 181756, "username": "rwesley007", "name": "", "links": { "alternate": { "href": "https://www.zotero.org/rwesley007", "type": "text/html" } } }, "creatorSummary": "Pawlak et al.", "parsedDate": "2004-09-28", "numChildren": 2 }, "data": { "key": "JJ478N5D", "version": 40, "itemType": "journalArticle", "title": "Effects of dietary glycaemic index on adiposity, glucose homoeostasis, and plasma lipids in animals", "creators": [ { "creatorType": "author", "firstName": "Dorota B", "lastName": "Pawlak" }, { "creatorType": "author", "firstName": "Jake A", "lastName": "Kushner" }, { "creatorType": "author", "firstName": "David S", "lastName": "Ludwig" } ], "abstractNote": "BACKGROUND: Clinical studies suggest a role for dietary glycaemic index (GI) in bodyweight regulation and diabetes risk. However, partly because manipulation of GI can produce changes in potentially confounding dietary factors such as fibre content, palatability, and energy density, its relevance to human health remains controversial. This study examined the independent effects of GI in animals.\nMETHODS: Partially pancreatectomised male Sprague-Dawley rats were given diets with identical nutrients, except for the type of starch: high-GI (n=11) or low-GI (n=10). The animals were fed in a controlled way to maintain the same mean bodyweight in the two groups for 18 weeks. Further experiments examined the effects of GI in rats in a cross-over design and C57BL/6J mice in a parallel design.\nFINDINGS: Despite having similar mean bodyweight (547.9 [SE 13.4] vs 549.2 [15.2] g), rats given high-GI food had more body fat (97.8 [13.6] vs 57.3 [7.2] g; p=0.0152) and less lean body mass (450.1 [9.6] vs 491.9 [11.7] g; p=0.0120) than those given low-GI food. The high-GI group also had greater increases over time in the areas under the curve for blood glucose and plasma insulin after oral glucose, lower plasma adiponectin concentrations, higher plasma triglyceride concentrations, and severe disruption of islet-cell architecture. Mice on the high-GI diet had almost twice the body fat of those on the low-GI diet after 9 weeks.\nINTERPRETATION: These findings provide a mechanistic basis for interpretation of studies of GI in human beings.\nRELEVANCE TO PRACTICE: The term GI describes how a food, meal, or diet affects blood sugar during the postprandial period. GI as an independent factor can cause obesity and increase risks of diabetes and heart disease in animals. Use of low-GI diets in prevention and treatment of human disease merits thorough examination.", "publicationTitle": "Lancet", "publisher": "", "place": "", "date": "2004 Aug 28-Sep 3", "volume": "364", "issue": "9436", "section": "", "partNumber": "", "partTitle": "", "pages": "778-785", "series": "", "seriesTitle": "", "seriesText": "", "journalAbbreviation": "Lancet", "DOI": "10.1016/S0140-6736(04)16937-7", "citationKey": "", "url": "", "accessDate": "", "PMID": "", "PMCID": "", "ISSN": "1474-547X", "archive": "", "archiveLocation": "", "shortTitle": "", "language": "eng", "libraryCatalog": "NCBI PubMed", "callNumber": "", "rights": "", "extra": "PMID: 15337404", "tags": [ { "tag": "Adiponectin", "type": 1 }, { "tag": "Adipose Tissue", "type": 1 }, { "tag": "Animals", "type": 1 }, { "tag": "Blood Glucose", "type": 1 }, { "tag": "Body Composition", "type": 1 }, { "tag": "Body Weight", "type": 1 }, { "tag": "Dietary Carbohydrates", "type": 1 }, { "tag": "Glucose Tolerance Test", "type": 1 }, { "tag": "Glycemic Index", "type": 1 }, { "tag": "Homeostasis", "type": 1 }, { "tag": "Insulin", "type": 1 }, { "tag": "Intercellular Signaling Peptides and Proteins", "type": 1 }, { "tag": "Islets of Langerhans", "type": 1 }, { "tag": "Leptin", "type": 1 }, { "tag": "Mice", "type": 1 }, { "tag": "Mice, Inbred C57BL", "type": 1 }, { "tag": "Obesity", "type": 1 }, { "tag": "Proteins", "type": 1 }, { "tag": "Rats", "type": 1 }, { "tag": "Rats, Sprague-Dawley", "type": 1 }, { "tag": "Triglycerides", "type": 1 }, { "tag": "carbohydrates" }, { "tag": "diet" } ], "collections": [], "relations": {}, "dateAdded": "2014-05-17T19:49:07Z", "dateModified": "2014-05-17T19:49:07Z" } }, { "key": "9WTXJR7T", "version": 35, "library": { "type": "group", "id": 139325, "name": "Carbohydrate Metabolism", "links": { "alternate": { "href": "https://www.zotero.org/groups/carbohydrate_metabolism", "type": "text/html" } } }, "links": { "self": { "href": 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Metabolism", "links": { "alternate": { "href": "https://www.zotero.org/groups/carbohydrate_metabolism", "type": "text/html" } } }, "links": { "self": { "href": "https://api.zotero.org/groups/139325/items/M8ITP6WE", "type": "application/json" }, "alternate": { "href": "https://www.zotero.org/groups/carbohydrate_metabolism/items/M8ITP6WE", "type": "text/html" }, "up": { "href": "https://api.zotero.org/groups/139325/items/2NWKVGNR", "type": "application/json" } }, "meta": { "createdByUser": { "id": 181756, "username": "rwesley007", "name": "", "links": { "alternate": { "href": "https://www.zotero.org/rwesley007", "type": "text/html" } } }, "numChildren": 0 }, "data": { "key": "M8ITP6WE", "version": 33, "parentItem": "2NWKVGNR", "itemType": "attachment", "linkMode": "imported_url", "title": "Ebbeling CB et al_2012_EFfects of dietary composition on energy expenditure during weight-loss.pdf", "accessDate": "2014-05-17T19:44:41Z", "url": "http://jama.jamanetwork.com/data/Journals/JAMA/24277/jpc120005_2627_2634.pdf", "note": "", "contentType": "application/pdf", "charset": "", "filename": "Ebbeling CB et al_2012_EFfects of dietary composition on energy expenditure during weight-loss.pdf", "md5": "71d5cab2083fc161850a80d7426fa71e", "mtime": 1400355886704, "tags": [], "relations": {}, "dateAdded": "2014-05-17T19:44:41Z", "dateModified": "2014-05-17T19:44:48Z" } }, { "key": "2NWKVGNR", "version": 34, "library": { "type": "group", "id": 139325, "name": "Carbohydrate Metabolism", "links": { "alternate": { "href": "https://www.zotero.org/groups/carbohydrate_metabolism", "type": "text/html" } } }, "links": { "self": { "href": "https://api.zotero.org/groups/139325/items/2NWKVGNR", "type": "application/json" }, "alternate": { "href": "https://www.zotero.org/groups/carbohydrate_metabolism/items/2NWKVGNR", "type": "text/html" } }, "meta": { "createdByUser": { "id": 181756, "username": "rwesley007", "name": "", "links": { "alternate": { "href": "https://www.zotero.org/rwesley007", "type": "text/html" } } }, "creatorSummary": "Ebbeling CB et al.", "parsedDate": "2012-06-27", "numChildren": 1 }, "data": { "key": "2NWKVGNR", "version": 34, "itemType": "journalArticle", "title": "EFfects of dietary composition on energy expenditure during weight-loss maintenance", "creators": [ { "creatorType": "author", "name": "Ebbeling CB" }, { "creatorType": "author", "name": "Swain JF" }, { "creatorType": "author", "name": "Feldman HA" }, { "creatorType": "author", "name": "et al" } ], "abstractNote": "Context Reduced energy expenditure following weight loss is thought to contribute to weight gain. However, the effect of dietary composition on energy expenditure during weight-loss maintenance has not been studied.Objective To examine the effects of 3 diets differing widely in macronutrient composition and glycemic load on energy expenditure following weight loss.Design, Setting, and Participants A controlled 3-way crossover design involving 21 overweight and obese young adults conducted at Children's Hospital Boston and Brigham and Women's Hospital, Boston, Massachusetts, between June 16, 2006, and June 21, 2010, with recruitment by newspaper advertisements and postings.Intervention After achieving 10% to 15% weight loss while consuming a run-in diet, participants consumed an isocaloric low-fat diet (60% of energy from carbohydrate, 20% from fat, 20% from protein; high glycemic load), low–glycemic index diet (40% from carbohydrate, 40% from fat, and 20% from protein; moderate glycemic load), and very low-carbohydrate diet (10% from carbohydrate, 60% from fat, and 30% from protein; low glycemic load) in random order, each for 4 weeks.Main Outcome Measures Primary outcome was resting energy expenditure (REE), with secondary outcomes of total energy expenditure (TEE), hormone levels, and metabolic syndrome components.Results Compared with the pre–weight-loss baseline, the decrease in REE was greatest with the low-fat diet (mean [95% CI], –205 [–265 to –144] kcal/d), intermediate with the low–glycemic index diet (–166 [–227 to –106] kcal/d), and least with the very low-carbohydrate diet (−138 [–198 to –77] kcal/d; overall P = .03; P for trend by glycemic load = .009). The decrease in TEE showed a similar pattern (mean [95% CI], −423 [–606 to –239] kcal/d; −297 [–479 to –115] kcal/d; and −97 [–281 to 86] kcal/d, respectively; overall P = .003; P for trend by glycemic load < .001). Hormone levels and metabolic syndrome components also varied during weight maintenance by diet (leptin, P < .001; 24-hour urinary cortisol, P = .005; indexes of peripheral [P = .02] and hepatic [P = .03] insulin sensitivity; high-density lipoprotein [HDL] cholesterol, P < .001; non-HDL cholesterol, P < .001; triglycerides, P < .001; plasminogen activator inhibitor 1, P for trend = .04; and C-reactive protein, P for trend = .05), but no consistent favorable pattern emerged.Conclusion Among overweight and obese young adults compared with pre–weight-loss energy expenditure, isocaloric feeding following 10% to 15% weight loss resulted in decreases in REE and TEE that were greatest with the low-fat diet, intermediate with the low–glycemic index diet, and least with the very low-carbohydrate diet.Trial Registration clinicaltrials.gov Identifier: NCT00315354", "publicationTitle": "JAMA", "publisher": "", "place": "", "date": "June 27, 2012", "volume": "307", "issue": "24", "section": "", "partNumber": "", "partTitle": "", "pages": "2627-2634", "series": "", "seriesTitle": "", "seriesText": "", "journalAbbreviation": "JAMA", "DOI": "10.1001/jama.2012.6607", "citationKey": "", "url": "http://dx.doi.org/10.1001/jama.2012.6607", "accessDate": "2014-05-17T19:44:41Z", "PMID": "", "PMCID": "", "ISSN": "0098-7484", "archive": "", "archiveLocation": "", "shortTitle": "", "language": "", "libraryCatalog": "Silverchair", "callNumber": "", "rights": "", "extra": "", "tags": [ { "tag": "carbohydrates" }, { "tag": "diet" }, { "tag": "obesity" } ], "collections": [], "relations": {}, "dateAdded": "2014-05-17T19:44:41Z", "dateModified": "2014-05-17T19:44:41Z" } }, { "key": "GM57DUER", "version": 31, "library": { "type": "group", "id": 139325, "name": "Carbohydrate Metabolism", "links": { "alternate": { "href": "https://www.zotero.org/groups/carbohydrate_metabolism", "type": "text/html" } } }, "links": { "self": { "href": "https://api.zotero.org/groups/139325/items/GM57DUER", "type": "application/json" }, "alternate": { "href": "https://www.zotero.org/groups/carbohydrate_metabolism/items/GM57DUER", "type": "text/html" }, "up": { "href": "https://api.zotero.org/groups/139325/items/H7ND8BRR", "type": "application/json" } }, "meta": { "createdByUser": { "id": 181756, "username": "rwesley007", "name": "", "links": { "alternate": { "href": "https://www.zotero.org/rwesley007", "type": "text/html" } } }, "numChildren": 0 }, "data": { "key": "GM57DUER", "version": 31, "parentItem": "H7ND8BRR", "itemType": "attachment", "linkMode": "imported_url", "title": "Ludwig DS_Friedman MI_2014_Increasing adiposity.pdf", "accessDate": "2014-05-17T19:35:02Z", "url": "http://jama.jamanetwork.com/data/Journals/JAMA/0/jvp140055.pdf", "note": "", "contentType": "application/pdf", "charset": "", "filename": "Ludwig DS_Friedman MI_2014_Increasing adiposity.pdf", "md5": "a9ff410240b6fa371f4b25eaac9750cb", "mtime": 1400355305836, "tags": [], "relations": {}, "dateAdded": "2014-05-17T19:35:02Z", "dateModified": "2014-05-17T19:35:07Z" } }, { "key": "H7ND8BRR", "version": 30, "library": { "type": "group", "id": 139325, "name": "Carbohydrate Metabolism", "links": { "alternate": { "href": "https://www.zotero.org/groups/carbohydrate_metabolism", "type": "text/html" } } }, "links": { "self": { "href": "https://api.zotero.org/groups/139325/items/H7ND8BRR", "type": "application/json" }, "alternate": { "href": "https://www.zotero.org/groups/carbohydrate_metabolism/items/H7ND8BRR", "type": "text/html" } }, "meta": { "createdByUser": { "id": 181756, "username": "rwesley007", "name": "", "links": { "alternate": { "href": "https://www.zotero.org/rwesley007", "type": "text/html" } } }, "creatorSummary": "Ludwig DS and Friedman MI", "parsedDate": "2014-05-16", "numChildren": 1 }, "data": { "key": "H7ND8BRR", "version": 30, "itemType": "journalArticle", "title": "Increasing adiposity: Consequence or cause of overeating?", "creators": [ { "creatorType": "author", "name": "Ludwig DS" }, { "creatorType": "author", "name": "Friedman MI" } ], "abstractNote": "Ninety years ago, an editorial in JAMA questioned the prevailing approach to obesity treatment: “When we read that ‘the fat woman has the remedy in her own hands—or rather between her own teeth’ . . . there is an implication that obesity is usually merely the result of unsatisfactory dietary bookkeeping. . . [Although logic suggests that body fat] may be decreased by altering the balance sheet through diminished intake, or increased output, or both . . . [t]he problem is not really so simple and uncomplicated as it is pictured.”1 Since then, billions of dollars have been spent on research into the biological factors affecting body weight, but the near-universal remedy remains virtually the same, to eat less and move more. According to an alternative view, chronic overeating represents a manifestation rather than the primary cause of increasing adiposity. Attempts to lower body weight without addressing the biological drivers of weight gain, including the quality of the diet, will inevitably fail for most individuals. 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